Gene expression profiling in the human hypothalamus-pituitary-adrenal axis and full-length cDNA cloning

Hu, Renming; Han, Ze‐Guang; Song, Huai-Dong; Peng, Yong; Huang, Qiu-Hua; Ren, Shuangxi; Gu, Ying; Huang, Chang-Jen; Li, Y.-B.; Jiang, Canwen; Fu, Gang; Zhang, Q.-H.; Gu, Bai-Wei; Dai, Mingqiu; Mao, Yuqing; Gao, Guozhen; Ren, Ruojin; Ye, M.; Zhou, Jun; Xu, Sheng; Gu, Jiafeng; Shi, Jun; Jin, Weihua; Zhang, C.-K.; Wu, Tao; Huang, Gege; Chen, Z.; Chen, M.-D.; Chen, J.-L.

doi:10.1073/pnas.160270997

Cited by 94 publications

(66 citation statements)

References 28 publications

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“…Human Insulin Receptor Tyrosine Kinase Substrate (IRTKS), also known as BAI1-associated protein 2-like 1 (BAIAP2L1), was previously cloned from endocrine organs in our laboratory (GenBank accession number: AF119666) [1] and encodes a member of the IRSp53/ MIM (missing-in-metastasis) homology domain family. Members of this family have been shown to play an important role in the formation of plasma membrane protrusions [2].…”

Section: Introductionmentioning

confidence: 99%

Deficiency of IRTKS as an adaptor of insulin receptor leads to insulin resistance

et al. 2013

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IRTKS encodes a member of the IRSp53/MIM homology domain family, which has been shown to play an important role in the formation of plasma membrane protrusions. Although the phosphorylation of IRTKS occurs in response to insulin stimulation, the role of this protein in insulin signaling remains unknown. Here we show that IRTKS-deficient mice exhibit insulin resistance, including hyperglycemia, hyperinsulinemia, glucose intolerance, decreased insulin sensitivity, and increased hepatic glucose production. The administration of ectopic IRTKS can ameliorate the insulin resistance of IRTKS-deficient and diabetic mice. In parallel, the expression level of IRTKS was significantly decreased in diabetic mouse model. Furthermore, DNA hypermethylation of the IRTKS promoter was also observed in these subjects. We also show that IRTKS, as an adaptor of the insulin receptor (IR), modulates IR-IRS1-PI3K-AKT signaling via regulating the phosphorylation of IR. These findings add new insights into our understanding of insulin signaling and resistance.

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Section: Introductionmentioning

confidence: 99%

Deficiency of IRTKS as an adaptor of insulin receptor leads to insulin resistance

et al. 2013

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“…The family members including ING1, ING2, ING3, ING4, and ING5 widely participate in regulating genetic transcription, cell proliferation, apoptosis, cell senescence, contact inhibition, DNA repair, and angiogenic inhibition [8][9][10][11][12][13][14][15]. ING4, as one of the new ING family members, was discovered in 2003 [8].…”

Section: Introductionmentioning

confidence: 99%

Low ING4 protein expression detected by paraffin-section immunohistochemistry is associated with poor prognosis in untreated patients with gastrointestinal stromal tumors

et al. 2013

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Background Inhibitor of growth 4 (ING4) has deserved attention as a tumor suppressor gene in many malignant tumors. In our study, we investigated ING4 immunoexpression in gastrointestinal stromal tumors (GISTs) and its prognostic value. Method The expression of ING4 and Ki67 was investigated in 41 samples of various risk gastrointestinal stromal tumors by immunohistochemical technique. The associations of ING4 expression and clinicopathological parameters, and prognosis of the patients, were analyzed by multivariate Cox regression analysis. Results ING4 expression showed a decreased trend from lower-risk to high-risk gastrointestinal stromal tumors, and an opposite trend for Ki67 expression. In lower-risk tumors, it was found the expression level of ING4 was 78.95 % ± 27.90 % and that of Ki67 was 4.42 % ± 3.75 %. However, in high-risk tumors, the expression level of ING4 was 9.23 % ± 7.66 % and that of Ki67 was 18.50 % ± 9.09 %. There was a strongly negative correlation between the expression levels of ING4 and Ki67. A significant difference was observed in the expression of ING4 between invasion and non-invasion (p \ 0.001). The expression of ING4 was markedly correlated with tumor size (p \ 0.001), mitotic index (p \ 0.001), tumor necrosis (p = 0.021), invasion (p \ 0.001), recurrence and metastasis (p = 0.021), and mortality (p \ 0.001). Conclusion The low expression level of ING4 protein was correlated with high-risk GISTs. ING4 might be involved in the progression of GISTs and inhibit its invasion. ING4 might be one of the prognostic indicators in GISTs.

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“…In previous studies of our group, cDNA libraries of human hypothalamus, pituitary, adrenal and insulinoma tissues were established and several novel full-length cDNAs cloned [25,26]. A novel full-length cDNA cloned from human hypothalamus tissue was selected for further study and found to be related with glucose metabolism (X. Wang and R. Hu, unpublished data).…”

Section: Introductionmentioning

confidence: 99%

Glucose metabolism-related protein 1 (GMRP1) regulates pancreatic beta cell proliferation and apoptosis via activation of Akt signalling pathway in rats and mice

et al. 2011

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Aims/hypothesis We attempted to elucidate the impacts on and possible mechanisms by which glucose metabolismrelated protein 1 (GMRP1) affects beta cell survival. Methods Adenovirus-mediated GMRP1 overproduction and siRNA-mediated knockdown were performed in INS-1E cells and rat islets, after which cell proliferation or apoptosis were determined, and phosphorylation of Akt and BCL2-associated agonist of cell death (BAD) investigated. INS-1E cells and rat islets were cultured at 5.6 (low) or 25 mmol/l (high) glucose for 24 or 48 h, and cell proliferation or apoptosis and GMRP1 levels were investigated. INS-1E cells were treated for 24 h with 0, 10, 50 and 100 nmol/l insulin, and GMRP1 levels were determined. After INS-1E cells were transfected with siRNA for 72 h, high glucose-induced cell proliferation and insulinstimulated Akt phosphorylation were investigated. Glucose-infused rat models were established and beta cell proliferation and mass were evaluated. Levels of GMRP1, and phosphorylation of Akt and BAD were determined in glucose-infused islets. The GMRP1-mediated Akt pathway was also investigated in db/db mice. Results Overproduction of GMRP1 promoted beta cell proliferation via increased phosphorylation of Akt. Knockdown of Gmrp1 (also known as Btbd10) reduced phosphorylation of Akt with enhanced beta cell apoptosis. High glucose increased GMRP1 levels and cell proliferation in INS-1E cells and islet cells. Knockdown of Gmrp1 decreased high glucose-induced cell proliferation and insulin-stimulated Akt phosphorylation. Increased GMRP1 levels were involved in the enhancement of beta cell proliferation and mass in glucose-infused islets. Decreased GMRP1 levels may participate in beta cell apoptosis of db/db mice. Conclusions/interpretation GMRP1 regulates pancreatic beta cell proliferation and apoptosis via activation of Akt signalling pathway.

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Gene expression profiling in the human hypothalamus-pituitary-adrenal axis and full-length cDNA cloning

Cited by 94 publications

References 28 publications

Deficiency of IRTKS as an adaptor of insulin receptor leads to insulin resistance

Deficiency of IRTKS as an adaptor of insulin receptor leads to insulin resistance

Low ING4 protein expression detected by paraffin-section immunohistochemistry is associated with poor prognosis in untreated patients with gastrointestinal stromal tumors

Glucose metabolism-related protein 1 (GMRP1) regulates pancreatic beta cell proliferation and apoptosis via activation of Akt signalling pathway in rats and mice

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