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Gene Information
Gene symbol: PSIP1
Gene name: PC4 and SFRS1 interacting protein 1
HGNC ID: 9527
Synonyms: p52, LEDGF, p75
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 7739516 | Carboxy-terminal deletion reduces the extent of maximal inhibition produced by rapamycin, from > 95% in the full-length p70 to 60 to 80% in p70 delta CT104, without altering the sensitivity to rapamycin inhibition (50% inhibitory concentration of 2 nM). |
| 2 | 8516328 | Nerve growth factor induces neuron-like differentiation of an insulin-secreting pancreatic beta cell line. |
| 3 | 8516328 | Here we demonstrate that RINm5F, a rat insulinoma cell line representing an early stage in pancreatic beta cell differentiation, expresses both the Trk and p75 NGF receptors and responds to NGF by extending neurite-like (neurofilament-containing) processes. |
| 4 | 8546031 | To investigate whether the failure of axonal regeneration could be related to a lack of NGF receptor production by Schwann cells, we examined the expression of p75 NGF receptors by Büngner bands immunocytochemically. |
| 5 | 8546031 | In comparison with other types of peripheral neuropathy, p75 NGF receptor expression appeared to take place normally. |
| 6 | 8546031 | To investigate whether the failure of axonal regeneration could be related to a lack of NGF receptor production by Schwann cells, we examined the expression of p75 NGF receptors by Büngner bands immunocytochemically. |
| 7 | 8546031 | In comparison with other types of peripheral neuropathy, p75 NGF receptor expression appeared to take place normally. |
| 8 | 9225754 | In this study we examined the expression of the neurotrophin receptor p75 (p75NTR) and the activation of macrophages in the sciatic nerve of rats at different time points after the induction of diabetes with streptozotocin (STZ). |
| 9 | 9237802 | We report the establishment and characterization of a T cell line (19KW) that reacts to purified 52 kDa islet protein (purified p52) from a subject with IDDM. |
| 10 | 9237802 | T cell lines specifically reactive to p52 may be useful for investigating further the role of this antigen in the pathogenesis of IDDM. |
| 11 | 9237802 | We report the establishment and characterization of a T cell line (19KW) that reacts to purified 52 kDa islet protein (purified p52) from a subject with IDDM. |
| 12 | 9237802 | T cell lines specifically reactive to p52 may be useful for investigating further the role of this antigen in the pathogenesis of IDDM. |
| 13 | 9664082 | TNF-alpha may play a role in mediating insulin resistance associated with obesity. |
| 14 | 9664082 | TNF elicits cellular responses via two receptors called p55 and p75. |
| 15 | 9664082 | In addition, high-fat diet-fed p75(-)/- mice had the lowest body weights and leptin levels, and improved insulin sensitivity. |
| 16 | 9664082 | Our data do not support the concept that TNF, acting via its receptors, is a major contributor to obesity-associated insulin resistance. |
| 17 | 10222115 | Immunoreactivity for the NGF receptors trkA and p75(NTR) was decreased and increased, respectively, between days 3 and 28 in right atria from diabetic rats and returned to pretreatment levels at day 49. |
| 18 | 10320052 | Mechanisms of TNF-alpha-induced insulin resistance. |
| 19 | 10320052 | There is now substantial evidence linking TNF-alpha to the presentation of insulin resistance in humans, animals and in vitro systems. |
| 20 | 10320052 | We explored the relationship between TNF-alpha and insulin resistance using knockout mice deficient for either TNF-alpha or one or both of its receptors, p55 and p75. |
| 21 | 10320052 | In studies of TNF-alpha-deficient knockout mice with diet-induced obesity, obese TNF-alpha knockouts responded to an exogenous dose of insulin or glucose much more efficiently than TNF-alpha wild-type animals. |
| 22 | 10320052 | This finding suggests that deletion of TNF-alpha leads to increased insulin sensitivity, ie decreased insulin resistance. |
| 23 | 10320052 | Since the improvement in sensitivity was slightly greater with double mutants, p55 alone cannot be responsible for TNF-alpha's promotion of insulin resistance in obese mice, despite the likelihood that it is more important than p75. |
| 24 | 10320052 | How TNF-alpha-related insulin resistance is mediated is not fully clear, although phosphorylation of serine residues on IRS-1 has previously been shown to be important. |
| 25 | 10320052 | When we monitored Glut 4 expression in obese TNF-alpha wild-type and knockout mice, we found no convincing evidence that TNF-alpha mediation of the down-regulation of Glut 4 mRNA expression is responsible for insulin resistance. |
| 26 | 10320052 | However, we found an approximately 2-fold increase in insulin-stimulated tyrosine phosphorylation of the insulin receptor in the muscle and adipose tissue of TNF-alpha knockout mice, suggesting that insulin receptor signalling is an important target for TNF-alpha. |
| 27 | 10320052 | Other possible mediators of TNF-alpha-induced insulin resistance include circulating free fatty acids (FFAs) and leptin. |
| 28 | 10440901 | Conversely, the mRNA expression of low-affinity neurotrophin receptor p75 was increased. |
| 29 | 10440901 | At birth, BDNF mRNA expression was affected with a significant generalized reduction,while in vibrissae we observed a reduction of BDNF and p75 mRNAs and an increase of NGF. |
| 30 | 10440901 | At postnatal day 14, pups from diabetic mothers showed reduced muscle levels of IGF-I, while we observed a partial impairment of substance P axonal transport at postnatal day 28. |
| 31 | 10440901 | In addition, these data suggest that nervous system abnormalities observed in diabetic embryopathy may also derive by insufficient neurotrophic factor biosynthesis involving sequentially NGF in the embryo and BDNF and IGF-I in the early postnatal days. |
| 32 | 10440901 | Conversely, the mRNA expression of low-affinity neurotrophin receptor p75 was increased. |
| 33 | 10440901 | At birth, BDNF mRNA expression was affected with a significant generalized reduction,while in vibrissae we observed a reduction of BDNF and p75 mRNAs and an increase of NGF. |
| 34 | 10440901 | At postnatal day 14, pups from diabetic mothers showed reduced muscle levels of IGF-I, while we observed a partial impairment of substance P axonal transport at postnatal day 28. |
| 35 | 10440901 | In addition, these data suggest that nervous system abnormalities observed in diabetic embryopathy may also derive by insufficient neurotrophic factor biosynthesis involving sequentially NGF in the embryo and BDNF and IGF-I in the early postnatal days. |
| 36 | 10567588 | The pronounced proteasome defect results in defective production and activation of the transcription factor NF-kappaB, which plays an important role in immune and inflammatory responses as well as in preventing apoptosis induced by tumor necrosis factor alpha. |
| 37 | 10567588 | The defect in proteasome function in NOD mouse splenocytes was evident from impaired NF-kappaB subunit p50 and p52 generation by proteolytic processing and impaired degradation of the NF-kappaB-inhibitory protein IkappaBalpha. |
| 38 | 10567588 | These data suggest that NOD proteasome dysfunction is due to a tissue- and developmental-stage-specific defect in expression of the MHC-linked Lmp2 gene, resulting in altered transcription factor NF-kappaB activity, and that this defect contributes to pathogenesis in NOD mice. |
| 39 | 10837808 | Effect of streptozotocin-induced diabetes on NGF, P75(NTR) and TrkA content of prevertebral and paravertebral rat sympathetic ganglia. |
| 40 | 10837808 | To test this hypothesis, we measured NGF content and NGF receptor expression, p75(NTR) (low affinity neurotrophin receptor) and trkA (high affinity NGF receptor), in control and diabetic rat SMG, CG and superior cervical ganglia (SCG). |
| 41 | 10837808 | Surprisingly, rather than a decrease, we observed an approximate doubling of NGF content in the diabetic SMG and CG, a result which reflects increased NGF content in the hyperplastic diabetic alimentary tract. |
| 42 | 10837808 | NGF receptor expression was not consistently altered in any of the autonomic ganglia. |
| 43 | 10837808 | Effect of streptozotocin-induced diabetes on NGF, P75(NTR) and TrkA content of prevertebral and paravertebral rat sympathetic ganglia. |
| 44 | 10837808 | To test this hypothesis, we measured NGF content and NGF receptor expression, p75(NTR) (low affinity neurotrophin receptor) and trkA (high affinity NGF receptor), in control and diabetic rat SMG, CG and superior cervical ganglia (SCG). |
| 45 | 10837808 | Surprisingly, rather than a decrease, we observed an approximate doubling of NGF content in the diabetic SMG and CG, a result which reflects increased NGF content in the hyperplastic diabetic alimentary tract. |
| 46 | 10837808 | NGF receptor expression was not consistently altered in any of the autonomic ganglia. |
| 47 | 11483249 | At postsurgical day 14, nerves were excised and analysed for levels of axonal markers, total and phosphorylated neurofilament, and Schwann cell receptors, ErbB2 and p75(NTR), using immunohistochemistry and Western blotting. |
| 48 | 11483249 | ErbB2 was decreased in grafts from diabetic rats (53% of control, P<0.05) and p75(NTR) levels were increased in both types of graft in diabetic rats (to 300-400% of controls, P<0.05). |
| 49 | 11483249 | At postsurgical day 14, nerves were excised and analysed for levels of axonal markers, total and phosphorylated neurofilament, and Schwann cell receptors, ErbB2 and p75(NTR), using immunohistochemistry and Western blotting. |
| 50 | 11483249 | ErbB2 was decreased in grafts from diabetic rats (53% of control, P<0.05) and p75(NTR) levels were increased in both types of graft in diabetic rats (to 300-400% of controls, P<0.05). |
| 51 | 11589428 | Sciatic nerve mRNA expression of IGF-I, IGF-1-receptor, NGF, and p75 (low affinity NGF receptor), as well as protein expression of C-FOS, were examined at various time points following crush injury and compared with age- and sex-matched nondiabetic BB/Wor rats. |
| 52 | 11589428 | Diabetic rats showed a delay in the early peak expression of IGF-1, C-FOS, NGF, and p75. |
| 53 | 11589428 | The delayed IGF-1 expression may affect C-FOS induction and may be responsible for the delay in the NGF response in diabetic rats. |
| 54 | 11589428 | Sciatic nerve mRNA expression of IGF-I, IGF-1-receptor, NGF, and p75 (low affinity NGF receptor), as well as protein expression of C-FOS, were examined at various time points following crush injury and compared with age- and sex-matched nondiabetic BB/Wor rats. |
| 55 | 11589428 | Diabetic rats showed a delay in the early peak expression of IGF-1, C-FOS, NGF, and p75. |
| 56 | 11589428 | The delayed IGF-1 expression may affect C-FOS induction and may be responsible for the delay in the NGF response in diabetic rats. |
| 57 | 11723053 | The levels of insulin-stimulated tyrosine phosphorylation of the insulin receptor beta-subunit, insulin receptor substrate (IRS)-2, and p52(Shc) were increased in diabetic compared with control heart, whereas tyrosine phosphorylation of IRS-1 was unchanged. |
| 58 | 11723053 | The amount of the p85 subunit of phosphatidylinositol 3-kinase (PI 3-kinase) and the level of PI 3-kinase activity associated with IRS-2 were also elevated in diabetes, whereas no changes in IRS-1-associated PI 3-kinase were observed. |
| 59 | 11723053 | Insulin-induced phosphorylation of Akt on Thr-308 was increased fivefold in diabetic heart, whereas Akt phosphorylation on Ser-473 was normal. |
| 60 | 11723053 | In contrast with Akt phosphorylation, insulin-induced phosphorylation of glycogen synthase kinase (GSK)-3, a major cellular substrate of Akt, was markedly reduced in diabetes. |
| 61 | 11723053 | In islet-transplanted rats, the majority of the alterations in insulin-signaling proteins found in diabetic rats were normalized, but insulin stimulation of IRS-2 tyrosine phosphorylation and association with PI 3-kinase was blunted. |
| 62 | 11723053 | In conclusion, in the diabetic heart, 1) IRS-1, IRS-2, and p52(Shc) are differently altered, 2) the levels of Akt phosphorylation on Ser-473 and Thr-308, respectively, are not coordinately regulated, and 3) the increased activity of proximal-signaling proteins (i.e., IRS-2 and PI 3-kinase) is not propagated distally to GSK-3. |
| 63 | 11723053 | The levels of insulin-stimulated tyrosine phosphorylation of the insulin receptor beta-subunit, insulin receptor substrate (IRS)-2, and p52(Shc) were increased in diabetic compared with control heart, whereas tyrosine phosphorylation of IRS-1 was unchanged. |
| 64 | 11723053 | The amount of the p85 subunit of phosphatidylinositol 3-kinase (PI 3-kinase) and the level of PI 3-kinase activity associated with IRS-2 were also elevated in diabetes, whereas no changes in IRS-1-associated PI 3-kinase were observed. |
| 65 | 11723053 | Insulin-induced phosphorylation of Akt on Thr-308 was increased fivefold in diabetic heart, whereas Akt phosphorylation on Ser-473 was normal. |
| 66 | 11723053 | In contrast with Akt phosphorylation, insulin-induced phosphorylation of glycogen synthase kinase (GSK)-3, a major cellular substrate of Akt, was markedly reduced in diabetes. |
| 67 | 11723053 | In islet-transplanted rats, the majority of the alterations in insulin-signaling proteins found in diabetic rats were normalized, but insulin stimulation of IRS-2 tyrosine phosphorylation and association with PI 3-kinase was blunted. |
| 68 | 11723053 | In conclusion, in the diabetic heart, 1) IRS-1, IRS-2, and p52(Shc) are differently altered, 2) the levels of Akt phosphorylation on Ser-473 and Thr-308, respectively, are not coordinately regulated, and 3) the increased activity of proximal-signaling proteins (i.e., IRS-2 and PI 3-kinase) is not propagated distally to GSK-3. |
| 69 | 11867071 | Macrophage infiltration and death in the nerve during the early phases of experimental diabetic neuropathy: a process concomitant with endoneurial induction of IL-1beta and p75NTR. |
| 70 | 11867071 | This study describes the infiltration and death of monocyte/macrophages and concomitant endoneurial expression of the pro-inflammatory cytokine interleukin-1beta (IL-1beta) and neurotrophin receptor p75 (p75NTR) in the sciatic nerve at the early phases of experimental diabetic neuropathy induced in Lewis rats by streptozotocin (STZ) intraperitoneal injection. |
| 71 | 11867071 | IL-1beta was evident in scattered macrophages, and along few isolated nerve fibers until week 5, when it became undetectable, in concomitance with complete endoneurial clearance of macrophages. p75NTR showed an up-regulation in the sciatic nerve of diabetic rats that began by week 3 after STZ administration, reached its peak by week 5, and returned then to a barely detectable level by week 6. |
| 72 | 11867071 | These findings seem to indicate that macrophages and IL-1beta may be involved in the pathogenesis of diabetic neuropathy, participating not only to nerve damage but also to the promotion of an attempt of regeneration via p75NTR induction. |
| 73 | 12031555 | A decreased axonal accumulation of endogenous nerve growth factor (NGF) and neurotrophin-3 (NT-3) in the vagus nerve of streptozotocin (STZ)-induced diabetic rats was previously shown. |
| 74 | 12031555 | In the current study, no changes in the NGF and NT-3 protein or mRNA levels in the stomach or atrium, two vagally innervated organs, were noted after 16 or 24 weeks of diabetes. |
| 75 | 12031555 | Moreover, the amounts of neurotrophin receptor (p75, TrkA, TrkC) mRNAs in the vagus nerve and vagal afferent nodose ganglion were not reduced in diabetic rats. |
| 76 | 12387452 | We have previously suggested that alterations in sequential early gene responses of trophic factors (IGF-1 -->c-fos-->NGF) contribute to impaired peripheral nerve regeneration in type 1 diabetic BB/W-rats. |
| 77 | 12387452 | The expression of IGF-1, c-fos, NGF and the receptors p75 and IGF-1R were determined at the protein and mRNA levels in sciatic nerve distal to the crush site by immunoblotting and semi-quantitative RT-PCR. |
| 78 | 12387452 | In situ hybridization was performed to assess the cellular localization of IGF-1, NGF, p75, and IGF-1R mRNA and immunohistochemistry served to localize the source of p75 and IGF-1R protein expression. |
| 79 | 12387452 | IGF-1R was expressed in Schwann cells and its expression was asynchronous to IGF-1 expression in type 1 rats but remained synchronous with IGF-1 in control and type 2 animals. |
| 80 | 12387452 | We have previously suggested that alterations in sequential early gene responses of trophic factors (IGF-1 -->c-fos-->NGF) contribute to impaired peripheral nerve regeneration in type 1 diabetic BB/W-rats. |
| 81 | 12387452 | The expression of IGF-1, c-fos, NGF and the receptors p75 and IGF-1R were determined at the protein and mRNA levels in sciatic nerve distal to the crush site by immunoblotting and semi-quantitative RT-PCR. |
| 82 | 12387452 | In situ hybridization was performed to assess the cellular localization of IGF-1, NGF, p75, and IGF-1R mRNA and immunohistochemistry served to localize the source of p75 and IGF-1R protein expression. |
| 83 | 12387452 | IGF-1R was expressed in Schwann cells and its expression was asynchronous to IGF-1 expression in type 1 rats but remained synchronous with IGF-1 in control and type 2 animals. |
| 84 | 15448099 | To evaluate the possible role of neuropeptide immunoreactive primary sensory neurons on the development of nociceptive dysfunction in diabetes, the absolute numbers of immunoreactive substance P and calcitonin gene-related peptide (CGRP) dorsal root ganglion (DRG) cell bodies were estimated in diabetic and nondiabetic BALB/C (p75(+/+)) and p75 receptor knockout (p75(-/-)) mice with unilateral sciatic nerve crush. |
| 85 | 15448099 | The total numbers of immunoreactive substance P A-cells, substance P B-cells, CGRP A-cells, and CGRP B-cells in L5DRG were estimated using semithick consecutive sections and the optical fractionator. |
| 86 | 15448099 | In p75(+/+) and p75(-/-) mice, there was no effect of diabetes on the immunoreactive CGRP B-cell number, nor was there any effect of diabetes on the immunoreactive substance P B-cell number. |
| 87 | 15448099 | It is concluded that experimental diabetes in the mouse is associated with loss of immunoreactive CGRP primary sensory neurons of the A-cell phenotype, that this loss could play a role for the touch-evoked nociception in the model, and that the neuronal immunoreactive CGRP abnormality possibly is mediated by activation of the p75 neurotrophin receptor. |
| 88 | 15589046 | Here, we report the occurrence of a decrease in general innervation within the islets in the nonobese diabetic (NOD) mouse, and the establishment of strands of Schwann cells, as detected via p75 and S-100 immunoreactivity (IR), and varicose nerve fibers expressing tyrosine kinase A (TrkA) in association with the immune cells. |
| 89 | 15665408 | Neurotrophins activate a number of signaling pathways relevant to neuroprotection; however, their poor pharmacological properties and their pleiotropic effects resulting from interaction with the p75(NTR)-Trk-sortilin three-receptor signaling system limit therapeutic application. |
| 90 | 15665408 | The expression of p75(NTR) by populations of neurons most vulnerable in Alzheimer's disease and the linkage of p75(NTR) signaling to aberrant signaling mechanisms occurring in this disorder, point to potential applications for p75(NTR)-based small molecule strategies. |
| 91 | 15665408 | Small molecules targeted to p75(NTR) in the settings of neurodegenerative disease and other forms of neural injury might serve to inhibit death signaling, block proNGF-mediated degenerative signaling and minimize deleterious effects promoted by pharmacologically upregulated Trk signaling. |
| 92 | 15665408 | Neurotrophins activate a number of signaling pathways relevant to neuroprotection; however, their poor pharmacological properties and their pleiotropic effects resulting from interaction with the p75(NTR)-Trk-sortilin three-receptor signaling system limit therapeutic application. |
| 93 | 15665408 | The expression of p75(NTR) by populations of neurons most vulnerable in Alzheimer's disease and the linkage of p75(NTR) signaling to aberrant signaling mechanisms occurring in this disorder, point to potential applications for p75(NTR)-based small molecule strategies. |
| 94 | 15665408 | Small molecules targeted to p75(NTR) in the settings of neurodegenerative disease and other forms of neural injury might serve to inhibit death signaling, block proNGF-mediated degenerative signaling and minimize deleterious effects promoted by pharmacologically upregulated Trk signaling. |
| 95 | 15665408 | Neurotrophins activate a number of signaling pathways relevant to neuroprotection; however, their poor pharmacological properties and their pleiotropic effects resulting from interaction with the p75(NTR)-Trk-sortilin three-receptor signaling system limit therapeutic application. |
| 96 | 15665408 | The expression of p75(NTR) by populations of neurons most vulnerable in Alzheimer's disease and the linkage of p75(NTR) signaling to aberrant signaling mechanisms occurring in this disorder, point to potential applications for p75(NTR)-based small molecule strategies. |
| 97 | 15665408 | Small molecules targeted to p75(NTR) in the settings of neurodegenerative disease and other forms of neural injury might serve to inhibit death signaling, block proNGF-mediated degenerative signaling and minimize deleterious effects promoted by pharmacologically upregulated Trk signaling. |
| 98 | 15857712 | Differential effect of p75 neurotrophin receptor on expression of pro-apoptotic proteins c-jun, p38 and caspase-3 in dorsal root ganglion cells after axotomy in experimental diabetes. |
| 99 | 15857712 | We have hypothesized that p75 neurotrophin receptor (p75(NTR))-mediated activation of the pro-apoptotic proteins c-jun, p38 and caspase-3 underlies the neuronal cell loss in dorsal root ganglia (DRG) neurons after axotomy in normal mice, and that this activation is exaggerated in experimental diabetes. |
| 100 | 15857712 | To test this hypothesized relationship, we compared the expression of pro-apoptotic proteins in fifth lumbar DRG (L5DRG) neurons of wildtype Balb/c (p75+/+) mice and p75(NTR) knockout (p75-/-) mice, assigned to either non-diabetic control groups or to diabetic (1 month) groups, all with a unilateral sciatic nerve crush produced 10 days before tissue preparation. |
| 101 | 15857712 | The absolute number of L5DRG neurons expressing immunoreactivities (IR) for phosphorylated c-jun (P-c-jun-IR), phosphorylated p-38 (P-p38-IR) and cleaved caspase-3 (caspase-3-IR) were estimated in semi-thick sections using the optical fractionator. |
| 102 | 15857712 | Nerve crush increased the numbers of P-c-jun-IR and caspase-3-IR neurons in all four groups. |
| 103 | 15857712 | On the crush side, diabetes did not exaggerate the increase of P-c-jun-IR or caspase-3-IR neurons in p75+/+ mice, whereas in p75-/- mice diabetes reduced the increase of P-c-jun-IR neurons. |
| 104 | 15857712 | This study demonstrates that (1) diabetes of 1 month's duration does not potentiate the expression of three pro-apoptotic markers p38, caspase-3 and P-c-jun neither in intact neurons nor after nerve crush, and that (2) p75(NTR) is required for activation of the pro-apoptosis signal caspase-3 after nerve crush in both diabetic and non-diabetic mice. |
| 105 | 15857712 | Differential effect of p75 neurotrophin receptor on expression of pro-apoptotic proteins c-jun, p38 and caspase-3 in dorsal root ganglion cells after axotomy in experimental diabetes. |
| 106 | 15857712 | We have hypothesized that p75 neurotrophin receptor (p75(NTR))-mediated activation of the pro-apoptotic proteins c-jun, p38 and caspase-3 underlies the neuronal cell loss in dorsal root ganglia (DRG) neurons after axotomy in normal mice, and that this activation is exaggerated in experimental diabetes. |
| 107 | 15857712 | To test this hypothesized relationship, we compared the expression of pro-apoptotic proteins in fifth lumbar DRG (L5DRG) neurons of wildtype Balb/c (p75+/+) mice and p75(NTR) knockout (p75-/-) mice, assigned to either non-diabetic control groups or to diabetic (1 month) groups, all with a unilateral sciatic nerve crush produced 10 days before tissue preparation. |
| 108 | 15857712 | The absolute number of L5DRG neurons expressing immunoreactivities (IR) for phosphorylated c-jun (P-c-jun-IR), phosphorylated p-38 (P-p38-IR) and cleaved caspase-3 (caspase-3-IR) were estimated in semi-thick sections using the optical fractionator. |
| 109 | 15857712 | Nerve crush increased the numbers of P-c-jun-IR and caspase-3-IR neurons in all four groups. |
| 110 | 15857712 | On the crush side, diabetes did not exaggerate the increase of P-c-jun-IR or caspase-3-IR neurons in p75+/+ mice, whereas in p75-/- mice diabetes reduced the increase of P-c-jun-IR neurons. |
| 111 | 15857712 | This study demonstrates that (1) diabetes of 1 month's duration does not potentiate the expression of three pro-apoptotic markers p38, caspase-3 and P-c-jun neither in intact neurons nor after nerve crush, and that (2) p75(NTR) is required for activation of the pro-apoptosis signal caspase-3 after nerve crush in both diabetic and non-diabetic mice. |
| 112 | 15857712 | Differential effect of p75 neurotrophin receptor on expression of pro-apoptotic proteins c-jun, p38 and caspase-3 in dorsal root ganglion cells after axotomy in experimental diabetes. |
| 113 | 15857712 | We have hypothesized that p75 neurotrophin receptor (p75(NTR))-mediated activation of the pro-apoptotic proteins c-jun, p38 and caspase-3 underlies the neuronal cell loss in dorsal root ganglia (DRG) neurons after axotomy in normal mice, and that this activation is exaggerated in experimental diabetes. |
| 114 | 15857712 | To test this hypothesized relationship, we compared the expression of pro-apoptotic proteins in fifth lumbar DRG (L5DRG) neurons of wildtype Balb/c (p75+/+) mice and p75(NTR) knockout (p75-/-) mice, assigned to either non-diabetic control groups or to diabetic (1 month) groups, all with a unilateral sciatic nerve crush produced 10 days before tissue preparation. |
| 115 | 15857712 | The absolute number of L5DRG neurons expressing immunoreactivities (IR) for phosphorylated c-jun (P-c-jun-IR), phosphorylated p-38 (P-p38-IR) and cleaved caspase-3 (caspase-3-IR) were estimated in semi-thick sections using the optical fractionator. |
| 116 | 15857712 | Nerve crush increased the numbers of P-c-jun-IR and caspase-3-IR neurons in all four groups. |
| 117 | 15857712 | On the crush side, diabetes did not exaggerate the increase of P-c-jun-IR or caspase-3-IR neurons in p75+/+ mice, whereas in p75-/- mice diabetes reduced the increase of P-c-jun-IR neurons. |
| 118 | 15857712 | This study demonstrates that (1) diabetes of 1 month's duration does not potentiate the expression of three pro-apoptotic markers p38, caspase-3 and P-c-jun neither in intact neurons nor after nerve crush, and that (2) p75(NTR) is required for activation of the pro-apoptosis signal caspase-3 after nerve crush in both diabetic and non-diabetic mice. |
| 119 | 15857712 | Differential effect of p75 neurotrophin receptor on expression of pro-apoptotic proteins c-jun, p38 and caspase-3 in dorsal root ganglion cells after axotomy in experimental diabetes. |
| 120 | 15857712 | We have hypothesized that p75 neurotrophin receptor (p75(NTR))-mediated activation of the pro-apoptotic proteins c-jun, p38 and caspase-3 underlies the neuronal cell loss in dorsal root ganglia (DRG) neurons after axotomy in normal mice, and that this activation is exaggerated in experimental diabetes. |
| 121 | 15857712 | To test this hypothesized relationship, we compared the expression of pro-apoptotic proteins in fifth lumbar DRG (L5DRG) neurons of wildtype Balb/c (p75+/+) mice and p75(NTR) knockout (p75-/-) mice, assigned to either non-diabetic control groups or to diabetic (1 month) groups, all with a unilateral sciatic nerve crush produced 10 days before tissue preparation. |
| 122 | 15857712 | The absolute number of L5DRG neurons expressing immunoreactivities (IR) for phosphorylated c-jun (P-c-jun-IR), phosphorylated p-38 (P-p38-IR) and cleaved caspase-3 (caspase-3-IR) were estimated in semi-thick sections using the optical fractionator. |
| 123 | 15857712 | Nerve crush increased the numbers of P-c-jun-IR and caspase-3-IR neurons in all four groups. |
| 124 | 15857712 | On the crush side, diabetes did not exaggerate the increase of P-c-jun-IR or caspase-3-IR neurons in p75+/+ mice, whereas in p75-/- mice diabetes reduced the increase of P-c-jun-IR neurons. |
| 125 | 15857712 | This study demonstrates that (1) diabetes of 1 month's duration does not potentiate the expression of three pro-apoptotic markers p38, caspase-3 and P-c-jun neither in intact neurons nor after nerve crush, and that (2) p75(NTR) is required for activation of the pro-apoptosis signal caspase-3 after nerve crush in both diabetic and non-diabetic mice. |
| 126 | 17884819 | Mice deficient in the NF-kappaB subunits p50 and p52 have retarded growth, suggesting that NF-kappaB is involved in bone growth. |
| 127 | 17884819 | To further define the underlying mechanisms, we studied the functional interaction between NF-kappaB p65 and BMP-2 in chondrocytes. |
| 128 | 17884819 | In cultured chondrocytes, the inhibition of NF-kappaB p65 activation (by PDTC and BAY) and expression (by p65 siRNA) led to the same findings observed in cultured metatarsal bones. |
| 129 | 17884819 | The addition of Noggin, a BMP-2 antagonist, neutralized the stimulatory effects of p65 on chondrocyte proliferation and differentiation, as well as its anti-apoptotic effect. |
| 130 | 17884819 | In conclusion, our findings indicate that NF-kappaB p65 expressed in growth plate chondrocytes facilitates growth plate chondrogenesis and longitudinal bone growth by inducing BMP-2 expression and activity. |
| 131 | 18566344 | Neurotrophin p75 receptor (p75NTR) promotes endothelial cell apoptosis and inhibits angiogenesis: implications for diabetes-induced impaired neovascularization in ischemic limb muscles. |
| 132 | 18566344 | The p75 receptor of neurotrophins (p75(NTR)), which is scarcely present in healthy endothelial cells (ECs), becomes strongly expressed by capillary ECs after induction of peripheral ischemia in type-1 diabetic mice. |
| 133 | 18566344 | Here, we show that gene transfer-induced p75(NTR) expression impairs the survival, proliferation, migration, and adhesion capacities of cultured ECs and endothelial progenitor cells (EPCs) and inhibits angiogenesis in vitro. |
| 134 | 18566344 | Moreover, intramuscular p75(NTR) gene delivery impairs neovascularization and blood flow recovery in a mouse model of limb ischemia. |
| 135 | 18566344 | In fact, p75(NTR) depresses the VEGF-A/Akt/eNOS/NO pathway and additionally reduces the mRNA levels of ITGB1 [beta (1) integrin], BIRC5 (survivin), PTTG1 (securin) and VEZF1. |
| 136 | 18566344 | Diabetic mice, which typically show impaired postischemic muscular neovascularization and blood perfusion recovery, have these defects corrected by intramuscular gene transfer of a dominant negative mutant form of p75(NTR). |
| 137 | 18566344 | Collectively, our data newly demonstrate the antiangiogenic action of p75(NTR) and open new avenues for the therapeutic use of p75(NTR) inhibition to combat diabetes-induced microvascular liabilities. |
| 138 | 18566344 | Neurotrophin p75 receptor (p75NTR) promotes endothelial cell apoptosis and inhibits angiogenesis: implications for diabetes-induced impaired neovascularization in ischemic limb muscles. |
| 139 | 18566344 | The p75 receptor of neurotrophins (p75(NTR)), which is scarcely present in healthy endothelial cells (ECs), becomes strongly expressed by capillary ECs after induction of peripheral ischemia in type-1 diabetic mice. |
| 140 | 18566344 | Here, we show that gene transfer-induced p75(NTR) expression impairs the survival, proliferation, migration, and adhesion capacities of cultured ECs and endothelial progenitor cells (EPCs) and inhibits angiogenesis in vitro. |
| 141 | 18566344 | Moreover, intramuscular p75(NTR) gene delivery impairs neovascularization and blood flow recovery in a mouse model of limb ischemia. |
| 142 | 18566344 | In fact, p75(NTR) depresses the VEGF-A/Akt/eNOS/NO pathway and additionally reduces the mRNA levels of ITGB1 [beta (1) integrin], BIRC5 (survivin), PTTG1 (securin) and VEZF1. |
| 143 | 18566344 | Diabetic mice, which typically show impaired postischemic muscular neovascularization and blood perfusion recovery, have these defects corrected by intramuscular gene transfer of a dominant negative mutant form of p75(NTR). |
| 144 | 18566344 | Collectively, our data newly demonstrate the antiangiogenic action of p75(NTR) and open new avenues for the therapeutic use of p75(NTR) inhibition to combat diabetes-induced microvascular liabilities. |
| 145 | 18566344 | Neurotrophin p75 receptor (p75NTR) promotes endothelial cell apoptosis and inhibits angiogenesis: implications for diabetes-induced impaired neovascularization in ischemic limb muscles. |
| 146 | 18566344 | The p75 receptor of neurotrophins (p75(NTR)), which is scarcely present in healthy endothelial cells (ECs), becomes strongly expressed by capillary ECs after induction of peripheral ischemia in type-1 diabetic mice. |
| 147 | 18566344 | Here, we show that gene transfer-induced p75(NTR) expression impairs the survival, proliferation, migration, and adhesion capacities of cultured ECs and endothelial progenitor cells (EPCs) and inhibits angiogenesis in vitro. |
| 148 | 18566344 | Moreover, intramuscular p75(NTR) gene delivery impairs neovascularization and blood flow recovery in a mouse model of limb ischemia. |
| 149 | 18566344 | In fact, p75(NTR) depresses the VEGF-A/Akt/eNOS/NO pathway and additionally reduces the mRNA levels of ITGB1 [beta (1) integrin], BIRC5 (survivin), PTTG1 (securin) and VEZF1. |
| 150 | 18566344 | Diabetic mice, which typically show impaired postischemic muscular neovascularization and blood perfusion recovery, have these defects corrected by intramuscular gene transfer of a dominant negative mutant form of p75(NTR). |
| 151 | 18566344 | Collectively, our data newly demonstrate the antiangiogenic action of p75(NTR) and open new avenues for the therapeutic use of p75(NTR) inhibition to combat diabetes-induced microvascular liabilities. |
| 152 | 18566344 | Neurotrophin p75 receptor (p75NTR) promotes endothelial cell apoptosis and inhibits angiogenesis: implications for diabetes-induced impaired neovascularization in ischemic limb muscles. |
| 153 | 18566344 | The p75 receptor of neurotrophins (p75(NTR)), which is scarcely present in healthy endothelial cells (ECs), becomes strongly expressed by capillary ECs after induction of peripheral ischemia in type-1 diabetic mice. |
| 154 | 18566344 | Here, we show that gene transfer-induced p75(NTR) expression impairs the survival, proliferation, migration, and adhesion capacities of cultured ECs and endothelial progenitor cells (EPCs) and inhibits angiogenesis in vitro. |
| 155 | 18566344 | Moreover, intramuscular p75(NTR) gene delivery impairs neovascularization and blood flow recovery in a mouse model of limb ischemia. |
| 156 | 18566344 | In fact, p75(NTR) depresses the VEGF-A/Akt/eNOS/NO pathway and additionally reduces the mRNA levels of ITGB1 [beta (1) integrin], BIRC5 (survivin), PTTG1 (securin) and VEZF1. |
| 157 | 18566344 | Diabetic mice, which typically show impaired postischemic muscular neovascularization and blood perfusion recovery, have these defects corrected by intramuscular gene transfer of a dominant negative mutant form of p75(NTR). |
| 158 | 18566344 | Collectively, our data newly demonstrate the antiangiogenic action of p75(NTR) and open new avenues for the therapeutic use of p75(NTR) inhibition to combat diabetes-induced microvascular liabilities. |
| 159 | 18566344 | Neurotrophin p75 receptor (p75NTR) promotes endothelial cell apoptosis and inhibits angiogenesis: implications for diabetes-induced impaired neovascularization in ischemic limb muscles. |
| 160 | 18566344 | The p75 receptor of neurotrophins (p75(NTR)), which is scarcely present in healthy endothelial cells (ECs), becomes strongly expressed by capillary ECs after induction of peripheral ischemia in type-1 diabetic mice. |
| 161 | 18566344 | Here, we show that gene transfer-induced p75(NTR) expression impairs the survival, proliferation, migration, and adhesion capacities of cultured ECs and endothelial progenitor cells (EPCs) and inhibits angiogenesis in vitro. |
| 162 | 18566344 | Moreover, intramuscular p75(NTR) gene delivery impairs neovascularization and blood flow recovery in a mouse model of limb ischemia. |
| 163 | 18566344 | In fact, p75(NTR) depresses the VEGF-A/Akt/eNOS/NO pathway and additionally reduces the mRNA levels of ITGB1 [beta (1) integrin], BIRC5 (survivin), PTTG1 (securin) and VEZF1. |
| 164 | 18566344 | Diabetic mice, which typically show impaired postischemic muscular neovascularization and blood perfusion recovery, have these defects corrected by intramuscular gene transfer of a dominant negative mutant form of p75(NTR). |
| 165 | 18566344 | Collectively, our data newly demonstrate the antiangiogenic action of p75(NTR) and open new avenues for the therapeutic use of p75(NTR) inhibition to combat diabetes-induced microvascular liabilities. |
| 166 | 18566344 | Neurotrophin p75 receptor (p75NTR) promotes endothelial cell apoptosis and inhibits angiogenesis: implications for diabetes-induced impaired neovascularization in ischemic limb muscles. |
| 167 | 18566344 | The p75 receptor of neurotrophins (p75(NTR)), which is scarcely present in healthy endothelial cells (ECs), becomes strongly expressed by capillary ECs after induction of peripheral ischemia in type-1 diabetic mice. |
| 168 | 18566344 | Here, we show that gene transfer-induced p75(NTR) expression impairs the survival, proliferation, migration, and adhesion capacities of cultured ECs and endothelial progenitor cells (EPCs) and inhibits angiogenesis in vitro. |
| 169 | 18566344 | Moreover, intramuscular p75(NTR) gene delivery impairs neovascularization and blood flow recovery in a mouse model of limb ischemia. |
| 170 | 18566344 | In fact, p75(NTR) depresses the VEGF-A/Akt/eNOS/NO pathway and additionally reduces the mRNA levels of ITGB1 [beta (1) integrin], BIRC5 (survivin), PTTG1 (securin) and VEZF1. |
| 171 | 18566344 | Diabetic mice, which typically show impaired postischemic muscular neovascularization and blood perfusion recovery, have these defects corrected by intramuscular gene transfer of a dominant negative mutant form of p75(NTR). |
| 172 | 18566344 | Collectively, our data newly demonstrate the antiangiogenic action of p75(NTR) and open new avenues for the therapeutic use of p75(NTR) inhibition to combat diabetes-induced microvascular liabilities. |
| 173 | 18566344 | Neurotrophin p75 receptor (p75NTR) promotes endothelial cell apoptosis and inhibits angiogenesis: implications for diabetes-induced impaired neovascularization in ischemic limb muscles. |
| 174 | 18566344 | The p75 receptor of neurotrophins (p75(NTR)), which is scarcely present in healthy endothelial cells (ECs), becomes strongly expressed by capillary ECs after induction of peripheral ischemia in type-1 diabetic mice. |
| 175 | 18566344 | Here, we show that gene transfer-induced p75(NTR) expression impairs the survival, proliferation, migration, and adhesion capacities of cultured ECs and endothelial progenitor cells (EPCs) and inhibits angiogenesis in vitro. |
| 176 | 18566344 | Moreover, intramuscular p75(NTR) gene delivery impairs neovascularization and blood flow recovery in a mouse model of limb ischemia. |
| 177 | 18566344 | In fact, p75(NTR) depresses the VEGF-A/Akt/eNOS/NO pathway and additionally reduces the mRNA levels of ITGB1 [beta (1) integrin], BIRC5 (survivin), PTTG1 (securin) and VEZF1. |
| 178 | 18566344 | Diabetic mice, which typically show impaired postischemic muscular neovascularization and blood perfusion recovery, have these defects corrected by intramuscular gene transfer of a dominant negative mutant form of p75(NTR). |
| 179 | 18566344 | Collectively, our data newly demonstrate the antiangiogenic action of p75(NTR) and open new avenues for the therapeutic use of p75(NTR) inhibition to combat diabetes-induced microvascular liabilities. |
| 180 | 18633731 | The content of both p65 and p52 was elevated in SOL and PL muscles, while p52 was decreased in RG. |
| 181 | 18633731 | Both p50 and RelB remained unchanged in all tissues examined. |
| 182 | 18708362 | During apoptosis, caspase-3 cleaved p52 to generate a p38 fragment that lacked the NH(2)-terminal PWWP domain and failed to transactivate the Hsp27 promoter in reporter assays. |
| 183 | 18708362 | However, p38 retained chromatin association properties and repressed the transactivation potential of LEDGF/p75. |
| 184 | 18708362 | During apoptosis, caspase-3 cleaved p52 to generate a p38 fragment that lacked the NH(2)-terminal PWWP domain and failed to transactivate the Hsp27 promoter in reporter assays. |
| 185 | 18708362 | However, p38 retained chromatin association properties and repressed the transactivation potential of LEDGF/p75. |
| 186 | 18771589 | The former pathway proceeds via phosphorylation and degradation of inhibitor of NF-kappaB (IkappaB) and leads most commonly to activation of the heterodimer RelA/NF-kappaB1(p50). |
| 187 | 18771589 | The latter pathway proceeds via phosphorylation and proteolytic processing of NF-kappaB2 (p100) and leads to activation, most commonly, of the heterodimer RelB/NF-kappaB2 (p52). |
| 188 | 18771589 | We discuss the involvement of NF-kappaB in self-reactive T and B lymphocyte development, survival and proliferation, and the maintenance of chronic inflammation due to cytokines such as tumor necrosis factor-alpha, IL-1, IL-6, and IL-8. |
| 189 | 19120268 | Lowered expressions of the NF-kappaB family members in dendritic cells from NOD mice are associated with a reduced expression of GATA-2. |
| 190 | 19120268 | In the present study, we compared transcription profiles of CD11c(+) bone marrow (BM)-derived DCs from NOD mice with those from NON mice, focusing on the NF-kappaB/Rel family members and associated molecules. |
| 191 | 19120268 | The BMDCs from NOD mice displayed reduced mRNA expressions of NF-kappaB components, p65, p50, p52, and RelB, compared to NON mice: the proportions of each molecule relative to those of NON DCs were 53.9, 54.1, 54.0, and 37.0%, respectively, which were accompanied with lowered expressions of downstream immunomodulatory molecules, including IL-6, CD80, CD86, 4-1BB, and CD40. |
| 192 | 19126759 | Conversely, the neurotrophin low-affinity p75(NTR) receptor induces apoptosis of endothelial cells and vascular smooth muscle cells and impairs angiogenesis. |
| 193 | 19591173 | More importantly, nuclear translocation of p65 and p52 of NF-kappaB by S100A4 was inhibited in the presence of ex-RAGE, confirming anti-inflammatory function of ex-RAGE. |
| 194 | 19591173 | In conclusion, ex-RAGE down-regulates RAGE expression and inhibits p65 and p52 activation in HSG, providing evidence that ex-RAGE functions as a "decoy" to RAGE-ligand interaction and thus potentially dampening inflammatory conditions. |
| 195 | 19591173 | More importantly, nuclear translocation of p65 and p52 of NF-kappaB by S100A4 was inhibited in the presence of ex-RAGE, confirming anti-inflammatory function of ex-RAGE. |
| 196 | 19591173 | In conclusion, ex-RAGE down-regulates RAGE expression and inhibits p65 and p52 activation in HSG, providing evidence that ex-RAGE functions as a "decoy" to RAGE-ligand interaction and thus potentially dampening inflammatory conditions. |
| 197 | 21326386 | Nuclear factor kappa B (NF-κB) is a ubiquitously expressed transcription factor comprised of various subunits (p50 (NF-κB1), p52 (NF-κB2), p65 (RelA), RelB, and c-Rel). |
| 198 | 21326386 | After 30 days, the heart, liver, spleen, and kidney were assessed for NF-κB activation and subunit composition with electrophoretic mobility shift assay (EMSA), and p50 and p65 subunit content was assessed with Western blotting. |
| 199 | 22460790 | p75 neurotrophin receptor regulates glucose homeostasis and insulin sensitivity. |
| 200 | 22460790 | Insulin-stimulated glucose uptake is mediated by the glucose transporter 4 (GLUT4), which is expressed mainly in skeletal muscle and adipose tissue. |
| 201 | 22460790 | Insulin-stimulated translocation of GLUT4 from its intracellular compartment to the plasma membrane is regulated by small guanosine triphosphate hydrolases (GTPases) and is essential for the maintenance of normal glucose homeostasis. |
| 202 | 22460790 | Here we show that the p75 neurotrophin receptor (p75(NTR)) is a regulator of glucose uptake and insulin resistance. p75(NTR) knockout mice show increased insulin sensitivity on normal chow diet, independent of changes in body weight. |
| 203 | 22460790 | Euglycemic-hyperinsulinemic clamp studies demonstrate that deletion of the p75(NTR) gene increases the insulin-stimulated glucose disposal rate and suppression of hepatic glucose production. |
| 204 | 22460790 | Genetic depletion or shRNA knockdown of p75(NTR) in adipocytes or myoblasts increases insulin-stimulated glucose uptake and GLUT4 translocation. |
| 205 | 22460790 | Conversely, overexpression of p75(NTR) in adipocytes decreases insulin-stimulated glucose transport. |
| 206 | 22460790 | In adipocytes, p75(NTR) forms a complex with the Rab5 family GTPases Rab5 and Rab31 that regulate GLUT4 trafficking. |
| 207 | 22460790 | Rab5 and Rab31 directly interact with p75(NTR) primarily via helix 4 of the p75(NTR) death domain. |
| 208 | 22460790 | Adipocytes from p75(NTR) knockout mice show increased Rab5 and decreased Rab31 activities, and dominant negative Rab5 rescues the increase in glucose uptake seen in p75(NTR) knockout adipocytes. |
| 209 | 22460790 | Our results identify p75(NTR) as a unique player in glucose metabolism and suggest that signaling from p75(NTR) to Rab5 family GTPases may represent a unique therapeutic target for insulin resistance and diabetes. |
| 210 | 22460790 | p75 neurotrophin receptor regulates glucose homeostasis and insulin sensitivity. |
| 211 | 22460790 | Insulin-stimulated glucose uptake is mediated by the glucose transporter 4 (GLUT4), which is expressed mainly in skeletal muscle and adipose tissue. |
| 212 | 22460790 | Insulin-stimulated translocation of GLUT4 from its intracellular compartment to the plasma membrane is regulated by small guanosine triphosphate hydrolases (GTPases) and is essential for the maintenance of normal glucose homeostasis. |
| 213 | 22460790 | Here we show that the p75 neurotrophin receptor (p75(NTR)) is a regulator of glucose uptake and insulin resistance. p75(NTR) knockout mice show increased insulin sensitivity on normal chow diet, independent of changes in body weight. |
| 214 | 22460790 | Euglycemic-hyperinsulinemic clamp studies demonstrate that deletion of the p75(NTR) gene increases the insulin-stimulated glucose disposal rate and suppression of hepatic glucose production. |
| 215 | 22460790 | Genetic depletion or shRNA knockdown of p75(NTR) in adipocytes or myoblasts increases insulin-stimulated glucose uptake and GLUT4 translocation. |
| 216 | 22460790 | Conversely, overexpression of p75(NTR) in adipocytes decreases insulin-stimulated glucose transport. |
| 217 | 22460790 | In adipocytes, p75(NTR) forms a complex with the Rab5 family GTPases Rab5 and Rab31 that regulate GLUT4 trafficking. |
| 218 | 22460790 | Rab5 and Rab31 directly interact with p75(NTR) primarily via helix 4 of the p75(NTR) death domain. |
| 219 | 22460790 | Adipocytes from p75(NTR) knockout mice show increased Rab5 and decreased Rab31 activities, and dominant negative Rab5 rescues the increase in glucose uptake seen in p75(NTR) knockout adipocytes. |
| 220 | 22460790 | Our results identify p75(NTR) as a unique player in glucose metabolism and suggest that signaling from p75(NTR) to Rab5 family GTPases may represent a unique therapeutic target for insulin resistance and diabetes. |
| 221 | 22460790 | p75 neurotrophin receptor regulates glucose homeostasis and insulin sensitivity. |
| 222 | 22460790 | Insulin-stimulated glucose uptake is mediated by the glucose transporter 4 (GLUT4), which is expressed mainly in skeletal muscle and adipose tissue. |
| 223 | 22460790 | Insulin-stimulated translocation of GLUT4 from its intracellular compartment to the plasma membrane is regulated by small guanosine triphosphate hydrolases (GTPases) and is essential for the maintenance of normal glucose homeostasis. |
| 224 | 22460790 | Here we show that the p75 neurotrophin receptor (p75(NTR)) is a regulator of glucose uptake and insulin resistance. p75(NTR) knockout mice show increased insulin sensitivity on normal chow diet, independent of changes in body weight. |
| 225 | 22460790 | Euglycemic-hyperinsulinemic clamp studies demonstrate that deletion of the p75(NTR) gene increases the insulin-stimulated glucose disposal rate and suppression of hepatic glucose production. |
| 226 | 22460790 | Genetic depletion or shRNA knockdown of p75(NTR) in adipocytes or myoblasts increases insulin-stimulated glucose uptake and GLUT4 translocation. |
| 227 | 22460790 | Conversely, overexpression of p75(NTR) in adipocytes decreases insulin-stimulated glucose transport. |
| 228 | 22460790 | In adipocytes, p75(NTR) forms a complex with the Rab5 family GTPases Rab5 and Rab31 that regulate GLUT4 trafficking. |
| 229 | 22460790 | Rab5 and Rab31 directly interact with p75(NTR) primarily via helix 4 of the p75(NTR) death domain. |
| 230 | 22460790 | Adipocytes from p75(NTR) knockout mice show increased Rab5 and decreased Rab31 activities, and dominant negative Rab5 rescues the increase in glucose uptake seen in p75(NTR) knockout adipocytes. |
| 231 | 22460790 | Our results identify p75(NTR) as a unique player in glucose metabolism and suggest that signaling from p75(NTR) to Rab5 family GTPases may represent a unique therapeutic target for insulin resistance and diabetes. |
| 232 | 22460790 | p75 neurotrophin receptor regulates glucose homeostasis and insulin sensitivity. |
| 233 | 22460790 | Insulin-stimulated glucose uptake is mediated by the glucose transporter 4 (GLUT4), which is expressed mainly in skeletal muscle and adipose tissue. |
| 234 | 22460790 | Insulin-stimulated translocation of GLUT4 from its intracellular compartment to the plasma membrane is regulated by small guanosine triphosphate hydrolases (GTPases) and is essential for the maintenance of normal glucose homeostasis. |
| 235 | 22460790 | Here we show that the p75 neurotrophin receptor (p75(NTR)) is a regulator of glucose uptake and insulin resistance. p75(NTR) knockout mice show increased insulin sensitivity on normal chow diet, independent of changes in body weight. |
| 236 | 22460790 | Euglycemic-hyperinsulinemic clamp studies demonstrate that deletion of the p75(NTR) gene increases the insulin-stimulated glucose disposal rate and suppression of hepatic glucose production. |
| 237 | 22460790 | Genetic depletion or shRNA knockdown of p75(NTR) in adipocytes or myoblasts increases insulin-stimulated glucose uptake and GLUT4 translocation. |
| 238 | 22460790 | Conversely, overexpression of p75(NTR) in adipocytes decreases insulin-stimulated glucose transport. |
| 239 | 22460790 | In adipocytes, p75(NTR) forms a complex with the Rab5 family GTPases Rab5 and Rab31 that regulate GLUT4 trafficking. |
| 240 | 22460790 | Rab5 and Rab31 directly interact with p75(NTR) primarily via helix 4 of the p75(NTR) death domain. |
| 241 | 22460790 | Adipocytes from p75(NTR) knockout mice show increased Rab5 and decreased Rab31 activities, and dominant negative Rab5 rescues the increase in glucose uptake seen in p75(NTR) knockout adipocytes. |
| 242 | 22460790 | Our results identify p75(NTR) as a unique player in glucose metabolism and suggest that signaling from p75(NTR) to Rab5 family GTPases may represent a unique therapeutic target for insulin resistance and diabetes. |
| 243 | 22460790 | p75 neurotrophin receptor regulates glucose homeostasis and insulin sensitivity. |
| 244 | 22460790 | Insulin-stimulated glucose uptake is mediated by the glucose transporter 4 (GLUT4), which is expressed mainly in skeletal muscle and adipose tissue. |
| 245 | 22460790 | Insulin-stimulated translocation of GLUT4 from its intracellular compartment to the plasma membrane is regulated by small guanosine triphosphate hydrolases (GTPases) and is essential for the maintenance of normal glucose homeostasis. |
| 246 | 22460790 | Here we show that the p75 neurotrophin receptor (p75(NTR)) is a regulator of glucose uptake and insulin resistance. p75(NTR) knockout mice show increased insulin sensitivity on normal chow diet, independent of changes in body weight. |
| 247 | 22460790 | Euglycemic-hyperinsulinemic clamp studies demonstrate that deletion of the p75(NTR) gene increases the insulin-stimulated glucose disposal rate and suppression of hepatic glucose production. |
| 248 | 22460790 | Genetic depletion or shRNA knockdown of p75(NTR) in adipocytes or myoblasts increases insulin-stimulated glucose uptake and GLUT4 translocation. |
| 249 | 22460790 | Conversely, overexpression of p75(NTR) in adipocytes decreases insulin-stimulated glucose transport. |
| 250 | 22460790 | In adipocytes, p75(NTR) forms a complex with the Rab5 family GTPases Rab5 and Rab31 that regulate GLUT4 trafficking. |
| 251 | 22460790 | Rab5 and Rab31 directly interact with p75(NTR) primarily via helix 4 of the p75(NTR) death domain. |
| 252 | 22460790 | Adipocytes from p75(NTR) knockout mice show increased Rab5 and decreased Rab31 activities, and dominant negative Rab5 rescues the increase in glucose uptake seen in p75(NTR) knockout adipocytes. |
| 253 | 22460790 | Our results identify p75(NTR) as a unique player in glucose metabolism and suggest that signaling from p75(NTR) to Rab5 family GTPases may represent a unique therapeutic target for insulin resistance and diabetes. |
| 254 | 22460790 | p75 neurotrophin receptor regulates glucose homeostasis and insulin sensitivity. |
| 255 | 22460790 | Insulin-stimulated glucose uptake is mediated by the glucose transporter 4 (GLUT4), which is expressed mainly in skeletal muscle and adipose tissue. |
| 256 | 22460790 | Insulin-stimulated translocation of GLUT4 from its intracellular compartment to the plasma membrane is regulated by small guanosine triphosphate hydrolases (GTPases) and is essential for the maintenance of normal glucose homeostasis. |
| 257 | 22460790 | Here we show that the p75 neurotrophin receptor (p75(NTR)) is a regulator of glucose uptake and insulin resistance. p75(NTR) knockout mice show increased insulin sensitivity on normal chow diet, independent of changes in body weight. |
| 258 | 22460790 | Euglycemic-hyperinsulinemic clamp studies demonstrate that deletion of the p75(NTR) gene increases the insulin-stimulated glucose disposal rate and suppression of hepatic glucose production. |
| 259 | 22460790 | Genetic depletion or shRNA knockdown of p75(NTR) in adipocytes or myoblasts increases insulin-stimulated glucose uptake and GLUT4 translocation. |
| 260 | 22460790 | Conversely, overexpression of p75(NTR) in adipocytes decreases insulin-stimulated glucose transport. |
| 261 | 22460790 | In adipocytes, p75(NTR) forms a complex with the Rab5 family GTPases Rab5 and Rab31 that regulate GLUT4 trafficking. |
| 262 | 22460790 | Rab5 and Rab31 directly interact with p75(NTR) primarily via helix 4 of the p75(NTR) death domain. |
| 263 | 22460790 | Adipocytes from p75(NTR) knockout mice show increased Rab5 and decreased Rab31 activities, and dominant negative Rab5 rescues the increase in glucose uptake seen in p75(NTR) knockout adipocytes. |
| 264 | 22460790 | Our results identify p75(NTR) as a unique player in glucose metabolism and suggest that signaling from p75(NTR) to Rab5 family GTPases may represent a unique therapeutic target for insulin resistance and diabetes. |
| 265 | 22460790 | p75 neurotrophin receptor regulates glucose homeostasis and insulin sensitivity. |
| 266 | 22460790 | Insulin-stimulated glucose uptake is mediated by the glucose transporter 4 (GLUT4), which is expressed mainly in skeletal muscle and adipose tissue. |
| 267 | 22460790 | Insulin-stimulated translocation of GLUT4 from its intracellular compartment to the plasma membrane is regulated by small guanosine triphosphate hydrolases (GTPases) and is essential for the maintenance of normal glucose homeostasis. |
| 268 | 22460790 | Here we show that the p75 neurotrophin receptor (p75(NTR)) is a regulator of glucose uptake and insulin resistance. p75(NTR) knockout mice show increased insulin sensitivity on normal chow diet, independent of changes in body weight. |
| 269 | 22460790 | Euglycemic-hyperinsulinemic clamp studies demonstrate that deletion of the p75(NTR) gene increases the insulin-stimulated glucose disposal rate and suppression of hepatic glucose production. |
| 270 | 22460790 | Genetic depletion or shRNA knockdown of p75(NTR) in adipocytes or myoblasts increases insulin-stimulated glucose uptake and GLUT4 translocation. |
| 271 | 22460790 | Conversely, overexpression of p75(NTR) in adipocytes decreases insulin-stimulated glucose transport. |
| 272 | 22460790 | In adipocytes, p75(NTR) forms a complex with the Rab5 family GTPases Rab5 and Rab31 that regulate GLUT4 trafficking. |
| 273 | 22460790 | Rab5 and Rab31 directly interact with p75(NTR) primarily via helix 4 of the p75(NTR) death domain. |
| 274 | 22460790 | Adipocytes from p75(NTR) knockout mice show increased Rab5 and decreased Rab31 activities, and dominant negative Rab5 rescues the increase in glucose uptake seen in p75(NTR) knockout adipocytes. |
| 275 | 22460790 | Our results identify p75(NTR) as a unique player in glucose metabolism and suggest that signaling from p75(NTR) to Rab5 family GTPases may represent a unique therapeutic target for insulin resistance and diabetes. |
| 276 | 22460790 | p75 neurotrophin receptor regulates glucose homeostasis and insulin sensitivity. |
| 277 | 22460790 | Insulin-stimulated glucose uptake is mediated by the glucose transporter 4 (GLUT4), which is expressed mainly in skeletal muscle and adipose tissue. |
| 278 | 22460790 | Insulin-stimulated translocation of GLUT4 from its intracellular compartment to the plasma membrane is regulated by small guanosine triphosphate hydrolases (GTPases) and is essential for the maintenance of normal glucose homeostasis. |
| 279 | 22460790 | Here we show that the p75 neurotrophin receptor (p75(NTR)) is a regulator of glucose uptake and insulin resistance. p75(NTR) knockout mice show increased insulin sensitivity on normal chow diet, independent of changes in body weight. |
| 280 | 22460790 | Euglycemic-hyperinsulinemic clamp studies demonstrate that deletion of the p75(NTR) gene increases the insulin-stimulated glucose disposal rate and suppression of hepatic glucose production. |
| 281 | 22460790 | Genetic depletion or shRNA knockdown of p75(NTR) in adipocytes or myoblasts increases insulin-stimulated glucose uptake and GLUT4 translocation. |
| 282 | 22460790 | Conversely, overexpression of p75(NTR) in adipocytes decreases insulin-stimulated glucose transport. |
| 283 | 22460790 | In adipocytes, p75(NTR) forms a complex with the Rab5 family GTPases Rab5 and Rab31 that regulate GLUT4 trafficking. |
| 284 | 22460790 | Rab5 and Rab31 directly interact with p75(NTR) primarily via helix 4 of the p75(NTR) death domain. |
| 285 | 22460790 | Adipocytes from p75(NTR) knockout mice show increased Rab5 and decreased Rab31 activities, and dominant negative Rab5 rescues the increase in glucose uptake seen in p75(NTR) knockout adipocytes. |
| 286 | 22460790 | Our results identify p75(NTR) as a unique player in glucose metabolism and suggest that signaling from p75(NTR) to Rab5 family GTPases may represent a unique therapeutic target for insulin resistance and diabetes. |
| 287 | 23091515 | Effects of Red Liriope platyphylla on NGF secretion ability, NGF receptor signaling pathway and γ-secretase components in NSE/hAPPsw transgenic mice expressing Alzheimer's Disease. |
| 288 | 23091515 | However, downstream effectors of the NGF receptor signaling pathway, including TrkA and p75(NTR) proteins, were suppressed in RLP-treated NSE/hAPPsw Tg mice. |
| 289 | 23091515 | Especially, Tg mice showed decreased levels of TrkA, p75(NTR), and RhoA expression. |
| 290 | 23091515 | Of the four components, the expression of APH-1 and Nicastrin (NCT) decreased in RLP-treated NSE/hAPPsw Tg mice, whereas expression of PS-2 and Pen-2 was maintained or increased within the same group. |
| 291 | 23091515 | Effects of Red Liriope platyphylla on NGF secretion ability, NGF receptor signaling pathway and γ-secretase components in NSE/hAPPsw transgenic mice expressing Alzheimer's Disease. |
| 292 | 23091515 | However, downstream effectors of the NGF receptor signaling pathway, including TrkA and p75(NTR) proteins, were suppressed in RLP-treated NSE/hAPPsw Tg mice. |
| 293 | 23091515 | Especially, Tg mice showed decreased levels of TrkA, p75(NTR), and RhoA expression. |
| 294 | 23091515 | Of the four components, the expression of APH-1 and Nicastrin (NCT) decreased in RLP-treated NSE/hAPPsw Tg mice, whereas expression of PS-2 and Pen-2 was maintained or increased within the same group. |
| 295 | 23365678 | Expression of proNGF, p75(NTR), cleaved-PARP, caspase-3 and p38MAPK/JNK were examined by Western-blot. |
| 296 | 23365678 | These effects were associated with significant upregulation of p75(NTR) and activation of RhoA. |
| 297 | 23365678 | Inhibiting RhoA kinase with Y27632 significantly reduced diabetes- and proNGF-induced activation of proapoptotic p38MAPK/JNK, expression of cleaved-PARP and caspase-3 and prevented retinal neurodegeneration in vivo and in vitro. |
| 298 | 23365678 | Taken together, these results provide compelling evidence for a causal role of proNGF in diabetes-induced retinal neurodegeneration through enhancing p75(NTR) expression and direct activation of RhoA and p38MAPK/JNK apoptotic pathways. |
| 299 | 23365678 | Expression of proNGF, p75(NTR), cleaved-PARP, caspase-3 and p38MAPK/JNK were examined by Western-blot. |
| 300 | 23365678 | These effects were associated with significant upregulation of p75(NTR) and activation of RhoA. |
| 301 | 23365678 | Inhibiting RhoA kinase with Y27632 significantly reduced diabetes- and proNGF-induced activation of proapoptotic p38MAPK/JNK, expression of cleaved-PARP and caspase-3 and prevented retinal neurodegeneration in vivo and in vitro. |
| 302 | 23365678 | Taken together, these results provide compelling evidence for a causal role of proNGF in diabetes-induced retinal neurodegeneration through enhancing p75(NTR) expression and direct activation of RhoA and p38MAPK/JNK apoptotic pathways. |
| 303 | 23365678 | Expression of proNGF, p75(NTR), cleaved-PARP, caspase-3 and p38MAPK/JNK were examined by Western-blot. |
| 304 | 23365678 | These effects were associated with significant upregulation of p75(NTR) and activation of RhoA. |
| 305 | 23365678 | Inhibiting RhoA kinase with Y27632 significantly reduced diabetes- and proNGF-induced activation of proapoptotic p38MAPK/JNK, expression of cleaved-PARP and caspase-3 and prevented retinal neurodegeneration in vivo and in vitro. |
| 306 | 23365678 | Taken together, these results provide compelling evidence for a causal role of proNGF in diabetes-induced retinal neurodegeneration through enhancing p75(NTR) expression and direct activation of RhoA and p38MAPK/JNK apoptotic pathways. |
| 307 | 23527709 | Splenocytes from adult db/db and CD1d-knockout mice of both genders and their wild-type, C57BL/6 and Balb/C counterparts were examined for tumor necrosis factor (TNF)-alpha and TNF-alpha receptor type 1. |
| 308 | 23527709 | Despite the absence of inflammatory infiltrates, the hearts of db/db mice showed alterations in TNF-alpha receptor-1 and NFkB activity, including increased expression of both the NFkB p52 and p65 subunits. |
| 309 | 23527709 | In the hearts of CD1d-knockout mice, p52 expression was reduced, while p65 expression remained largely unchanged. |
| 310 | 23527709 | These results provide evidence for CD1d-mediated NFkB activation and diastolic dysfunction in the hearts of db/db mice. |
| 311 | 23527709 | Therefore, CD1d-associated abnormalities of innate immune responses and TNF-alpha production in splenic tissue may contribute to NFkB activation and cardiac dysfunction in type 2 diabetes. |
| 312 | 23527709 | Splenocytes from adult db/db and CD1d-knockout mice of both genders and their wild-type, C57BL/6 and Balb/C counterparts were examined for tumor necrosis factor (TNF)-alpha and TNF-alpha receptor type 1. |
| 313 | 23527709 | Despite the absence of inflammatory infiltrates, the hearts of db/db mice showed alterations in TNF-alpha receptor-1 and NFkB activity, including increased expression of both the NFkB p52 and p65 subunits. |
| 314 | 23527709 | In the hearts of CD1d-knockout mice, p52 expression was reduced, while p65 expression remained largely unchanged. |
| 315 | 23527709 | These results provide evidence for CD1d-mediated NFkB activation and diastolic dysfunction in the hearts of db/db mice. |
| 316 | 23527709 | Therefore, CD1d-associated abnormalities of innate immune responses and TNF-alpha production in splenic tissue may contribute to NFkB activation and cardiac dysfunction in type 2 diabetes. |
| 317 | 23577003 | We have provided an overview of functional BRET studies associated with the RTK superfamily involving: neurotrophic receptors [e.g., tropomyosin-related kinase (Trk) and p75 neurotrophin receptor (p75NTR)]; insulinotropic receptors [e.g., insulin receptor (IR) and insulin-like growth factor receptor (IGFR)] and growth factor receptors [e.g., ErbB receptors including the EGFR, the fibroblast growth factor receptor (FGFR), the vascular endothelial growth factor receptor (VEGFR) and the c-kit and platelet-derived growth factor receptor (PDGFR)]. |
| 318 | 23577003 | In addition, we review BRET-mediated studies of other tyrosine kinase-associated receptors including cytokine receptors, i.e., leptin receptor (OB-R) and the growth hormone receptor (GHR). |
| 319 | 23918145 | Modulation of p75(NTR) prevents diabetes- and proNGF-induced retinal inflammation and blood-retina barrier breakdown in mice and rats. |
| 320 | 23998130 | Additional cultures were treated with mutant-proNGF in the presence of specific pharmacological inhibitors of TrkA and p75(NTR) receptors. |
| 321 | 23998130 | Treatment of retinal endothelial cells with mutant-proNGF activated phosphorylation of TrkA and p38MAPK; however, it did not alter p75(NTR) expression. |
| 322 | 23998130 | Inhibition of TrkA but not p75(NTR) significantly reduced mutant-proNGF-induced cell proliferation, cell migration, and tube formation. |
| 323 | 23998130 | Additional cultures were treated with mutant-proNGF in the presence of specific pharmacological inhibitors of TrkA and p75(NTR) receptors. |
| 324 | 23998130 | Treatment of retinal endothelial cells with mutant-proNGF activated phosphorylation of TrkA and p38MAPK; however, it did not alter p75(NTR) expression. |
| 325 | 23998130 | Inhibition of TrkA but not p75(NTR) significantly reduced mutant-proNGF-induced cell proliferation, cell migration, and tube formation. |
| 326 | 23998130 | Additional cultures were treated with mutant-proNGF in the presence of specific pharmacological inhibitors of TrkA and p75(NTR) receptors. |
| 327 | 23998130 | Treatment of retinal endothelial cells with mutant-proNGF activated phosphorylation of TrkA and p38MAPK; however, it did not alter p75(NTR) expression. |
| 328 | 23998130 | Inhibition of TrkA but not p75(NTR) significantly reduced mutant-proNGF-induced cell proliferation, cell migration, and tube formation. |