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Gene Information
Gene symbol: SYP
Gene name: synaptophysin
HGNC ID: 11506
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 1969977 | The diagnosis remained unclear until immunohistochemical studies of the resected specimen revealed somatostatin and synaptophysin, suggesting a somatostatinoma. |
| 2 | 3117578 | A minireview with particular reference to synaptophysin and chromogranin A as neuroendocrine markers and to the ontogeny of argyrophil insulin immunoreactive cells in the rabbit. |
| 3 | 3117578 | In addition, the distribution of the newly discovered neuroendocrine markers synaptophysin and chromogranin A has been reviewed immunohistochemically in normal and neoplastic islet parenchyma cells; the insulin cells do not seem to contain chromogranin A. |
| 4 | 3117578 | A minireview with particular reference to synaptophysin and chromogranin A as neuroendocrine markers and to the ontogeny of argyrophil insulin immunoreactive cells in the rabbit. |
| 5 | 3117578 | In addition, the distribution of the newly discovered neuroendocrine markers synaptophysin and chromogranin A has been reviewed immunohistochemically in normal and neoplastic islet parenchyma cells; the insulin cells do not seem to contain chromogranin A. |
| 6 | 7485492 | Phosphorylated IRS-1 then interacts with the p85 alpha subunit of phosphatidylinositol 3-kinase (PI3K), Nck, growth factor receptor-bound protein 2 (GRB2), and Syp, thus branching insulin's signal for both mitogenic and metabolic responses. |
| 7 | 7485492 | IR and PI3K p85 alpha protein levels were significantly lower in KKAy mice than in control nondiabetic mice, whereas IRS-1 protein levels were not altered. |
| 8 | 7485492 | In contrast, the protein levels of GRB2, Nck, Syp, and GLUT-1 were dramatically elevated in KKAy fat, with less striking changes in liver. |
| 9 | 7485492 | Phosphorylated IRS-1 then interacts with the p85 alpha subunit of phosphatidylinositol 3-kinase (PI3K), Nck, growth factor receptor-bound protein 2 (GRB2), and Syp, thus branching insulin's signal for both mitogenic and metabolic responses. |
| 10 | 7485492 | IR and PI3K p85 alpha protein levels were significantly lower in KKAy mice than in control nondiabetic mice, whereas IRS-1 protein levels were not altered. |
| 11 | 7485492 | In contrast, the protein levels of GRB2, Nck, Syp, and GLUT-1 were dramatically elevated in KKAy fat, with less striking changes in liver. |
| 12 | 7531695 | We now show that, in addition, simultaneous occupancy of both SH2 domains of the phosphotyrosine phosphatase SH-PTP2 (Syp, PTP 1D, PTP-2C) by a tethered peptide with two IRS-1-derived phosphorylation sites potently stimulates phosphatase activity. |
| 13 | 7626133 | Tyrosine-phosphorylation of IRS-1 causes it to associate with the src-homology-2 (SH2) domains of at least four other proteins: phosphatidylinositol 3'-kinase (PI3K), growth factor receptor-bound protein-2 (GRB2), Nck, and Syp. |
| 14 | 7626133 | In liver tissue of diabetic rats, the levels of Nck and Syp were significantly decreased to 71 +/- 6% and 61 +/- 4% control, respectively, while in fat tissue only the Syp levels were significantly reduced to 72 +/- 9% control. |
| 15 | 7626133 | Tyrosine-phosphorylation of IRS-1 causes it to associate with the src-homology-2 (SH2) domains of at least four other proteins: phosphatidylinositol 3'-kinase (PI3K), growth factor receptor-bound protein-2 (GRB2), Nck, and Syp. |
| 16 | 7626133 | In liver tissue of diabetic rats, the levels of Nck and Syp were significantly decreased to 71 +/- 6% and 61 +/- 4% control, respectively, while in fat tissue only the Syp levels were significantly reduced to 72 +/- 9% control. |
| 17 | 7763633 | Synaptophysin-containing microvesicles transport heat-shock protein hsp60 in insulin-secreting beta cells. |
| 18 | 7763633 | However, we have recently documented that, in addition to mitochondria, a hsp60-like protein is present in secretory granules of insulin-secreting beta cells. |
| 19 | 8144631 | SH-PTP2/Syp SH2 domain binding specificity is defined by direct interactions with platelet-derived growth factor beta-receptor, epidermal growth factor receptor, and insulin receptor substrate-1-derived phosphopeptides. |
| 20 | 8144631 | The cytoplasmic phosphotyrosine phosphatase SH-PTP2 (Syp, PTP 1D, PTP-2C) contains two SH2 domains (N and C) which mediate its association with and activation by the platelet-derived growth factor (PDGF) and epidermal growth factor receptors and IRS-1. |
| 21 | 8144631 | The sequence surrounding Tyr1009 bound with greatest affinity (ID50 = 14 microM) of eight PDGF receptor-derived phosphopeptides tested. |
| 22 | 8144631 | These findings are consistent with recent mutational analyses of the PDGF receptor and predict site-specific interactions between SH-PTP2 and each of these phosphoproteins. |
| 23 | 8144631 | SH-PTP2/Syp SH2 domain binding specificity is defined by direct interactions with platelet-derived growth factor beta-receptor, epidermal growth factor receptor, and insulin receptor substrate-1-derived phosphopeptides. |
| 24 | 8144631 | The cytoplasmic phosphotyrosine phosphatase SH-PTP2 (Syp, PTP 1D, PTP-2C) contains two SH2 domains (N and C) which mediate its association with and activation by the platelet-derived growth factor (PDGF) and epidermal growth factor receptors and IRS-1. |
| 25 | 8144631 | The sequence surrounding Tyr1009 bound with greatest affinity (ID50 = 14 microM) of eight PDGF receptor-derived phosphopeptides tested. |
| 26 | 8144631 | These findings are consistent with recent mutational analyses of the PDGF receptor and predict site-specific interactions between SH-PTP2 and each of these phosphoproteins. |
| 27 | 8568932 | Immunolocalization of GLUT1 and GLUT3 glucose transporters in primary cultured neurons and glia. |
| 28 | 8568932 | Immunofluorescence analysis was used to study the cellular localization of glucose transporters 1 and 3 (GLUT1 and GLUT3) in primary rat neuronal and glial cultures. |
| 29 | 8568932 | GLUT3 distribution corresponded most closely with the neural cell adhesion molecule (NCAM), and showed overlapping but distinct distributions compared to synaptophysin, microtubule-associated protein 2 (MAP2), neurofilament protein, and growth-associated protein (GAP43). |
| 30 | 8568932 | GLUT1, but not GLUT3, was detected in glial fibrillary acidic protein (GFAP)-positive astrocytes present in mixed neuronal-glial cultures derived from cerebellum and cerebral cortex, as well as in cortical astrocyte cultures. |
| 31 | 8621530 | Interaction between the Grb10 SH2 domain and the insulin receptor carboxyl terminus. |
| 32 | 8621530 | We identified and isolated the Grb10 SH2 domain based on its interaction with the intracellular domain of the insulin receptor beta-subunit using the yeast two-hybrid system. |
| 33 | 8621530 | The interaction was specific for the insulin receptor and the insulin-like growth factor-1 receptor, and it required a catalytically active receptor kinase domain and an intact Grb10 SH2 domain. |
| 34 | 8621530 | Glutathione S-transferase fusion proteins containing the Grb10 SH2 domain associated in an insulin-dependent manner with insulin receptors from cell lysates and with purified insulin receptors. |
| 35 | 8621530 | Co-precipitation experiments revealed the association of cellular Grb10 with hormone-stimulated insulin receptors in cell extracts. |
| 36 | 8621530 | The Grb10 SH2 domain did not bind to an insulin receptor lacking 43 amino acids at the carboxyl terminus, and it exhibited highest affinity for a phosphopeptide containing Tyr(P)-1322. |
| 37 | 8621530 | Unlike p85 and Syp, which also bind to Tyr(P)-1322, Grb10 was not found to associate with insulin receptor substrate-1. |
| 38 | 8621530 | These results suggest that Grb10 is a novel insulin receptor interactive protein and provide direct evidence for an insulin receptor substrate-1-independent function of the insulin receptor carboxyl terminus in protein binding. |
| 39 | 9139984 | Insulin replacement partially restored (attenuated the loss of) synaptophysin immunoreactivity and maintained neurostimulated intracavernous pressure responses to control levels while having no effect on penile reflexes. |
| 40 | 9388271 | Activation of protein kinase C stimulates tyrosine phosphorylation and activation of ErbB2 and ErbB3. |
| 41 | 9388271 | Purification of the 190-kDa tyrosine-phosphorylated protein revealed that it consists of both ErbB2 and ErbB3. |
| 42 | 9388271 | Following PMA-induced tyrosine phosphorylation, ErbB2 and ErbB3 were able to associate with the SH2 domains of several signaling proteins including the p85alpha subunit of phosphatidylinositol 3-kinase, Syp, and Grb2. |
| 43 | 9388271 | Both ErbB2 and paxillin also exhibit reduced migration on SDS-polyacrylamide gel electrophoresis following PMA treatment, suggesting that they are also phosphorylated on serine/threonine residues. |
| 44 | 9388271 | The activation of ErbB2 and ErbB3 that is initiated by PMA may contribute to the tumor promoting activity of these compounds. |
| 45 | 9392487 | Localization and functional role of synaptotagmin III in insulin secretory vesicles in pancreatic beta-cells. |
| 46 | 9392487 | In the present study, we generated a polyclonal antibody against synaptotagmin III, and found that synaptotagmin III immunoreactivity was present at high levels in insulin-containing pancreatic islet cells and insulin-secreting clonal MIN6 cells. |
| 47 | 9392487 | In subcellular fractionations of MIN6 cells, synaptotagmin III was recovered in the vesicular fractions containing both insulin and vesicle-associated membrane protein-2 (VAMP-2), but not in synaptophysin-positive fractions. |
| 48 | 9392487 | The secretory vesicles immunoprecipitated by anti-VAMP-2 antibody contained synaptotagmin III and insulin. |
| 49 | 9392487 | In addition, treatment of streptolysin-O-permeabilized MIN6 cells with anti-synaptotagmin III antibody significantly inhibited Ca2+-triggered insulin secretion. |
| 50 | 9392487 | These results indicate that synaptotagmin III is localized in insulin-containing dense-core vesicles in pancreatic beta-cells, and further strongly suggest that synaptotagmin III is the Ca2+ sensor in the exocytosis of insulin secretory vesicles. |
| 51 | 10079028 | Chromaffin cells were characterized by immunohistochemical staining against synaptophysin and tyrosine hydroxylase. |
| 52 | 10636906 | Pantophysin is a phosphoprotein component of adipocyte transport vesicles and associates with GLUT4-containing vesicles. |
| 53 | 10636906 | Pantophysin, a protein related to the neuroendocrine-specific synaptophysin, recently has been identified in non-neuronal tissues. |
| 54 | 10636906 | Sucrose gradient ultracentrifugation demonstrated that pantophysin and GLUT4 exhibited overlapping distribution profiles. |
| 55 | 10636906 | Furthermore, immunopurified GLUT4 vesicles contained pantophysin, and both GLUT4 and pantophysin were depleted from this vesicle population following treatment with insulin. |
| 56 | 10636906 | Additionally, a subpopulation of immunopurified pantophysin vesicles contained insulin-responsive GLUT4. |
| 57 | 10636906 | Consistent with the interaction of synaptophysin with vesicle-associated membrane protein 2 in neuroendocrine tissues, pantophysin associated with vesicle-associated membrane protein 2 in adipocytes. |
| 58 | 10636906 | This phosphorylation was unchanged in response to insulin; however, insulin stimulated the phosphorylation of a 77-kDa protein associated with alpha-pantophysin immunoprecipitates. |
| 59 | 10636906 | Although the functional role of pantophysin in vesicle trafficking is unclear, its presence on GLUT4 vesicles is consistent with the emerging role of soluble N-ethylmaleimide-sensitive protein receptor (SNARE) factor complex and related proteins in regulated vesicle transport in adipocytes. |
| 60 | 10636906 | Pantophysin is a phosphoprotein component of adipocyte transport vesicles and associates with GLUT4-containing vesicles. |
| 61 | 10636906 | Pantophysin, a protein related to the neuroendocrine-specific synaptophysin, recently has been identified in non-neuronal tissues. |
| 62 | 10636906 | Sucrose gradient ultracentrifugation demonstrated that pantophysin and GLUT4 exhibited overlapping distribution profiles. |
| 63 | 10636906 | Furthermore, immunopurified GLUT4 vesicles contained pantophysin, and both GLUT4 and pantophysin were depleted from this vesicle population following treatment with insulin. |
| 64 | 10636906 | Additionally, a subpopulation of immunopurified pantophysin vesicles contained insulin-responsive GLUT4. |
| 65 | 10636906 | Consistent with the interaction of synaptophysin with vesicle-associated membrane protein 2 in neuroendocrine tissues, pantophysin associated with vesicle-associated membrane protein 2 in adipocytes. |
| 66 | 10636906 | This phosphorylation was unchanged in response to insulin; however, insulin stimulated the phosphorylation of a 77-kDa protein associated with alpha-pantophysin immunoprecipitates. |
| 67 | 10636906 | Although the functional role of pantophysin in vesicle trafficking is unclear, its presence on GLUT4 vesicles is consistent with the emerging role of soluble N-ethylmaleimide-sensitive protein receptor (SNARE) factor complex and related proteins in regulated vesicle transport in adipocytes. |
| 68 | 11718847 | Triple label immunofluorescence staining of brain sections for galanin, GnRH and the presynaptic vesicle marker synaptophysin coupled with confocal microscopy was employed to identify galanin synapses to GnRH perikarya. |
| 69 | 12047718 | Galanin synaptic input onto gonadotropin-releasing hormone (GnRH) neuronal cell bodies was analysed in female mice using the presynaptic vesicle-specific protein, synaptophysin (Syn) as a marker. |
| 70 | 12047718 | In the first experiment, forebrain sections from normal ovariectomized ovarian steroid-primed mice exhibiting a surge of luteinizing hormone were processed for immunohistochemical labelling for GnRH, synaptophysin, galanin and Fos. |
| 71 | 12047718 | Galanin synaptic input onto gonadotropin-releasing hormone (GnRH) neuronal cell bodies was analysed in female mice using the presynaptic vesicle-specific protein, synaptophysin (Syn) as a marker. |
| 72 | 12047718 | In the first experiment, forebrain sections from normal ovariectomized ovarian steroid-primed mice exhibiting a surge of luteinizing hormone were processed for immunohistochemical labelling for GnRH, synaptophysin, galanin and Fos. |
| 73 | 12242483 | Immunohistochemically, small cells are positive for PDX-1, synaptophysin, insulin, glucagon, somatostatin, pancreatic polypeptide, alpha-fetaprotein and Bcl-2 and negative for cytokeratin 19 and nestin. |
| 74 | 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. |
| 75 | 12403815 | The present study demonstrates that adult human pancreatic duct cells can be converted into insulin-expressing cells after ectopic, adenovirus-mediated expression of the class B basic helix-loop-helix factor neurogenin 3 (ngn3), which is a critical factor in embryogenesis of the mouse endocrine pancreas. |
| 76 | 12403815 | Infection with adenovirus ngn3 (Adngn3) induced gene and/or protein expression of NeuroD/beta2, Pax4, Nkx2.2, Pax6, and Nkx6.1, all known to be essential for beta-cell differentiation in mouse embryos. |
| 77 | 12403815 | Expression of ngn3 in adult human duct cells induced Notch ligands Dll1 and Dll4 and neuroendocrine- and beta-cell-specific markers: it increased the percentage of synaptophysin- and insulin-positive cells 15-fold in ngn3-infected versus control cells. |
| 78 | 12403815 | Infection with NeuroD/beta2 (a downstream target of ngn3) induced similar effects. |
| 79 | 14726964 | CD56-positive cells with or without synaptophysin expression are recognized in the pancreatic duct epithelium: a study with adult and fetal tissues and specimens from chronic pancreatitis. |
| 80 | 15789763 | [The investigation of Syn and NPY expression in brain tissues of diabetic model rat induced by streptozotocin]. |
| 81 | 15789763 | The synaptophysin (Syn) and neuropeptide Y (NPY) expressions in brain tissue of diabetic model rats were investigated. 20 adult Sprague-Dawley male rats were randomly divided into two groups. 10 rats were injected with streptozotocin to induce diabetes, which was identified by blood & urinary sugar level; and the others were injected with sodium citrate buffer as the control. |
| 82 | 15789763 | Afterward freeze sections from the frontal cortex and hippocampus were made and stained with Nissl and Syn, NPY Immunohistochemistry staining. |
| 83 | 15789763 | Both the number of neurons and the light densities of Syn and NPY immunostaining reaction in the frontal cortex and hippocampus of brain tissue sections significantly decreased in the diabetic model rats. |
| 84 | 15789763 | It is suggested that the decrease in neuron number and Syn, NPY expression in frontal cortex and hippocampus may be one of the factors leading to diabetic dementia. |
| 85 | 15789763 | [The investigation of Syn and NPY expression in brain tissues of diabetic model rat induced by streptozotocin]. |
| 86 | 15789763 | The synaptophysin (Syn) and neuropeptide Y (NPY) expressions in brain tissue of diabetic model rats were investigated. 20 adult Sprague-Dawley male rats were randomly divided into two groups. 10 rats were injected with streptozotocin to induce diabetes, which was identified by blood & urinary sugar level; and the others were injected with sodium citrate buffer as the control. |
| 87 | 15789763 | Afterward freeze sections from the frontal cortex and hippocampus were made and stained with Nissl and Syn, NPY Immunohistochemistry staining. |
| 88 | 15789763 | Both the number of neurons and the light densities of Syn and NPY immunostaining reaction in the frontal cortex and hippocampus of brain tissue sections significantly decreased in the diabetic model rats. |
| 89 | 15789763 | It is suggested that the decrease in neuron number and Syn, NPY expression in frontal cortex and hippocampus may be one of the factors leading to diabetic dementia. |
| 90 | 15789763 | [The investigation of Syn and NPY expression in brain tissues of diabetic model rat induced by streptozotocin]. |
| 91 | 15789763 | The synaptophysin (Syn) and neuropeptide Y (NPY) expressions in brain tissue of diabetic model rats were investigated. 20 adult Sprague-Dawley male rats were randomly divided into two groups. 10 rats were injected with streptozotocin to induce diabetes, which was identified by blood & urinary sugar level; and the others were injected with sodium citrate buffer as the control. |
| 92 | 15789763 | Afterward freeze sections from the frontal cortex and hippocampus were made and stained with Nissl and Syn, NPY Immunohistochemistry staining. |
| 93 | 15789763 | Both the number of neurons and the light densities of Syn and NPY immunostaining reaction in the frontal cortex and hippocampus of brain tissue sections significantly decreased in the diabetic model rats. |
| 94 | 15789763 | It is suggested that the decrease in neuron number and Syn, NPY expression in frontal cortex and hippocampus may be one of the factors leading to diabetic dementia. |
| 95 | 15789763 | [The investigation of Syn and NPY expression in brain tissues of diabetic model rat induced by streptozotocin]. |
| 96 | 15789763 | The synaptophysin (Syn) and neuropeptide Y (NPY) expressions in brain tissue of diabetic model rats were investigated. 20 adult Sprague-Dawley male rats were randomly divided into two groups. 10 rats were injected with streptozotocin to induce diabetes, which was identified by blood & urinary sugar level; and the others were injected with sodium citrate buffer as the control. |
| 97 | 15789763 | Afterward freeze sections from the frontal cortex and hippocampus were made and stained with Nissl and Syn, NPY Immunohistochemistry staining. |
| 98 | 15789763 | Both the number of neurons and the light densities of Syn and NPY immunostaining reaction in the frontal cortex and hippocampus of brain tissue sections significantly decreased in the diabetic model rats. |
| 99 | 15789763 | It is suggested that the decrease in neuron number and Syn, NPY expression in frontal cortex and hippocampus may be one of the factors leading to diabetic dementia. |
| 100 | 15789763 | [The investigation of Syn and NPY expression in brain tissues of diabetic model rat induced by streptozotocin]. |
| 101 | 15789763 | The synaptophysin (Syn) and neuropeptide Y (NPY) expressions in brain tissue of diabetic model rats were investigated. 20 adult Sprague-Dawley male rats were randomly divided into two groups. 10 rats were injected with streptozotocin to induce diabetes, which was identified by blood & urinary sugar level; and the others were injected with sodium citrate buffer as the control. |
| 102 | 15789763 | Afterward freeze sections from the frontal cortex and hippocampus were made and stained with Nissl and Syn, NPY Immunohistochemistry staining. |
| 103 | 15789763 | Both the number of neurons and the light densities of Syn and NPY immunostaining reaction in the frontal cortex and hippocampus of brain tissue sections significantly decreased in the diabetic model rats. |
| 104 | 15789763 | It is suggested that the decrease in neuron number and Syn, NPY expression in frontal cortex and hippocampus may be one of the factors leading to diabetic dementia. |
| 105 | 15791482 | Transversal sections of head, body and tail segments were stained with synaptophysin combined with Congo red to map/quantify islet tissue and amyloid. |
| 106 | 16226381 | The regulation of microtubule-associated protein 2, synaptophysin and postsynaptic density-95 was examined in two different animal models of hypercorticosteronemia: corticosterone administration and streptozotocin-induced diabetes using both a short-term (1 week) and long-term (5 weeks) treatment. |
| 107 | 16226381 | Glucocorticoids and/or hyperglycemia increased synaptophysin expression in CA1, CA3 and the dentate gyrus, regions that exhibit synaptic plasticity in response to glucocorticoid exposure. |
| 108 | 16226381 | The regulation of microtubule-associated protein 2, synaptophysin and postsynaptic density-95 was examined in two different animal models of hypercorticosteronemia: corticosterone administration and streptozotocin-induced diabetes using both a short-term (1 week) and long-term (5 weeks) treatment. |
| 109 | 16226381 | Glucocorticoids and/or hyperglycemia increased synaptophysin expression in CA1, CA3 and the dentate gyrus, regions that exhibit synaptic plasticity in response to glucocorticoid exposure. |
| 110 | 16443778 | In islets from the diabetic patients, insulin responses to 8.3 and 16.7 mmol/l glucose were markedly reduced compared with control islets (4.7 +/- 0.3 and 8.4 +/- 1.8 vs. 17.5 +/- 0.1 and 24.3 +/- 1.2 microU . islet(-1) . h(-1), respectively; P < 0.001). |
| 111 | 16443778 | Western blot analysis revealed decreased amounts of islet SNARE complex and SNARE-modulating proteins in diabetes: syntaxin-1A (21 +/- 5% of control levels), SNAP-25 (12 +/- 4%), VAMP-2 (7 +/- 4%), nSec1 (Munc 18; 34 +/- 13%), Munc 13-1 (27 +/- 4%), and synaptophysin (64 +/- 7%). |
| 112 | 16443778 | Microarray gene chip analysis, confirmed by quantitative PCR, showed that gene expression was decreased in diabetes islets: syntaxin-1A (27 +/- 2% of control levels), SNAP-25 (31 +/- 7%), VAMP-2 (18 +/- 3%), nSec1 (27 +/- 5%), synaptotagmin V (24 +/- 2%), and synaptophysin (12 +/- 2%). |
| 113 | 16443778 | In islets from the diabetic patients, insulin responses to 8.3 and 16.7 mmol/l glucose were markedly reduced compared with control islets (4.7 +/- 0.3 and 8.4 +/- 1.8 vs. 17.5 +/- 0.1 and 24.3 +/- 1.2 microU . islet(-1) . h(-1), respectively; P < 0.001). |
| 114 | 16443778 | Western blot analysis revealed decreased amounts of islet SNARE complex and SNARE-modulating proteins in diabetes: syntaxin-1A (21 +/- 5% of control levels), SNAP-25 (12 +/- 4%), VAMP-2 (7 +/- 4%), nSec1 (Munc 18; 34 +/- 13%), Munc 13-1 (27 +/- 4%), and synaptophysin (64 +/- 7%). |
| 115 | 16443778 | Microarray gene chip analysis, confirmed by quantitative PCR, showed that gene expression was decreased in diabetes islets: syntaxin-1A (27 +/- 2% of control levels), SNAP-25 (31 +/- 7%), VAMP-2 (18 +/- 3%), nSec1 (27 +/- 5%), synaptotagmin V (24 +/- 2%), and synaptophysin (12 +/- 2%). |
| 116 | 18487452 | Angiotensin II type 1 receptor signaling contributes to synaptophysin degradation and neuronal dysfunction in the diabetic retina. |
| 117 | 18551299 | The subtotally resected lesion consisted of synaptophysin-immunoreactive lobules of (a) large, polygonal, amphophilic, PAS-positive cells immunoreactive for ACTH, beta-endorphin, alpha melanocyte stimulating hormone (MSH), and keratin (CAM5.2) in some cells showing Crooke hyaline change, (b) less frequent acidophilic, growth hormone (GH) immunoreactive cells, and (c) rare luteinizing hormone (LH) and/or alpha subunit immunopositive cells. |
| 118 | 18551299 | Also conspicuous were smaller cells resembling Rathke-type epithelium forming rosettes to sizable glands immunoreactive for EMA, keratin, S-100 protein, galectin-3 and rarely for synaptophysin and/or one of the above-noted adenohypophysial hormones. |
| 119 | 18551299 | Transcription factors, including Neuro-D1 and Pit-1, were present in ACTH- and GH-producing cells, respectively, but only in occasional Rathke-type cells. |
| 120 | 18551299 | The subtotally resected lesion consisted of synaptophysin-immunoreactive lobules of (a) large, polygonal, amphophilic, PAS-positive cells immunoreactive for ACTH, beta-endorphin, alpha melanocyte stimulating hormone (MSH), and keratin (CAM5.2) in some cells showing Crooke hyaline change, (b) less frequent acidophilic, growth hormone (GH) immunoreactive cells, and (c) rare luteinizing hormone (LH) and/or alpha subunit immunopositive cells. |
| 121 | 18551299 | Also conspicuous were smaller cells resembling Rathke-type epithelium forming rosettes to sizable glands immunoreactive for EMA, keratin, S-100 protein, galectin-3 and rarely for synaptophysin and/or one of the above-noted adenohypophysial hormones. |
| 122 | 18551299 | Transcription factors, including Neuro-D1 and Pit-1, were present in ACTH- and GH-producing cells, respectively, but only in occasional Rathke-type cells. |
| 123 | 20347724 | Diabetes induces changes in ILK, PINCH and components of related pathways in the spinal cord of rats. |
| 124 | 20347724 | Expression of ILK, PINCH, PI3K, GSK-3beta, tau, MAP2, synaptophysin and drebrin in the lumbar spinal cord of non-diabetic and streptozotocin-diabetic rats was assessed by Western-blot analysis and immunocytochemistry after 8 and 20weeks of diabetes. |
| 125 | 20347724 | ILK and PINCH proteins levels were significantly decreased and both colocalized to neurons and oligodendrocytes. |
| 126 | 20347724 | Phosphorylation of tau and MAP2A/B protein expression were significantly increased, and expression of synaptophysin and drebrin were reduced in diabetic rats. |
| 127 | 20347724 | Decreased ILK and PINCH as well as alterations of components of related signaling pathways are associated with tau hyperphosphorylation, MAP2 overexpression and reduction of synaptic proteins in the spinal cord of diabetic rats, suggesting that ILK and PINCH contribute to stabilization of axonal and dendritic structures. |
| 128 | 20347724 | Diabetes induces changes in ILK, PINCH and components of related pathways in the spinal cord of rats. |
| 129 | 20347724 | Expression of ILK, PINCH, PI3K, GSK-3beta, tau, MAP2, synaptophysin and drebrin in the lumbar spinal cord of non-diabetic and streptozotocin-diabetic rats was assessed by Western-blot analysis and immunocytochemistry after 8 and 20weeks of diabetes. |
| 130 | 20347724 | ILK and PINCH proteins levels were significantly decreased and both colocalized to neurons and oligodendrocytes. |
| 131 | 20347724 | Phosphorylation of tau and MAP2A/B protein expression were significantly increased, and expression of synaptophysin and drebrin were reduced in diabetic rats. |
| 132 | 20347724 | Decreased ILK and PINCH as well as alterations of components of related signaling pathways are associated with tau hyperphosphorylation, MAP2 overexpression and reduction of synaptic proteins in the spinal cord of diabetic rats, suggesting that ILK and PINCH contribute to stabilization of axonal and dendritic structures. |
| 133 | 20600668 | Diabetes affected differentially the content of synaptic proteins (VAMP-2, SNAP-25, syntaxin-1, synapsin-1 and synaptophysin) in hippocampal and retinal nerve terminals. |
| 134 | 20600668 | The content of synaptotagmin-1 and rabphilin 3a in nerve terminals of both tissues was not affected. |
| 135 | 22144984 | The renin-angiotensin system (RAS) and reactive oxygen species (ROS) both cause OP impairment and reduced levels of synaptophysin, a synaptic vesicle protein for neurotransmitter release, most likely through excessive protein degradation by the ubiquitin-proteasome system. |
| 136 | 22940631 | The protein levels of synaptophysin, a marker of synaptic integrity, and caspase 9 activity were also evaluated in cortical and hippocampal homogenates. |
| 137 | 22940631 | In addition, higher MDA levels and decreased GSH/GSSG, α-tocopherol levels, and aconitase, glutathione peroxidase and MnSOD activities were observed in both groups of animals. |
| 138 | 23271319 | Furthermore, PMQ significantly activated the Akt/cAMP response element-binding protein pathway and increased the expression of memory-related proteins in the downstream part of the Akt/cAMP response element-binding protein pathway, such as synaptophysin and glutamate receptor 1. |
| 139 | 23271319 | The results suggest that insulin resistance could predominantly reduce Akt/cAMP response element-binding protein activation in the brain, which is associated with a higher risk of cognitive dysfunction. |
| 140 | 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. |
| 141 | 23766563 | High-mobility group box-1 induces decreased brain-derived neurotrophic factor-mediated neuroprotection in the diabetic retina. |
| 142 | 23766563 | To test the hypothesis that brain-derived neurotrophic factor-(BDNF-) mediated neuroprotection is reduced by high-mobility group box-1 (HMGB1) in diabetic retina, paired vitreous and serum samples from 46 proliferative diabetic retinopathy and 34 nondiabetic patients were assayed for BDNF, HMGB1, soluble receptor for advanced glycation end products (sRAGE), soluble intercellular adhesion molecule-1 (sICAM-1), monocyte chemoattractant protein-1 (MCP-1), and TBARS. |
| 143 | 23766563 | The effect of the HMGB1 inhibitor glycyrrhizin on diabetes-induced changes in retinal BDNF expressions was studied. |
| 144 | 23766563 | BDNF levels were significantly lower in serum samples from diabetic patients compared with nondiabetics, whereas HMGB1, sRAGE, sICAM-1, and TBARS levels were significantly higher in diabetic serum samples. |
| 145 | 23766563 | There was significant inverse correlation between serum levels of BDNF and HMGB1. |
| 146 | 23766563 | Diabetes and intravitreal administration of HMGB1 induced significant upregulation of the expression of HMGB1, TBARS, and cleaved caspase-3, whereas the expression of BDNF and synaptophysin was significantly downregulated in rat retinas. |
| 147 | 23766563 | Our results suggest that HMGB1-induced downregulation of BDNF might be involved in pathogenesis of diabetic retinal neurodegeneration. |
| 148 | 23776493 | Diabetes alters KIF1A and KIF5B motor proteins in the hippocampus. |
| 149 | 23776493 | We investigated the effect of diabetes (2 and 8 weeks duration) on KIF1A, KIF5B and dynein motor proteins, which are important for axonal transport, in the hippocampus. |
| 150 | 23776493 | Diabetes increased the expression and immunoreactivity of KIF1A and KIF5B in the hippocampus, but no alterations in dynein were detected. |
| 151 | 23776493 | Nevertheless, high glucose increased the number of fluorescent accumulations of KIF1A and synaptotagmin-1 and decreased KIF5B, SNAP-25 and synaptophysin immunoreactivity specifically in axons of hippocampal neurons. |
| 152 | 23897760 | Enrichment of human embryonic stem cell-derived NKX6.1-expressing pancreatic progenitor cells accelerates the maturation of insulin-secreting cells in vivo. |
| 153 | 23897760 | We previously described a differentiation protocol to generate pancreatic progenitor cells from hESCs, composed of mainly pancreatic endoderm (PDX1/NKX6.1-positive), endocrine precursors (NKX2.2/synaptophysin-positive, hormone/NKX6.1-negative), and polyhormonal cells (insulin/glucagon-positive, NKX6.1-negative). |
| 154 | 23897760 | However, the relative contributions of NKX6.1-negative versus NKX6.1-positive cell fractions to the maturation of functional β-cells remained unclear. |
| 155 | 23897760 | Prior to transplant, both populations contained a high proportion of PDX1-expressing cells (~85%-90%) but were distinguished by their relatively high (~80%) or low (~25%) expression of NKX6.1. |
| 156 | 23897760 | Fasting human C-peptide levels were similar between groups throughout the study, but only NKX6.1-high grafts displayed robust meal-, glucose- and arginine-responsive insulin secretion as early as 3 months post-transplant. |
| 157 | 23897760 | Theracyte devices from both groups contained almost exclusively pancreatic endocrine tissue, but NKX6.1-high grafts contained a greater proportion of insulin-positive and somatostatin-positive cells, whereas NKX6.1-low grafts contained mainly glucagon-expressing cells. |
| 158 | 23897760 | Insulin-positive cells in NKX6.1-high, but not NKX6.1-low grafts expressed nuclear MAFA. |