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Gene Information
Gene symbol: DES
Gene name: desmin
HGNC ID: 2770
Synonyms: CMD1I, CSM1, CSM2
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 1306850 | Finally, in order to evaluate possible diabetes-related changes of the pituicyte cytoskeleton, we measured by densitometry actin, tubulin, vimentin, and desmin in immunocytochemically stained pituitary sections. |
| 2 | 1306850 | In diabetic compared with control cells of the studied pituitary region, we observed: (a) cytoplasmic atrophy; (b) the number of secretory granules per unit area increased in the total cytoplasm, and decreased in the SPL cytoplasm (lowered regulated secretion); (c) decreased IG labelling in the SPL granules (reduced amount of hormone transported by each granule towards the cell membrane); (d) decreased IG labelling in the integranular SPL cytoplasm (reduced constitutive secretion), and (e) strongly increased actin and desmin, yet unchanged tubulin and vimentin immunoreactivity. |
| 3 | 1306850 | Finally, in order to evaluate possible diabetes-related changes of the pituicyte cytoskeleton, we measured by densitometry actin, tubulin, vimentin, and desmin in immunocytochemically stained pituitary sections. |
| 4 | 1306850 | In diabetic compared with control cells of the studied pituitary region, we observed: (a) cytoplasmic atrophy; (b) the number of secretory granules per unit area increased in the total cytoplasm, and decreased in the SPL cytoplasm (lowered regulated secretion); (c) decreased IG labelling in the SPL granules (reduced amount of hormone transported by each granule towards the cell membrane); (d) decreased IG labelling in the integranular SPL cytoplasm (reduced constitutive secretion), and (e) strongly increased actin and desmin, yet unchanged tubulin and vimentin immunoreactivity. |
| 5 | 1420061 | Apha smooth muscle actin or desmin, both markers of the myogenically differentiated and chronically contractile subpopulation could be detected in a large majority of the examined membranes. |
| 6 | 1710892 | Increased weight gain, nitrogen retention and muscle protein synthesis following treatment of diabetic rats with insulin-like growth factor (IGF)-I and des(1-3)IGF-I. |
| 7 | 1710892 | We have examined the effects of infusing recombinant human growth hormone (hGH), insulin-like growth factor-I (IGF-I), the truncated IGF-I analogue, des(1-3)IGF-I, and insulin over a 7-day period in streptozotocin-induced diabetic rats. |
| 8 | 1710892 | IGF-I at a dose of 1.05 or 1.08 mg/kg per day in two experiments increased body weight and nitrogen retention above those of vehicle-infused controls to about 30% of the improvement achieved with 25 or 30 units of insulin/kg per day, but only in the second experiment were the differences statistically significant (P less than 0.05). |
| 9 | 1710892 | A 2.5-fold higher IGF-I dose, or des(1-3)IGF-I at 1.08 mg/kg per day, gave effects that were approx. 70% of those obtained with insulin. hGH at 1.38 mg/kg per day was not effective. |
| 10 | 1710892 | Des(1-3)IGF-I induced binding proteins, but had only a slight effect on measured IGF-I concentrations. |
| 11 | 1710892 | Moreover, des(1-3)IGF-I is at least as potent as the full-length IGF-I. |
| 12 | 1729686 | Apart from insulin-secreting cells, the 58-kDa antigen was only found to be expressed by neuroblastoma cells and was identified as peripherin, an intermediate filament protein previously characterized in well-defined neuronal populations. |
| 13 | 1889766 | In addition, the topographic distribution of fibronectin was analyzed and the localization of the epidermal growth factor receptor, which is the coreceptor for the transforming growth factor alpha, was examined by staining procedures. |
| 14 | 1889766 | We used antibodies against macrophages (Ki-M7), cytokeratin, vimentin, desmin, glial fibrillary acidic protein and against the proliferation antigen Ki-67. |
| 15 | 1889766 | Among the cellular receptors necessary for signal transduction of mitogenic substances, we localized the coreceptor for the epidermal growth factor and the transforming growth factor alpha among actively proliferating macrophages in a PVR membrane. |
| 16 | 7578889 | Necrobiosis lipoidica (NL), a skin disease, is associated with insulin-dependent diabetes mellitus (IDDM). |
| 17 | 7578889 | Isotype-specific enzyme-linked immunosorbent assays (ELISAs) were used to detect NAbs against actin, myosin, keratin, desmin, troponin, tropomyosin, thyroglobulin, insulin, single-stranded DNA and the hapten trinitrophenyl. |
| 18 | 7578889 | High proportion of NL sera exhibited increased IgG anti-tropomyosin (69%), anti-troponin, anti-desmin and anti-keratin (50% each), anti-insulin (44%) and anti-trinitrophenyl (31%) activities, as well as increased IgA and IgM anti-keratin activities (26% and 31%, respectively). |
| 19 | 7578889 | Necrobiosis lipoidica (NL), a skin disease, is associated with insulin-dependent diabetes mellitus (IDDM). |
| 20 | 7578889 | Isotype-specific enzyme-linked immunosorbent assays (ELISAs) were used to detect NAbs against actin, myosin, keratin, desmin, troponin, tropomyosin, thyroglobulin, insulin, single-stranded DNA and the hapten trinitrophenyl. |
| 21 | 7578889 | High proportion of NL sera exhibited increased IgG anti-tropomyosin (69%), anti-troponin, anti-desmin and anti-keratin (50% each), anti-insulin (44%) and anti-trinitrophenyl (31%) activities, as well as increased IgA and IgM anti-keratin activities (26% and 31%, respectively). |
| 22 | 9077489 | We studied the immunolocalization of Dp116 (a 116 kDa protein product of the dystrophin gene), vinculin, talin, vimentin, desmin, spectrin and titin in the sural nerve biopsies of 25 patients with peripheral neuropathies of different origin. 4 patients presented with HMSN type 1, 4 with HMSN type 2, 2 with HNPP, 4 with CIDP, 5 with chronic axonal neuropathy of unknown origin, 3 with vasculitic neuropathy, 3 with diabetic neuropathy. |
| 23 | 9077489 | Expression and localization of Dp116, vinculin, vimentin, desmin, spectrin and titin did not differ from normal control cases. |
| 24 | 9077489 | Spectrin and titin immunoreactivities were absent and desmin was occasionally found in few epineurial vessels. |
| 25 | 9077489 | We studied the immunolocalization of Dp116 (a 116 kDa protein product of the dystrophin gene), vinculin, talin, vimentin, desmin, spectrin and titin in the sural nerve biopsies of 25 patients with peripheral neuropathies of different origin. 4 patients presented with HMSN type 1, 4 with HMSN type 2, 2 with HNPP, 4 with CIDP, 5 with chronic axonal neuropathy of unknown origin, 3 with vasculitic neuropathy, 3 with diabetic neuropathy. |
| 26 | 9077489 | Expression and localization of Dp116, vinculin, vimentin, desmin, spectrin and titin did not differ from normal control cases. |
| 27 | 9077489 | Spectrin and titin immunoreactivities were absent and desmin was occasionally found in few epineurial vessels. |
| 28 | 9077489 | We studied the immunolocalization of Dp116 (a 116 kDa protein product of the dystrophin gene), vinculin, talin, vimentin, desmin, spectrin and titin in the sural nerve biopsies of 25 patients with peripheral neuropathies of different origin. 4 patients presented with HMSN type 1, 4 with HMSN type 2, 2 with HNPP, 4 with CIDP, 5 with chronic axonal neuropathy of unknown origin, 3 with vasculitic neuropathy, 3 with diabetic neuropathy. |
| 29 | 9077489 | Expression and localization of Dp116, vinculin, vimentin, desmin, spectrin and titin did not differ from normal control cases. |
| 30 | 9077489 | Spectrin and titin immunoreactivities were absent and desmin was occasionally found in few epineurial vessels. |
| 31 | 9439529 | Insulin-like growth factor binding protein production in bovine retinal endothelial cells. |
| 32 | 9439529 | Bovine retinal endothelial cells (BRECs) were cultured to investigate if insulin, insulin-like growth factors (IGFs), IGF binding proteins (IGFBPs), and a chronic high-glucose condition could control endothelial cell growth. |
| 33 | 9439529 | Insulin, which does not bind to IGFBPs, was a potent mitogenic factor in these cells at a high concentration (10 nmol/L), suggesting a cross-reaction to IGF-I receptor. |
| 34 | 9439529 | These IGFBPs, except the 24-kd form (IGFBP-4), were modulated by both IGF-I and IGF-II, with a maximum effect at 100 and 10 nmol/L, respectively. |
| 35 | 9439529 | In fact, (1) IGFBP mRNA levels were not modified after stimulation with 100 nmol/L IGF-I, (2) 100 nmol/L IGF plus an equimolar concentration of alpha IR3 did not affect IGFBP production, (3) Des(1-3)IGF-I had no effect on IGFBP modulation, whereas at 10 nmol/L it enhanced BREC thymidine cell incorporation, and (4) 100 nmol/L insulin, which at this concentration can cross-react with the IGF-I receptor, did not modify the IGFBP pattern. |
| 36 | 9439529 | In conclusion, we showed that conditions mimicking hyperinsulinemia, rather than high levels of IGFs, could regulate BREC growth and that the IGF-I analog, Des(1-3), even with reduced affinity for IGFBPs but in part capable of binding to IGFBP-3, significantly stimulated BRECs growth only at 10 nmol/L. |
| 37 | 9439529 | Insulin-like growth factor binding protein production in bovine retinal endothelial cells. |
| 38 | 9439529 | Bovine retinal endothelial cells (BRECs) were cultured to investigate if insulin, insulin-like growth factors (IGFs), IGF binding proteins (IGFBPs), and a chronic high-glucose condition could control endothelial cell growth. |
| 39 | 9439529 | Insulin, which does not bind to IGFBPs, was a potent mitogenic factor in these cells at a high concentration (10 nmol/L), suggesting a cross-reaction to IGF-I receptor. |
| 40 | 9439529 | These IGFBPs, except the 24-kd form (IGFBP-4), were modulated by both IGF-I and IGF-II, with a maximum effect at 100 and 10 nmol/L, respectively. |
| 41 | 9439529 | In fact, (1) IGFBP mRNA levels were not modified after stimulation with 100 nmol/L IGF-I, (2) 100 nmol/L IGF plus an equimolar concentration of alpha IR3 did not affect IGFBP production, (3) Des(1-3)IGF-I had no effect on IGFBP modulation, whereas at 10 nmol/L it enhanced BREC thymidine cell incorporation, and (4) 100 nmol/L insulin, which at this concentration can cross-react with the IGF-I receptor, did not modify the IGFBP pattern. |
| 42 | 9439529 | In conclusion, we showed that conditions mimicking hyperinsulinemia, rather than high levels of IGFs, could regulate BREC growth and that the IGF-I analog, Des(1-3), even with reduced affinity for IGFBPs but in part capable of binding to IGFBP-3, significantly stimulated BRECs growth only at 10 nmol/L. |
| 43 | 12107504 | Nestin is an intermediate filament protein expressed by neuroepithelial stem cells and which has been proposed to represent also a marker for putative islet stem cells. |
| 44 | 12107504 | These cells also expressed desmin, vimentin, and glial fibrillary acidic protein which are known to represent stellate cell markers. |
| 45 | 12107504 | Nestin is an intermediate filament protein expressed by neuroepithelial stem cells and which has been proposed to represent also a marker for putative islet stem cells. |
| 46 | 12107504 | These cells also expressed desmin, vimentin, and glial fibrillary acidic protein which are known to represent stellate cell markers. |
| 47 | 12197670 | Heat shock protein (HSP) 47, a collagen-binding stress protein, has a specific role in the intracellular processing of procollagen molecules during collagen synthesis. |
| 48 | 12197670 | The expression pattern of alpha-smooth muscle actin (to identify mesangial cell damage), vimentin (to identify tubular epithelial cell damage), and desmin (to identify glomerular epithelial cell damage) was also determined in kidneys of these diabetic rats. |
| 49 | 12197670 | Antibodies specific for HSP47, type III and type IV collagens, alpha-smooth muscle actin, vimentin, and desmin were used to assess the relative expression of their proteins in paraffin-embedded kidney sections by immunohistochemistry. |
| 50 | 12197670 | Similarly, compared to kidneys of control and acute diabetic rats, an increased expression of alpha-smooth muscle actin (in mesangial cells), vimentin (in tubular epithelial cells), and desmin (in glomerular epithelial cells) was detected in the kidneys of chronic diabetic rats; by dual immunostaining, these phenotypically-altered renal cells in kidneys of chronic diabetic rats were found to be HSP47-producing cells. |
| 51 | 12197670 | Heat shock protein (HSP) 47, a collagen-binding stress protein, has a specific role in the intracellular processing of procollagen molecules during collagen synthesis. |
| 52 | 12197670 | The expression pattern of alpha-smooth muscle actin (to identify mesangial cell damage), vimentin (to identify tubular epithelial cell damage), and desmin (to identify glomerular epithelial cell damage) was also determined in kidneys of these diabetic rats. |
| 53 | 12197670 | Antibodies specific for HSP47, type III and type IV collagens, alpha-smooth muscle actin, vimentin, and desmin were used to assess the relative expression of their proteins in paraffin-embedded kidney sections by immunohistochemistry. |
| 54 | 12197670 | Similarly, compared to kidneys of control and acute diabetic rats, an increased expression of alpha-smooth muscle actin (in mesangial cells), vimentin (in tubular epithelial cells), and desmin (in glomerular epithelial cells) was detected in the kidneys of chronic diabetic rats; by dual immunostaining, these phenotypically-altered renal cells in kidneys of chronic diabetic rats were found to be HSP47-producing cells. |
| 55 | 12197670 | Heat shock protein (HSP) 47, a collagen-binding stress protein, has a specific role in the intracellular processing of procollagen molecules during collagen synthesis. |
| 56 | 12197670 | The expression pattern of alpha-smooth muscle actin (to identify mesangial cell damage), vimentin (to identify tubular epithelial cell damage), and desmin (to identify glomerular epithelial cell damage) was also determined in kidneys of these diabetic rats. |
| 57 | 12197670 | Antibodies specific for HSP47, type III and type IV collagens, alpha-smooth muscle actin, vimentin, and desmin were used to assess the relative expression of their proteins in paraffin-embedded kidney sections by immunohistochemistry. |
| 58 | 12197670 | Similarly, compared to kidneys of control and acute diabetic rats, an increased expression of alpha-smooth muscle actin (in mesangial cells), vimentin (in tubular epithelial cells), and desmin (in glomerular epithelial cells) was detected in the kidneys of chronic diabetic rats; by dual immunostaining, these phenotypically-altered renal cells in kidneys of chronic diabetic rats were found to be HSP47-producing cells. |
| 59 | 12360045 | Immunohistochemically, all lesions were KP1 (CD68) and vimentin positive and lysozyme, S-100 protein, HMB-45, epithelial membrane antigen, cytokeratins, factor VIIIrag, CD34, muscle-specific actin, alpha-smooth muscle actin, desmin (D33), desmin (Der-11), chromogranin, synaptophysin, neurofilament protein, and glial fibrillary acidic protein negative. |
| 60 | 12498975 | A number of proteins, including mitochondrial ATP synthase beta-chain, desmin, actin, and myosin, were found carbonylated. |
| 61 | 12745670 | Des(1-3)IGF-1 treatment normalizes type 1 IGF receptor and phospho-Akt (Thr 308) immunoreactivity in predegenerative retina of diabetic rats. |
| 62 | 12745670 | This study tested the hypothesis that immediate, systemic treatment with an insulin-like growth factor (IGF)-1 analog can prevent abnormal accumulations of type 1 IGF receptor, and phospho-Akt (Thr 308) immunoreactivity in predegenerative retinas of streptozotocin (STZ) diabetic rats. |
| 63 | 12745670 | Hyperglycemia/failure of weight gain in diabetic rats continued despite systemic des(1-3)IGF-1. |
| 64 | 14649687 | Immunohistochemical staining for anticollagen type IV, integrin alpha5, laminin, smooth muscle beta-actin, procollagen type I, and desmin was evaluated. |
| 65 | 14711882 | The term myofibrillar myopathy (MFM) was proposed in 1996 as a non-committal term for a pathological pattern of myofibrillar dissolution associated with accumulation of myofibrillar degradation products and ectopic expression of multiple proteins that include desmin, alphaB-crystallin (alphaBC), dystrophin and congophilic amyloid material. |
| 66 | 14711882 | Semiquantitative analysis in each case indicates that among the abnormal fibres, an average of 90, 75, 75, 70 and 70% abnormally express myotilin, desmin, alphaBC, dystrophin and beta-amyloid precursor protein, respectively. |
| 67 | 14711882 | In all patients, we searched for mutations in desmin and alphaBC, as well as in telethonin, a Z-disk-associated protein, or in syncoilin, which together with plectin links desmin to the Z-disk. |
| 68 | 14711882 | Two of the 63 patients carry truncation mutations in the C-terminal domain of alphaBC, four carry missense mutations in the head or tail region of desmin, and none carries a mutation in syncoilin or telethonin. |
| 69 | 14711882 | The term myofibrillar myopathy (MFM) was proposed in 1996 as a non-committal term for a pathological pattern of myofibrillar dissolution associated with accumulation of myofibrillar degradation products and ectopic expression of multiple proteins that include desmin, alphaB-crystallin (alphaBC), dystrophin and congophilic amyloid material. |
| 70 | 14711882 | Semiquantitative analysis in each case indicates that among the abnormal fibres, an average of 90, 75, 75, 70 and 70% abnormally express myotilin, desmin, alphaBC, dystrophin and beta-amyloid precursor protein, respectively. |
| 71 | 14711882 | In all patients, we searched for mutations in desmin and alphaBC, as well as in telethonin, a Z-disk-associated protein, or in syncoilin, which together with plectin links desmin to the Z-disk. |
| 72 | 14711882 | Two of the 63 patients carry truncation mutations in the C-terminal domain of alphaBC, four carry missense mutations in the head or tail region of desmin, and none carries a mutation in syncoilin or telethonin. |
| 73 | 14711882 | The term myofibrillar myopathy (MFM) was proposed in 1996 as a non-committal term for a pathological pattern of myofibrillar dissolution associated with accumulation of myofibrillar degradation products and ectopic expression of multiple proteins that include desmin, alphaB-crystallin (alphaBC), dystrophin and congophilic amyloid material. |
| 74 | 14711882 | Semiquantitative analysis in each case indicates that among the abnormal fibres, an average of 90, 75, 75, 70 and 70% abnormally express myotilin, desmin, alphaBC, dystrophin and beta-amyloid precursor protein, respectively. |
| 75 | 14711882 | In all patients, we searched for mutations in desmin and alphaBC, as well as in telethonin, a Z-disk-associated protein, or in syncoilin, which together with plectin links desmin to the Z-disk. |
| 76 | 14711882 | Two of the 63 patients carry truncation mutations in the C-terminal domain of alphaBC, four carry missense mutations in the head or tail region of desmin, and none carries a mutation in syncoilin or telethonin. |
| 77 | 14711882 | The term myofibrillar myopathy (MFM) was proposed in 1996 as a non-committal term for a pathological pattern of myofibrillar dissolution associated with accumulation of myofibrillar degradation products and ectopic expression of multiple proteins that include desmin, alphaB-crystallin (alphaBC), dystrophin and congophilic amyloid material. |
| 78 | 14711882 | Semiquantitative analysis in each case indicates that among the abnormal fibres, an average of 90, 75, 75, 70 and 70% abnormally express myotilin, desmin, alphaBC, dystrophin and beta-amyloid precursor protein, respectively. |
| 79 | 14711882 | In all patients, we searched for mutations in desmin and alphaBC, as well as in telethonin, a Z-disk-associated protein, or in syncoilin, which together with plectin links desmin to the Z-disk. |
| 80 | 14711882 | Two of the 63 patients carry truncation mutations in the C-terminal domain of alphaBC, four carry missense mutations in the head or tail region of desmin, and none carries a mutation in syncoilin or telethonin. |
| 81 | 14966942 | [Early expression of TGF-beta1, vimentin and desmin genes in renal cortex of diabetic rats]. |
| 82 | 15378652 | We examined the effects of streptozotocin (STZ)-induced diabetes in rats on the level of the astrocyte intermediate filament protein, glial fibrillary acidic protein (GFAP), number of astrocytes, and levels of the astrocyte glutamate transporters, glutamate transporter-1 (GLT-1) and glutamate/aspartate transporter (GLAST), in the cerebral cortex, hippocampus, and cerebellum by Western blotting (WB) and immunohistochemistry (IH). |
| 83 | 15922737 | We used a human-specific antibody against the intermediate filament protein nestin, a marker of regenerating skeletal muscle, to identify functional contribution of MSC to myotube formation. |
| 84 | 16462907 | There is a substantial body of information to indicate alterations in myofibrillar proteins including actin, myosin, tropomyosin, troponin, titin, desmin, and myosin-binding protein C in conditions such as hyperthyroidism, hypothyroidism, and diabetes. |
| 85 | 17333128 | There was a correlation between albumin excretion and desmin-positive glomerular area. |
| 86 | 17581414 | Sertoliform endometrioid carcinoma of the endometrium with dual immunophenotypes for epithelial membrane antigen and inhibin alpha: case report and literature review. |
| 87 | 17581414 | The tumor cells were diffusely immunoreactive for epithelial membrane antigen, estrogen receptor, and progesterone receptor (PR), and focally for vimentin. |
| 88 | 17581414 | The tumor cells were also diffusely positive for inhibin alpha and CD99. |
| 89 | 17581414 | Immunostains for other sex cord markers (calretinin, WT-1, and Melan-A) were also positive in approximately 30% to 40% of the tumor cells. |
| 90 | 17581414 | Immunostains for CD10, smooth muscle actin, desmin, or HHF35 were negative. |
| 91 | 17581414 | Two ovarian sertoliform endometrioid carcinomas from our archived tissue were, however, immunoreactive for epithelial membrane antigen but negative for inhibin alpha. |
| 92 | 18433871 | We found that a sizable proportion of hybridomas produced monoclonal antibodies reactive to peripherin, an intermediate filament protein mainly found in the peripheral nervous system. |
| 93 | 19089939 | CABG versus DES PCI in diabetics with multivessel disease: back to the BARI registry. |
| 94 | 19424163 | When compared to OZR-RD animals, OZR-HFD animals exhibited significantly higher levels of total renal cortical reactive oxygen species (ROS) production, plasma lipids, insulin, C-reactive protein, blood urea nitrogen (BUN), creatinine (Cr), and urinary albumin excretion (P < 0.05); these changes were accompanied by a significant decrease in plasma high-density lipoprotein levels (P < 0.05). |
| 95 | 19424163 | The mRNA expression levels of desmin, tumor necrosis factor-alpha (TNF-alpha), nuclear factor kappaB (NFkappaB), and NAD(P)H oxidase-1 (NOX-1) were significantly higher in the renal cortical tissues of OZR-HFD animals; NFkappaB p65 DNA binding activity as determined by electrophoretic mobility shift assay was also significantly higher in these animals. |
| 96 | 19706787 | Microarray analysis using mRNA collected from whole LVs revealed downregulation of known inhibitors of proliferation, p53 and p21, in the diabetic group, consistent with our proliferation data. |
| 97 | 19706787 | We explored the potential signaling underlying the downregulation of these cell cycle mediators and determined that activated Akt, a signal that inhibits p53, was elevated in the diabetic group. |
| 98 | 19706787 | Surprisingly, the hearts from the diabetic group contained lower levels of the myofibroblast marker α-smooth muscle actin (α-SMA) and higher levels of desmin and platelet endothelial cell adhesion molecule (PECAM). |
| 99 | 19890475 | Targets of S100A1 include proteins involved in calcium signaling (ryanidine receptors 1 & 2, Serca2a, phopholamban), neurotransmitter release (synapsins I & II), cytoskeletal and filament associated proteins (CapZ, microtubules, intermediate filaments, tau, mocrofilaments, desmin, tubulin, F-actin, titin, and the glial fibrillary acidic protein GFAP), transcription factors and their regulators (e.g. myoD, p53), enzymes (e.g. aldolase, phosphoglucomutase, malate dehydrogenase, glycogen phosphorylase, photoreceptor guanyl cyclases, adenylate cyclases, glyceraldehydes-3-phosphate dehydrogenase, twitchin kinase, Ndr kinase, and F1 ATP synthase), and other Ca2+-activated proteins (annexins V & VI, S100B, S100A4, S100P, and other S100 proteins). |
| 100 | 19952939 | Immunostaining demonstrated that the tumor cells were positive for alpha-smooth muscle actin, desmin, estrogen receptor, and progesterone receptor. |
| 101 | 20061119 | The target antigen was identified as peripherin, a 55kDa - type III intermediate filament protein. |
| 102 | 20113007 | Some studies have described the intermediate filament protein peripherin (PRPH) as an autoantigen associated with T1D in non-obese diabetic (NOD) mice. |
| 103 | 20610922 | Pathological examination revealed hypercellularity of spindle cells, that showed positive for CD34, vimentin, desmin and Mic-2, and negative for S100, alphaSMA, c-kit, AE1/3, p53 and bcl-2. |
| 104 | 20630940 | Proteomic analysis identifies insulin-like growth factor-binding protein-related protein-1 as a podocyte product. |
| 105 | 20630940 | As validation, we confirmed that one of these proteins, insulin-like growth factor-binding protein-related protein-1 (IGFBP-rP1), was expressed in mRNA and protein of cultured podocytes. |
| 106 | 20630940 | In addition, transforming growth factor-β1 stimulation increased IGFBP-rP1 in conditioned medium. |
| 107 | 20630940 | IGFBP-rP1 was absent from podocytes of normal mice and was expressed in podocytes and pseudocrescents of transgenic mice, where it was coexpressed with desmin, a podocyte injury marker. |
| 108 | 21185309 | Ubiquitin is a novel substrate for human insulin-degrading enzyme. |
| 109 | 21185309 | Insulin-degrading enzyme (IDE) can degrade insulin and amyloid-β, peptides involved in diabetes and Alzheimer's disease, respectively. |
| 110 | 21185309 | From these criteria, we predict that IDE can cleave and inactivate ubiquitin (Ub). |
| 111 | 21185309 | IDE is known to bind the cytoplasmic intermediate filament protein nestin with high affinity. |
| 112 | 21185309 | We found that nestin potently inhibits the cleavage of Ub by IDE. |
| 113 | 21228103 | An increase in the renal levels of VEGF-A, VEGFR-2, transforming growth factor (TGF)-β1, and monocyte chemoattractant protein-1 in diabetic animals was significantly suppressed by AdhVASH-1 (immunoblotting). |
| 114 | 21228103 | AdhVASH-1 treatment significantly recovered the loss and altered the distribution patterns of nephrin and zonula occludens (ZO)-1 and suppressed the increase in the number of fibroblast-specific protein-1 (FSP-1(+)) and desmin(+) podocytes in diabetic mice. |
| 115 | 21228103 | In vitro, recombinant human VASH-1 (rhVASH-1) dose dependently suppressed the upregulation of VEGF induced by high ambient glucose (25 mM) in cultured mouse podocytes. |
| 116 | 21228103 | In addition, rhVASH-1 significantly recovered the mRNA levels of nephrin and the protein levels of ZO-1 and P-cadherin and suppressed the increase in protein levels of desmin, FSP-1, Snail, and Slug in podocytes under high-glucose condition. |
| 117 | 21228103 | An increase in the renal levels of VEGF-A, VEGFR-2, transforming growth factor (TGF)-β1, and monocyte chemoattractant protein-1 in diabetic animals was significantly suppressed by AdhVASH-1 (immunoblotting). |
| 118 | 21228103 | AdhVASH-1 treatment significantly recovered the loss and altered the distribution patterns of nephrin and zonula occludens (ZO)-1 and suppressed the increase in the number of fibroblast-specific protein-1 (FSP-1(+)) and desmin(+) podocytes in diabetic mice. |
| 119 | 21228103 | In vitro, recombinant human VASH-1 (rhVASH-1) dose dependently suppressed the upregulation of VEGF induced by high ambient glucose (25 mM) in cultured mouse podocytes. |
| 120 | 21228103 | In addition, rhVASH-1 significantly recovered the mRNA levels of nephrin and the protein levels of ZO-1 and P-cadherin and suppressed the increase in protein levels of desmin, FSP-1, Snail, and Slug in podocytes under high-glucose condition. |
| 121 | 21354350 | Among the decreased proteins, 3 are involved in heart structure (one isoform of desmin, troponin T2 and α-cardiac actin), 3 are involved in energy metabolism (mitochondrial ATP synthase β subunit, adenylate kinase and creatine kinase) and one is a component of the citric acid cycle (isocitrate dehydrogenase 3). |
| 122 | 21913214 | The roles of connective tissue growth factor and integrin-linked kinase in high glucose-induced phenotypic alterations of podocytes. |
| 123 | 21913214 | Connective tissue growth factor (CTGF) and integrin-linked kinase (ILK) are involved in the progression of DN. |
| 124 | 21913214 | The study aimed to investigate the roles of CTGF and ILK in high glucose-induced phenotypic alterations of podocytes and determine whether ILK signaling is downstream of CTGF. |
| 125 | 21913214 | The epithelial marker of nephrin and the mesenchymal marker of desmin were investigated by real-time RT-PCR and Western blotting. |
| 126 | 21913214 | The results demonstrated that podocytes displayed a spreading, arborized morphology in normal glucose, whereas they had a cobblestone morphology in high glucose conditions, accompanied by decreased nephrin expression and increased desmin expression, suggesting podocytes underwent EMT. |
| 127 | 21913214 | In response to high glucose, CTGF and ILK expression in podocytes were increased in a dose- and time-dependent manner, whereas the increase did not occur in the osmotic control. |
| 128 | 21913214 | Furthermore, the inhibition of CTGF with anti-CTGF antibody prevented the phenotypic transition, as demonstrated by the preservation of epithelial morphology, the suppression of high glucose-induced desmin overexpression and the restoration of nephrin. |
| 129 | 21913214 | Of note, the upregulation of ILK induced by high glucose was partially blocked by the inhibition of CTGF. |
| 130 | 21913214 | In summary, these findings suggested that CTGF and ILK were involved in high glucose-induced phenotypic alterations of podocytes. |
| 131 | 21913214 | ILK acted as a downstream kinase of CTGF and high glucose-induced ILK expression might occur through CTGF-dependent and -independent pathways. |
| 132 | 21913214 | The roles of connective tissue growth factor and integrin-linked kinase in high glucose-induced phenotypic alterations of podocytes. |
| 133 | 21913214 | Connective tissue growth factor (CTGF) and integrin-linked kinase (ILK) are involved in the progression of DN. |
| 134 | 21913214 | The study aimed to investigate the roles of CTGF and ILK in high glucose-induced phenotypic alterations of podocytes and determine whether ILK signaling is downstream of CTGF. |
| 135 | 21913214 | The epithelial marker of nephrin and the mesenchymal marker of desmin were investigated by real-time RT-PCR and Western blotting. |
| 136 | 21913214 | The results demonstrated that podocytes displayed a spreading, arborized morphology in normal glucose, whereas they had a cobblestone morphology in high glucose conditions, accompanied by decreased nephrin expression and increased desmin expression, suggesting podocytes underwent EMT. |
| 137 | 21913214 | In response to high glucose, CTGF and ILK expression in podocytes were increased in a dose- and time-dependent manner, whereas the increase did not occur in the osmotic control. |
| 138 | 21913214 | Furthermore, the inhibition of CTGF with anti-CTGF antibody prevented the phenotypic transition, as demonstrated by the preservation of epithelial morphology, the suppression of high glucose-induced desmin overexpression and the restoration of nephrin. |
| 139 | 21913214 | Of note, the upregulation of ILK induced by high glucose was partially blocked by the inhibition of CTGF. |
| 140 | 21913214 | In summary, these findings suggested that CTGF and ILK were involved in high glucose-induced phenotypic alterations of podocytes. |
| 141 | 21913214 | ILK acted as a downstream kinase of CTGF and high glucose-induced ILK expression might occur through CTGF-dependent and -independent pathways. |
| 142 | 21913214 | The roles of connective tissue growth factor and integrin-linked kinase in high glucose-induced phenotypic alterations of podocytes. |
| 143 | 21913214 | Connective tissue growth factor (CTGF) and integrin-linked kinase (ILK) are involved in the progression of DN. |
| 144 | 21913214 | The study aimed to investigate the roles of CTGF and ILK in high glucose-induced phenotypic alterations of podocytes and determine whether ILK signaling is downstream of CTGF. |
| 145 | 21913214 | The epithelial marker of nephrin and the mesenchymal marker of desmin were investigated by real-time RT-PCR and Western blotting. |
| 146 | 21913214 | The results demonstrated that podocytes displayed a spreading, arborized morphology in normal glucose, whereas they had a cobblestone morphology in high glucose conditions, accompanied by decreased nephrin expression and increased desmin expression, suggesting podocytes underwent EMT. |
| 147 | 21913214 | In response to high glucose, CTGF and ILK expression in podocytes were increased in a dose- and time-dependent manner, whereas the increase did not occur in the osmotic control. |
| 148 | 21913214 | Furthermore, the inhibition of CTGF with anti-CTGF antibody prevented the phenotypic transition, as demonstrated by the preservation of epithelial morphology, the suppression of high glucose-induced desmin overexpression and the restoration of nephrin. |
| 149 | 21913214 | Of note, the upregulation of ILK induced by high glucose was partially blocked by the inhibition of CTGF. |
| 150 | 21913214 | In summary, these findings suggested that CTGF and ILK were involved in high glucose-induced phenotypic alterations of podocytes. |
| 151 | 21913214 | ILK acted as a downstream kinase of CTGF and high glucose-induced ILK expression might occur through CTGF-dependent and -independent pathways. |
| 152 | 22056625 | The phosphoinositide 3-kinase (PI3K) inhibitor, wortmannin, simultaneously regulates Rac1 and Cdc42, which destabilize the podocyte actin cytoskeleton during early DN. |
| 153 | 22056625 | In this study, in order to evaluate the reno-protective effects of wortmannin in early DN by regulating Rac1 and Cdc42, streptozotocin (STZ)-induced proteinuric renal disease (SPRD) rats were treated with wortmannin. |
| 154 | 22056625 | Changes in the expression level of nephrin, podocin and Rac1/Cdc42, which is related to actin cytoskeleton in podocytes, by wortmannin administration were confirmed by Western blotting. |
| 155 | 22056625 | The expression levels of nephrin (79.66 ± 0.02), podocin (87.81 ± 0.03) and Rac1/Cdc42 (86.12 ± 0.02) in the wortmannin group were higher than the expression levels of nephrin (55.32 ± 0.03), podocin (53.40 ± 0.06) and Rac1/Cdc42 (54.05 ± 0.04) in the SPRD group. |
| 156 | 22056625 | In addition, expression and localization of nephrin, podocin and desmin were confirmed by immunofluorescence. |
| 157 | 22076171 | Immunohistochemical results of the tumor were as follows: α-methylacyl-coenzyme A rasemase (AMACR) +++, vimentin +++, cytokeratin (CK) 18 +++, CD10 +++, S-100 protein +, MUC1 ++, MUC2 ++, MUC5AC ++, MUC6 ++, panCK Cam5.2 +, CK7 +, CK8 +, CK14 +, CK19 +, CK20 +, p53 +, HepPar1 +, CD68 +, platelet-derived growth factor-α (PDGFRA) +, PanCK AE1/3 -, PanCK WSS -, PanCK MNF115 -, CK 35BE12 -, CK5/6 -, EMA -, desmin -, smooth muscle antigen -, α-fetoprotein -, CEA -, estrogen receptor -, progesterone receptor -, HER2 -, p63 -, and KIT -. |
| 158 | 22076171 | These results suggest that OPRCC can express colloidal iron, low molecular weight CKs, S100 protein, MUC1, MUC2, MUC5AC, MUC6, p53, PDGFRA, and HepPar1. |
| 159 | 22311732 | Tadalafil reversed the coordinated alterations of cytoskeletal/contractile proteins such as myosin light chain (MLY) 2 and 4, myosin heavy chain α and myosin-binding protein C which contributes to contractile dysfunction. |
| 160 | 22311732 | The expression of intermediate filament protein vimentin and extra-cellular matrix proteins like cysteine and glycine rich protein-3 and collagen type VI α were upregulated in db/db mice indicating cardiac remodeling in diabetes. |
| 161 | 22311732 | Tadalafil also enhanced antioxidant enzyme glutathione S-transferase Kappa-1 (GSKT-1) and downregulated redox regulatory chaperones like heat shock protein 8 (HSPA8), and 75 kD glucose regulatory protein (75GRP). |
| 162 | 22317894 | Formalin fixed and paraffin embedded specimens of 14 normal and 17 Type 1 diabetic term placentas were used for picrosirius staining, vimentin and desmin immunohistochemistry and confocal microscopy. 3D models of villi and villous capillaries were constructed from stacks of confocal optical sections. |
| 163 | 23000950 | The expression of intermediate filament protein nestin and its association with cyclin-dependent kinase 5 in the glomeruli of rats with diabetic nephropathy. |
| 164 | 23722292 | Immunohistochemically, tumor cells were positive for vimentin, synaptophysin, chromogranin, and CD56 and negative for AE1/AE3, CK, EMA, CD10, SMA, Melan A, HMB-45, desmin, and S100-P. |
| 165 | 23780909 | Ligand-independent, constitutive activation of Hedgehog signalling in mice expressing a mutant, activated SmoM2 allele results in the development of multifocal, highly differentiated tumours that express myogenic markers (including desmin, actin, MyoD and myogenin). |