Artykuły w czasopismach: „Insulin receptor gene”

1

Seino, S., M. Seino i G. I. Bell. "Human Insulin-Receptor Gene". Diabetes 39, nr 2 (1.02.1990): 129–33. http://dx.doi.org/10.2337/diab.39.2.129.

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Seino, S., M. Seino i G. I. Bell. "Human insulin-receptor gene". Diabetes 39, nr 2 (1.02.1990): 129–33. http://dx.doi.org/10.2337/diabetes.39.2.129.

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Brunetti, Antonio, i I. D. Goldfine. "Insulin receptor gene expression and insulin resistance". Journal of Endocrinological Investigation 18, nr 5 (maj 1995): 398–405. http://dx.doi.org/10.1007/bf03347847.

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Morris, Brian J. "Insulin Receptor Gene in Hypertension". Clinical and Experimental Hypertension 19, nr 5-6 (styczeń 1997): 551–65. http://dx.doi.org/10.3109/10641969709083169.

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Greenhill, Claire. "Insulin and the insulin receptor regulate gene expression". Nature Reviews Endocrinology 15, nr 6 (11.04.2019): 315. http://dx.doi.org/10.1038/s41574-019-0206-6.

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Soler, A. P., K. A. Thompson, R. M. Smith i L. Jarett. "Immunological demonstration of the accumulation of insulin, but not insulin receptors, in nuclei of insulin-treated cells". Proceedings of the National Academy of Sciences 86, nr 17 (wrzesień 1989): 6640–44. http://dx.doi.org/10.1073/pnas.86.17.6640.

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Although insulin is known to regulate nuclear-related processes, such as cell growth and gene transcription, the mechanisms involved are poorly understood. Previous studies suggested that translocation of insulin or its receptor to cell nuclei might be involved in some of these processes. The present investigation demonstrated that intact insulin, but not the insulin receptor, accumulated in nuclei of insulin-treated cells. Cell fractionation studies demonstrated that the nuclear accumulation of 125I-labeled insulin was time-, temperature-, and insulin-concentration-dependent. Electron microscopic immunocytochemistry demonstrated that the insulin that accumulated in the nucleus was immunologically intact and associated with the heterochromatin. Only 1% of the 125I-labeled insulin extracted from isolated nuclei was eluted from a Sephadex G-50 column as 125I-labeled tyrosine. Plasma membrane insulin receptors were not detected in the nucleus by immuno electron microscopy or when wheat germ agglutinin-purified extracts of the nuclei were subjected to PAGE, electrotransfer, and immunoblotting with anti-insulin receptor antibodies. These results suggested that internalized insulin dissociated from its receptor and accumulated in the nucleus without its membrane receptor. We propose that some of insulin's effects on nuclear function may be caused by the translocation of the intact and biologically active hormone to the nucleus and its binding to nuclear components in the heterochromatin.

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Rojek, Aleksandra, i Marek Niedziela. "Insulin Receptor and its Relationship with Different Forms of Insulin Resistance". Advances in Cell Biology 2, nr 2 (1.02.2010): 59–90. http://dx.doi.org/10.2478/v10052-010-0004-8.

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SummaryInsulin plays an important role in maintaining the whole organism’s homeostasis. The presence of insulin receptors in all vertebrates and invertebrates cells reflects the diversity of regulatory processes in which this hormone is involved. Furthermore, many different factors may influence the level of insulin receptor expression. These factors include e.g. the sole insulin or stage of development. Mutations in the receptor may lead to the development of insulin resistance. These mutations differ in the level of severity and are frequently associated with diabetes mellitus, hypertension, cardiovascular disorders, heart failure, metabolic syndrome and infertility in women. More than 50 mutations in insulin receptor gene have already been characterized. These mutations are associated with rare forms of insulin resistance like leprechaunism, insulin resistance type A or Rabson-Mendenhall syndrome. Molecular analysis of insulin receptor gene may lead to a better understanding of molecular mechanisms underlying various types of insulin resistance and help to develop more efficient treatment.

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TAYLOR, SIMEON I., ALESSANDRO CAMA, DOMENICO ACCILI, FABRIZIO BARBETTI, MICHAEL J. QUON, MARIA DE LA LUZ SIERRA, YOSHIFUMI SUZUKI i in. "Mutations in the Insulin Receptor Gene". Endocrine Reviews 13, nr 3 (sierpień 1992): 566–95. http://dx.doi.org/10.1210/edrv-13-3-566.

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Taylor, S. I., T. Kadowaki, H. Kadowaki, D. Accili, A. Cama i C. McKeon. "Mutations in Insulin-Receptor Gene in Insulin-Resistant Patients". Diabetes Care 13, nr 3 (1.03.1990): 257–79. http://dx.doi.org/10.2337/diacare.13.3.257.

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Kitamura, Tadahiro, Yoshiaki Kido, Serge Nef, Jussi Merenmies, Luis F. Parada i Domenico Accili. "Preserved Pancreatic β-Cell Development and Function in Mice Lacking the Insulin Receptor-Related Receptor". Molecular and Cellular Biology 21, nr 16 (15.08.2001): 5624–30. http://dx.doi.org/10.1128/mcb.21.16.5624-5630.2001.

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ABSTRACT Receptors of the insulin/insulinlike growth factor (IGF) family have been implicated in the regulation of pancreatic β-cell growth and insulin secretion. The insulin receptor-related receptor (IRR) is an orphan receptor of the insulin receptor gene (Ir) subfamily. It is expressed at considerably higher levels in β cells than either insulin or IGF-1 receptors, and it has been shown to engage in heterodimer formation with insulin or IGF-1 receptors. To address whether IRR plays a physiologic role in β-cell development and regulation of insulin secretion, we have characterized mice lacking IRR and generated a combined knockout of Irand Irr. We report that islet morphology, β-cell mass, and secretory function are not affected in IRR-deficient mice. Moreover, lack of IRR does not impair compensatory β-cell hyperplasia in insulin-resistant Ir +/− mice, nor does it affect β-cell development and function inIr −/− mice. We conclude that glucose-stimulated insulin secretion and embryonic β-cell development occur normally in mice lacking Irr.

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Kusari, J., J. M. Olefsky, C. Strahl i D. A. McClain. "Insulin-Receptor cDNA Sequence in NIDDM Patient Homozygous for Insulin-Receptor Gene RFLP". Diabetes 40, nr 2 (1.02.1991): 249–54. http://dx.doi.org/10.2337/diab.40.2.249.

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Kusari, J., J. M. Olefsky, C. Strahl i D. A. McClain. "Insulin-receptor cDNA sequence in NIDDM patient homozygous for insulin-receptor gene RFLP". Diabetes 40, nr 2 (1.02.1991): 249–54. http://dx.doi.org/10.2337/diabetes.40.2.249.

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Veenstra, Jan A. "Ambulacrarian insulin-related peptides and their putative receptors suggest how insulin and similar peptides may have evolved from insulin-like growth factor". PeerJ 9 (14.07.2021): e11799. http://dx.doi.org/10.7717/peerj.11799.

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Background Some insulin/IGF-related peptides (irps) stimulate a receptor tyrosine kinase (RTK) that transfers the extracellular hormonal signal into an intracellular response. Other irps, such as relaxin, do not use an RTK, but a G-protein coupled receptor (GPCR). This is unusual since evolutionarily related hormones typically either use the same or paralogous receptors. In arthropods three different irps, i.e. arthropod IGF, gonadulin and Drosophila insulin-like peptide 7 (dilp7), likely evolved from a gene triplication, as in several species genes encoding these three peptides are located next to one another on the same chromosomal fragment. These arthropod irps have homologs in vertebrates, suggesting that the initial gene triplication was perhaps already present in the last common ancestor of deuterostomes and protostomes. It would be interesting to know whether this is indeed so and how insulin might be related to this trio of irps. Methodology Genes encoding irps as well as their putative receptors were identified in genomes and transcriptomes from echinoderms and hemichordates. Results A similar triplet of genes coding for irps also occurs in some ambulacrarians. Two of these are orthologs of arthropod IGF and dilp7 and the third is likely a gonadulin ortholog. In echinoderms, two novel irps emerged, gonad stimulating substance (GSS) and multinsulin, likely from gene duplications of the IGF and dilp7-like genes respectively. The structures of GSS diverged considerably from IGF, which would suggest they use different receptors from IGF, but no novel irp receptors evolved. If IGF and GSS use different receptors, and the evolution of GSS from a gene duplication of IGF is not associated with the appearance of a novel receptor, while irps are known to use two different types of receptors, the ancestor of GSS and IGF might have acted on both types of receptors while one or both of its descendants act on only one. There are three ambulacrarian GPCRs that have amino acid sequences suggestive of being irp GPCRs, two of these are orthologs of the gonadulin and dilp7 receptors. This suggests that the third might be an IGF receptor, and that by deduction, GSS only acts on the RTK. The evolution of GSS from IGF may represent a pattern, where IGF gene duplications lead to novel genes coding for shorter peptides that activate an RTK. It is likely this is how insulin and the insect neuroendocrine irps evolved independently from IGF. Conclusion The local gene triplication described from arthropods that yielded three genes encoding irps was already present in the last common ancestor of protostomes and deuterostomes. It seems plausible that irps, such as those produced by neuroendocrine cells in the brain of insects and echinoderm GSS evolved independently from IGF and, thus, are not true orthologs, but the result of convergent evolution.

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Morgan, R., A. Bishop, DR Owens i A. Rees. "Insulin Receptor Gene Variants in Non-Insulin Dependent Diabetes Mellitus". Clinical Science 74, s18 (1.01.1988): 41P. http://dx.doi.org/10.1042/cs074041pb.

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Taylor, Simeon I., Alessandro Cama, Hiroko Kadowaki, Takashi Kadowaki i Domenico Accili. "Mutations of the human insulin receptor gene". Trends in Endocrinology & Metabolism 1, nr 3 (styczeń 1990): 134–39. http://dx.doi.org/10.1016/1043-2760(90)90024-w.

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Ojamaa, Kaie, Jose A. Hedo, Charles T. Roberts, Victoria Y. Moncada, Phillip Gorden, Axel Ullrich i Simeon I. Taylor. "Defects in Human Insulin Receptor Gene Expression". Molecular Endocrinology 2, nr 3 (marzec 1988): 242–47. http://dx.doi.org/10.1210/mend-2-3-242.

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Accili, Domenico. "Molecular defects of the insulin receptor gene". Diabetes / Metabolism Reviews 11, nr 1 (kwiecień 1995): 47–62. http://dx.doi.org/10.1002/dmr.5610110105.

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Laustsen, Palle G., Steven J. Russell, Lei Cui, Amelia Entingh-Pearsall, Martin Holzenberger, Ronglih Liao i C. Ronald Kahn. "Essential Role of Insulin and Insulin-Like Growth Factor 1 Receptor Signaling in Cardiac Development and Function". Molecular and Cellular Biology 27, nr 5 (22.12.2006): 1649–64. http://dx.doi.org/10.1128/mcb.01110-06.

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ABSTRACT Cardiovascular disease is the leading cause of death in people with type 2 diabetes and is linked to insulin resistance even in the absence of diabetes. Here we show that mice with combined deficiency of the insulin receptor and insulin-like growth factor 1 (IGF-1) receptor in cardiac and skeletal muscle develop early-onset dilated cardiomyopathy and die from heart failure within the first month of life despite having a normal glucose homeostasis. Mice lacking the insulin receptor show impaired cardiac performance at 6 months, and mice lacking the insulin receptor plus one Igf1r allele have slightly increased mortality. By contrast, mice lacking the IGF-1 receptor or the IGF-1 receptor plus one Ir allele appear normal. Morphological characterization and oligonucleotide array analysis of gene expression demonstrate that prior to development of these physiological defects, mice with combined deficiency of both insulin and IGF-1 receptors have a coordinated down-regulation of genes encoding components of the electron transport chain and mitochondrial fatty acid beta-oxidation pathways and altered expression of contractile proteins. Thus, while neither the insulin receptor nor IGF-1 receptor in muscle is critical for glucose homeostasis during the first month of life, signaling from these receptors, particularly the insulin receptor, is required for normal cardiac metabolism and function.

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Mamluk, Roni, Nitzan Levy, Bo Rueda, John S. Davis i Rina Meidan. "Characterization and Regulation of Type A Endothelin Receptor Gene Expression in Bovine Luteal Cell Types". Endocrinology 140, nr 5 (1.05.1999): 2110–16. http://dx.doi.org/10.1210/endo.140.5.6690.

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Abstract Our previous studies demonstrated that endothelin-1 (ET-1), a 21-amino acid vasoconstrictor peptide, has a paracrine regulatory role in bovine corpus luteum (CL). The peptide is produced within the gland where it inhibits progesterone production by acting via the selective type A endothelin (ETA) receptors. The present study was designed to characterize ETA receptor gene expression in different ovarian cell types and its hormonal regulation. ETA receptor messenger RNA (mRNA) levels were high in follicular cells as well as in CL during luteal regression. At this latter stage, high ETA receptor expression concurred with low prostaglandin F2α receptor mRNA. The ETA receptor gene was expressed by all three major cell populations of the bovine CL; i.e. small and large luteal cells, as well as in luteal endothelial cells. Among these various cell populations, the highest ETA receptor mRNA levels were found in endothelial cells. cAMP elevating agents, forskolin and LH, suppressed ETA receptor mRNA expression in luteinized theca cells (LTC). This inhibition was dose dependent and was evident already after 24 h of incubation. In luteinized granulosa cells (LGC), 10 and 100 ng/ml of insulin-like growth factor I and insulin (only at a concentration of 2000 ng/ml) markedly decreased ETA receptor mRNA levels. In both LGC and LTC there was an inverse relationship between ETA receptor gene expression and progesterone production; insulin (in LGC) and forskolin (in LTC) enhanced progesterone production while inhibiting ETA receptor mRNA levels. Our findings may therefore suggest that, during early stages of luteinization when peak levels of both LH and insulin-like growth factor I exist, the expression of ETA receptors in the gland are suppressed. This study demonstrates physiologically relevant regulatory mechanisms controlling ETA receptor gene expression and further supports the inhibitory role of ET-1 in CL function.

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Vaßen, Lothar, Wojciech Wegrzyn i Ludger Klein-Hitpass. "Human Insulin Receptor Substrate-2 (IRS-2) Is a Primary Progesterone Response Gene". Molecular Endocrinology 13, nr 3 (1.03.1999): 485–94. http://dx.doi.org/10.1210/mend.13.3.0256.

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Abstract Elevated cAMP has been shown to unmask agonist activity of antiprogestin/antiglucocorticoid RU486. In our search for cellular target genes induced through this cross-talk mechanism, we identified human insulin receptor substrate-2 (IRS-2), a cytoplasmic signaling molecule that mediates effects of insulin, insulin-like growth factor-1 (IGF-I), and other cytokines by acting as a molecular adaptor between diverse receptor tyrosine kinases and downstream effectors. Our analysis of the regulation of IRS-2 in HeLa cell models shows that synergistic induction of IRS-2 by cAMP and RU486 can be mediated by progesterone receptors (PR) and glucocorticoid receptors (GR) and occurs through a relative slow mechanism that requires ongoing protein synthesis. Importantly, we demonstrate that IRS-2 mRNA is also inducible by progesterone, while glucocorticoid effects are only observed in the presence of cAMP. Up-regulation of IRS-2 by progesterone depends strictly on the presence of PR and occurs through a rapid mechanism, suggesting that it represents a primary transcriptional response. Furthermore, we show that expression of IRS-1, which also binds to receptors of insulin, IGF-I, and cytokines, is unaffected by progesterone. Thus, our results demonstrate that progesterone alters the ratio of IRS-1 and IRS-2 in PR-positive cells and implicate a mechanism through which progesterone can modulate the effects of insulin, IGF-I, and cytokines on cell proliferation, differentiation, and homeostasis.

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Jiang, Shan, Qichen Fang, Feng Zhang, Hui Wan, Rong Zhang, Congrong Wang, Yuqian Bao i in. "Functional characterization of insulin receptor gene mutations contributing to Rabson-Mendenhall syndrome - phenotypic heterogeneity of insulin receptor gene mutations". Endocrine Journal 58, nr 11 (2011): 931–40. http://dx.doi.org/10.1507/endocrj.ej11-0032.

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Clark, A. R., M. E. Wilson, N. J. M. London, R. F. L. James i K. Docherty. "Identification and characterization of a functional retinoic acid/thyroid hormone-response element upstream of the human insulin gene enhancer". Biochemical Journal 309, nr 3 (1.08.1995): 863–70. http://dx.doi.org/10.1042/bj3090863.

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A deletion analysis of the human insulin gene extending to 2 kb upstream of the transcription start site provided evidence of regulatory sequences located upstream of the insulin-linked polymorphic region (ILPR). Within this ILPR-distal region is a sequence (Ink, for insulin kilobase upstream) which contains three potential nuclear hormone-receptor half-sites, closely matching the consensus sequence AGGTCA. These sequences are arranged as a palindromic element with zero spacing over-lapping a direct repeat with 2 bp spacing. The Ink sequence was used in electrophoretic mobility-shift assays within nuclear extracts from COS-7 cells overexpressing the vitamin D, thyroid hormone or retinoic acid receptors, or from an insulin-expressing hamster cell line, HIT-T15. These studies suggest that the insulin-expressing cell line contains thyroid hormone and retinoic acid receptors at least, and that these receptors are able to recognize the Ink sequence. Three copies of the Ink sequence were placed upstream of the thymidine kinase promoter and firefly luciferase reporter gene. In COS-7 cells expressing the appropriate nuclear hormone receptor, this construct was responsive to both thyroid hormone (18-fold) and all-trans-retinoic acid (31-fold). In HIT-T15 cells the same construct responded to all-trans-retinoic acid, but not to thyroid hormone. Within the context of a 2 kb insulin gene fragment, the Ink sequence was shown to be activated by retinoic acid and by the retinoic acid receptor, but acted as a negative element in the presence of both retinoic acid and the retinoic acid receptor. Mutagenesis studies demonstrated that the palindromic sequence was important for the retinoic acid response, and for binding of complexes containing retinoic acid receptor. In human islets of Langerhans, retinoic acid was shown to stimulate insulin mRNA levels. These results demonstrate that a functional nuclear hormone-receptor-response element is located upstream of the human ILPR. As retinoic acid and thyroid hormone are frequently involved in developmental regulatory processes, it is possible that this element may be important in the process of islet cell differentiation.

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Muller-Wieland, D., R. Taub, D. S. Tewari, K. M. Kriaciunas, S. Sethu, K. Reddy i C. R. Kahn. "Insulin-Receptor Gene and Its Expression in Patients With Insulin Resistance". Diabetes 38, nr 1 (1.01.1989): 31–38. http://dx.doi.org/10.2337/diab.38.1.31.

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LUDWIG, SORA, DIRK MULLER-WIELAND, BARRY J. GOLDSTEIN i C. RONALD KAHN. "The Insulin Receptor Gene and Its Expression in Insulin-Resistant Mice*". Endocrinology 123, nr 1 (lipiec 1988): 594–600. http://dx.doi.org/10.1210/endo-123-1-594.

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Muller-Wieland, D., R. Taub, D. S. Tewari, K. M. Kriauciunas, S. Sethu, K. Reddy i C. R. Kahn. "Insulin-receptor gene and its expression in patients with insulin resistance". Diabetes 38, nr 1 (1.01.1989): 31–38. http://dx.doi.org/10.2337/diabetes.38.1.31.

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SHIMADA, F. "Insulin-resistant diabetes associated with partial deletion of insulin-receptor gene". Lancet 335, nr 8699 (maj 1990): 1179–81. http://dx.doi.org/10.1016/0140-6736(90)92695-e.

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Duan, Chaojun, Hongyan Yang, Morris F. White i Liangyou Rui. "Disruption of the SH2-B Gene Causes Age-Dependent Insulin Resistance and Glucose Intolerance". Molecular and Cellular Biology 24, nr 17 (1.09.2004): 7435–43. http://dx.doi.org/10.1128/mcb.24.17.7435-7443.2004.

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ABSTRACT Insulin regulates glucose homeostasis by binding and activating the insulin receptor, and defects in insulin responses (insulin resistance) induce type 2 diabetes. SH2-B, an Src homology 2 (SH2) and pleckstrin homology domain-containing adaptor protein, binds via its SH2 domain to insulin receptor in response to insulin; however, its physiological role remains unclear. Here we show that SH2-B was expressed in the liver, skeletal muscle, and fat. Systemic deletion of SH2-B impaired insulin receptor activation and signaling in the liver, skeletal muscle, and fat, including tyrosine phosphorylation of insulin receptor substrate 1 (IRS1) and IRS2 and activation of the phosphatidylinositol 3-kinase/Akt and the Erk1/2 pathways. Consequently, SH2-B−/− knockout mice developed age-dependent hyperinsulinemia, hyperglycemia, and glucose intolerance. Moreover, SH2-B directly enhanced autophosphorylation of insulin receptor and tyrosine phosphorylation of IRS1 and IRS2 in an SH2 domain-dependent manner in cultured cells. Our data suggest that SH2-B is a physiological enhancer of insulin receptor activation and is required for maintaining normal insulin sensitivity and glucose homeostasis during aging.

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Payankaulam, Sandhya, Ana-Maria Raicu i David N. Arnosti. "Transcriptional Regulation of INSR, the Insulin Receptor Gene". Genes 10, nr 12 (29.11.2019): 984. http://dx.doi.org/10.3390/genes10120984.

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The insulin receptor gene encodes an evolutionarily conserved signaling protein with a wide spectrum of functions in metazoan development. The insulin signaling pathway plays key roles in processes such as metabolic regulation, growth control, and neuronal function. Misregulation of the pathway features in diabetes, cancer, and neurodegenerative diseases, making it an important target for clinical interventions. While much attention has been focused on differential pathway activation through ligand availability, sensitization of overall signaling may also be mediated by differential expression of the insulin receptor itself. Although first characterized as a “housekeeping” gene with stable expression, comparative studies have shown that expression levels of the human INSR mRNA differ by tissue and in response to environmental signals. Our recent analysis of the transcriptional controls affecting expression of the Drosophila insulin receptor gene indicates that a remarkable amount of DNA is dedicated to encoding sophisticated feedback and feed forward signals. The human INSR gene is likely to contain a similar level of transcriptional complexity; here, we summarize over three decades of molecular biology and genetic research that points to a still incompletely understood regulatory control system. Further elucidation of transcriptional controls of INSR will provide the basis for understanding human genetic variation that underlies population-level physiological differences and disease.

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Hauguel-de-Mouzon, S., C. Mrejen, F. Alengrin i E. Van Obberghen. "Glucose-induced stimulation of human insulin-receptor mRNA and tyrosine kinase activity in cultured cells". Biochemical Journal 305, nr 1 (1.01.1995): 119–24. http://dx.doi.org/10.1042/bj3050119.

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The effects of high glucose on insulin-receptor tyrosine kinase activity and gene expression were investigated in 3T3-HIR cells. Cells incubated for 48 h in the presence of 25 mM glucose showed a 5-fold increase in the amount of insulin receptors per cell, receptor autophosphorylation and phosphorylation of the exogenous substrate poly(Glu/Tyr) compared with cells grown in the absence of glucose but in the presence of 25 mM fructose. These effects were associated with a 4-fold stimulation in steady-state levels of insulin-receptor mRNA. Significant cellular glucose utilization and lactate production were observed in the presence of high glucose in the culture medium, indicating a functional glycolytic pathway in glucose-treated cells, but not in cells treated with fructose. Such a differential response to hexoses favours the hypothesis of a carbohydrate regulation via a glycolytic intermediate. This was further supported by a similar glucose-induced increase in mRNA levels of the enzyme glyceraldehyde-3-phosphate dehydrogenase. To test the hypothesis that the stimulatory effect of glucose on amount of insulin receptors and phosphorylation state could result from post-transcriptional modifications, cells exposed to glucose were incubated with actinomycin D, a potent inhibitor of gene transcription. In cells challenged with high glucose plus inhibitor, insulin-receptor mRNA half-life was increased from 1 to 3 h, indicating that posttranscriptional mechanisms are involved in these processes of glucose regulation. Inhibition of protein synthesis by cycloheximide induced an overexpression of insulin-receptor mRNA levels in the presence of glucose, suggesting that labile repressor protein(s) could be implicated in the effects of glucose. We conclude that (1) long-term culture with high glucose increases the amount of insulin receptors and their tyrosine kinase activity and (2) the glucose-induced increase in insulin-receptor mRNA levels can be accounted for, at least in part, by posttranscriptional events.

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Levy, J. R., i V. Hug. "Regulation of insulin receptor gene expression. Cell cycle-mediated effects on insulin receptor mRNA stability." Journal of Biological Chemistry 267, nr 35 (grudzień 1992): 25289–95. http://dx.doi.org/10.1016/s0021-9258(19)74038-1.

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Otsu, Koji, Yoshiyuki Toya, Jin Oshikawa, Reiko Kurotani, Takuya Yazawa, Motohiko Sato, Utako Yokoyama i in. "Caveolin gene transfer improves glucose metabolism in diabetic mice". American Journal of Physiology-Cell Physiology 298, nr 3 (marzec 2010): C450—C456. http://dx.doi.org/10.1152/ajpcell.00077.2009.

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Caveolin, a member of the membrane-anchoring protein family, accumulates various growth receptors in caveolae and inhibits their function. Upregulation of caveolin attenuates cellular proliferation and growth. However, the role of caveolin in regulating insulin signals remains controversial. Here, we demonstrate that caveolin potently enhances insulin receptor (IR) signaling when overexpressed in the liver in vivo. Adenovirus-mediated gene transfer was used to overexpress caveolin specifically in the liver of diabetic obese mice, which were generated with a high-fat diet. Expression of molecules involved in IR signaling, such as IR or Akt, remained unchanged after gene transfer. However, hepatic glycogen synthesis was markedly increased with a decrease in phosphoenolpyruvate carboxykinase protein expression. Insulin sensitivity was increased after caveolin gene transfer as determined by decreased blood glucose levels in response to insulin injection and fasting blood glucose levels. Glucose tolerant test performance was also improved. Similar improvements were obtained in KKA y genetically diabetic mice. Adenovirus-mediated overexpression of caveolin-3 in hepatic cells also enhanced IR signaling, as shown by increased phosphorylation of IR in response to insulin stimulation and higher glycogen synthesis at baseline. These effects were attributed mostly to increased insulin receptor activity and caveolin-mediated, direct inhibition of protein tyrosine phosphatase 1B, which was increased in obese mouse livers. In conclusion, our results suggest that caveolin is an important regulator of glucose metabolism that can enhance insulin signals.

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Bennett, William L., Shaonin Ji i Joseph L. Messina. "Insulin regulation of growth hormone receptor gene expression". Molecular and Cellular Endocrinology 274, nr 1-2 (sierpień 2007): 53–59. http://dx.doi.org/10.1016/j.mce.2007.05.020.

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Abbott, A. M., R. Bueno, M. T. Pedrini, J. M. Murray i R. J. Smith. "Insulin-like growth factor I receptor gene structure." Journal of Biological Chemistry 267, nr 15 (maj 1992): 10759–63. http://dx.doi.org/10.1016/s0021-9258(19)50083-7.

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Kulkarni, Rohit N., i Terumasa Okada. "Tissue-Specific Targeting of the Insulin Receptor Gene". Endocrine 19, nr 3 (2002): 257–66. http://dx.doi.org/10.1385/endo:19:3:257.

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Sibley, E., T. Kastelic, T. J. Kelly i M. D. Lane. "Characterization of the mouse insulin receptor gene promoter." Proceedings of the National Academy of Sciences 86, nr 24 (1.12.1989): 9732–36. http://dx.doi.org/10.1073/pnas.86.24.9732.

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Persson, Kristin, Giovanni Pacini, Frank Sundler i Bo Ahrén. "Islet Function Phenotype in Gastrin-Releasing Peptide Receptor Gene-Deficient Mice". Endocrinology 143, nr 10 (1.10.2002): 3717–26. http://dx.doi.org/10.1210/en.2002-220371.

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Abstract Gastrin-releasing peptide (GRP) is an islet neuropeptide that stimulates insulin secretion. To explore whether islet GRP contributes to neurally mediated insulin secretion, we studied GRP receptor (GRPR)-deleted mice. By using RT-PCR we showed that GRPR mRNA is expressed in islets of wild-type mice, but is lost in GRPR-deleted mice. Functional studies revealed that GRP potentiates glucose-stimulated insulin secretion in wild-type animals, but not in GRPR-deleted mice. This shows that GRPR is the receptor subtype mediating GRP-induced insulin secretion and that GRPR-deleted mice are tools for studying the physiological role of islet GRP. We found that GRPR-deleted mice display 1) augmentation of the insulin response to glucose by a mechanism inhibited by ganglionic blockade; 2) increased insulin responsiveness also to the cholinergic agonist carbachol, but not to arginine; 3) impaired insulin and glucagon responses to autonomic nerve activation by 2-deoxyglucose; 4) normal islet adaptation to high fat-induced insulin resistance and fasting; and 5) normal islet cytoarchitecture, as revealed by immunocytochemistry of insulin and glucagon. In conclusion, 1) GRPR is the receptor subtype mediating the islet effects of GRP; 2) GRP contributes to insulin secretion induced by activation of the autonomic nerves; and 3) deletion of GRPR is compensated by increased cholinergic sensitivity.

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Shier, P. "Tissue-specific expression of the rat insulin receptor-related receptor gene". Molecular Endocrinology 6, nr 5 (1.05.1992): 723–29. http://dx.doi.org/10.1210/me.6.5.723.

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Shier, P., i V. M. Watt. "Tissue-specific expression of the rat insulin receptor-related receptor gene." Molecular Endocrinology 6, nr 5 (maj 1992): 723–29. http://dx.doi.org/10.1210/mend.6.5.1603082.

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Shen, Wen-jun, Haeyoung S. Kim i Sophia Y. Tsai. "Stimulation of Human Insulin Receptor Gene Expression by Retinoblastoma Gene Product". Journal of Biological Chemistry 270, nr 35 (1.09.1995): 20525–29. http://dx.doi.org/10.1074/jbc.270.35.20525.

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Jensen, Maja, Jane Palsgaard, Rehannah Borup, Pierre de Meyts i Lauge Schäffer. "Activation of the insulin receptor (IR) by insulin and a synthetic peptide has different effects on gene expression in IR-transfected L6 myoblasts". Biochemical Journal 412, nr 3 (28.05.2008): 435–45. http://dx.doi.org/10.1042/bj20080279.

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Single-chain peptides have been recently produced that display either mimetic or antagonistic properties against the insulin and IGF-1 (insulin-like growth factor 1) receptors. We have shown previously that the insulin mimetic peptide S597 leads to significant differences in receptor activation and initiation of downstream signalling cascades despite similar binding affinity and in vivo hypoglycaemic potency. It is still unclear how two ligands can initiate different signalling responses through the IR (insulin receptor). To investigate further how the activation of the IR by insulin and S597 differentially activates post-receptor signalling, we studied the gene expression profile in response to IR activation by either insulin or S597 using microarray technology. We found striking differences between the patterns induced by these two ligands. Most remarkable was that almost half of the genes differentially regulated by insulin and S597 were involved in cell proliferation and growth. Insulin either selectively regulated the expression of these genes or was a more potent regulator. Furthermore, we found that half of the differentially regulated genes interact with the genes involved with the MAPK (mitogen-activated protein kinase) pathway. These findings support our signalling results obtained previously and confirm that the main difference between S597 and insulin stimulation resides in the activation of the MAPK pathway. In conclusion, we show that insulin and S597 acting via the same receptor differentially affect gene expression in cells, resulting in a different mitogenicity of the two ligands, a finding which has critical therapeutic implications.

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Wadley, G. D., R. J. Tunstall, A. Sanigorski, G. R. Collier, M. Hargreaves i D. Cameron-Smith. "Differential effects of exercise on insulin-signaling gene expression in human skeletal muscle". Journal of Applied Physiology 90, nr 2 (1.02.2001): 436–40. http://dx.doi.org/10.1152/jappl.2001.90.2.436.

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Skeletal muscle insulin sensitivity is enhanced after acute exercise and short-term endurance training. We investigated the impact of exercise on the gene expression of key insulin-signaling proteins in humans. Seven untrained subjects (4 women and 3 men) completed 9 days of cycling at 63 ± 2% of peak O2 uptake for 60 min/day. Muscle biopsies were taken before, immediately after, and 3 h after the exercise bouts (on days 1 and 9). The gene expression of insulin receptor substrate-2 and the p85α subunit of phosphatidylinositol 3-kinase was significantly higher 3 h after a single exercise bout, although short-term training ameliorated this effect. Gene expression of insulin receptor and insulin receptor substrate-1 was not significantly altered at any time point. These results suggest that exercise may have a transitory impact on the expression of insulin receptor substrate-2 and phosphatidylinositol 3-kinase; however, the predominant actions of exercise on insulin sensitivity appear not to reside in the transcriptional activation of the genes encoding major insulin-signaling proteins.

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Toyoshima, Yuka, Christopher Monson, Cunming Duan, Yingjie Wu, Chuan Gao, Shoshana Yakar, Kirsten C. Sadler i Derek LeRoith. "The Role of Insulin Receptor Signaling in Zebrafish Embryogenesis". Endocrinology 149, nr 12 (7.08.2008): 5996–6005. http://dx.doi.org/10.1210/en.2008-0329.

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Insulin receptor (IR) signaling is considered to be important in growth and development in addition to its major role in metabolic homeostasis. The metabolic role of insulin in carbohydrate and lipid metabolism is extensively studied. In contrast, the role of IR activation during embryogenesis is less understood. To address this, we examined the function of the IR during zebrafish development. Zebrafish express two isoforms of IR (insra and insrb). Both isoforms were cloned and show high homology to the human insulin receptor and can functionally substitute for the human IR in fibroblasts derived from insr gene-deleted mice. Gene expression studies reveal that these receptors are expressed at moderate levels in the central nervous system during development. Morpholino-mediated selective knockdown of each of the IR isoforms causes growth retardation and profound morphogenetic defects in the brain and eye. These results clearly demonstrate that IR signaling plays essential roles in vertebrate embryogenesis and growth.

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Jin, Jing, Xinxin Liang, Jie Wei i Lingling Xu. "A New Mutation of the INSR Gene in a 13-Year-Old Girl with Severe Insulin Resistance Syndrome in China". BioMed Research International 2021 (25.02.2021): 1–4. http://dx.doi.org/10.1155/2021/8878149.

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Background. Mutations in insulin receptor genes can cause severe insulin resistance syndrome. Compared with Rabson-Mendenhall Syndrome and Donohue’s Syndrome, type A insulin resistance syndrome is generally not serious. The main manifestations in woman with type A insulin resistance syndrome are hyperinsulinemia, insulin resistance, acanthosis nigricans, hyperandrogenism, and polycystic ovary. Case Presentation. A 13-year-old girl (Han nationality) visited the hospital due to hairiness and acanthosis nigricans. Further examination revealed severe hyperinsulinemia, insulin resistance, elevated blood glucose, hyperandrogenism, and polycystic ovary. Analysis of the insulin receptor gene by sequencing showed the presence of a nucleotide change in intron 7 (c. 1610+1G > A). The mutation was a splicing mutation, which can obviously affect the mRNA splicing of the insulin receptor and cause its function loss. The patient was finally diagnosed with type A insulin resistance syndrome. After 2 months of metformin treatment, the patient had spontaneous menstrual cramps and significantly improved acanthosis nigricans and sex hormones. Conclusion. We report for the first time a new splicing mutation on the insulin receptor gene at the 7th intron (c.1610+1G > A), which leads to type A insulin resistance syndrome. In clinically suspected patients with polycystic ovary syndrome, if there are extremely high blood levels of insulin in the blood, genetic testing should be performed to detect insulin receptor gene mutation of type A insulin resistance syndrome.

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Schultz, GA, A. Hogan, AJ Watson, RM Smith i S. Heyner. "Insulin, insulin-like growth factors and glucose transporters: temporal patterns of gene expression in early murine and bovine embryos". Reproduction, Fertility and Development 4, nr 4 (1992): 361. http://dx.doi.org/10.1071/rd9920361.

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mRNA phenotyping by the reverse transcription-polymerase chain reaction (RT-PCR) method was used to compare the patterns of expression of insulin and insulin-like growth factor (IGF) ligand and receptor genes in preimplantation bovine embryos with those established previously for preimplantation murine embryos. In the early bovine embryo, transcripts for IGF-I, IGF-II and mRNAs encoding receptors for insulin, IGF-I and IGF-II were all detectable at all embryo stages from the 1-cell zygote to the blastocyst. In the mouse, IGF-II ligand and receptor mRNAs were not expressed until the 2-cell stage, and the insulin and IGF-I receptor mRNAs were not detectable until the 8-cell stage. Since transcriptional activation of the embryonic genome occurs at the 8- to 16-cell stage in the bovine embryo and at the 2-cell stage in the murine embryo, it is suggested that these transcripts are products of both the maternal and embryonic genomes in the bovine embryo whereas in the mouse they are present only after activation of the embryonic genome. Transcripts for insulin were not detected in preimplantation embryos of either species. Colloidal-gold immunocytochemistry with antibodies directed against the insulin receptor, IGF-I receptor and IGF-I ligand has confirmed the presence of these molecules in bovine blastocysts. RT-PCR and indirect immunofluorescence procedures demonstrated that the glucose transporter (GLUT) isoform 1 is present in murine embryos from the oocyte to blastocyst stage whereas GLUT 2 expression begins at the 8-cell stage.

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Inukai, Kouichi, Youhei Nakashima, Masaki Watanabe, Nobuki Takata, Takahiro Sawa, Susumu Kurihara, Takuya Awata i Shigehiro Katayama. "Regulation of adiponectin receptor gene expression in diabetic mice". American Journal of Physiology-Endocrinology and Metabolism 288, nr 5 (maj 2005): E876—E882. http://dx.doi.org/10.1152/ajpendo.00118.2004.

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Adiponectin is an adipocyte-derived factor that plays pivotal roles in lipid and glucose metabolism in muscle and liver. The following two adiponectin receptor types were recently identified: AdipoR1 is abundantly expressed in muscle, whereas AdipoR2 is predominantly expressed in the liver. To clarify the regulation of adiponectin receptor gene expression in diabetic states, we examined mRNA levels of AdipoR1 in the muscles of diabetic animals by Northern blotting. The level of AdipoR1 mRNA was increased ∼2.5-fold in muscle of streptozotocin (STZ) diabetic mice, but the normal level was restored by insulin administration, indicating that insulin has an inhibitory effect on AdipoR1 expression. To confirm this inhibitory effect of insulin, we performed in vitro experiments using C2C12 skeletal muscle cells. Insulin treatment for 24 h decreased AdipoR1 expression by ∼60% in C2C12 cells. In addition, this effect was mediated by the phosphatidylinositol 3-kinase-dependent pathway rather than the mitogen-activated protein kinase pathway. AdipoR1 expression in insulin-resistant diabetic mice was also investigated. AdipoR1 expression was decreased by 36% in type 2 diabetic obese db/db mice compared with lean mice. In contrast, hepatic AdipoR2 expression was not significantly changed in either STZ mice or genetically obese mice. Our results indicate that regulation of AdipoR1, but not that of AdipoR2, may be involved in glucose and lipid metabolism in diabetic states.

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Al-Sultany, Fadia ‎. H., Ali H. Al- Saadi ‎ i Ibtihal M. Al-Husainy. "Evaluated the Up –regulation in Gene ‎Expression of Hepatic Insulin Gene and ‎Hepatic Insulin Receptor Gene in Type 1 ‎Diabetic Rats Treated with Cuscuta chinesis ‎Lam.‎". JOURNAL OF UNIVERSITY OF BABYLON for Pure and Applied Sciences 26, nr 4 (1.02.2018): 75–93. http://dx.doi.org/10.29196/jub.v26i4.687.

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This research was conducted to study the hypoglycemic activity of C. chinesis Lam on type 1 diabetic disease and investigate the molecular and histological mechanism of its action .many parameters was investigated , Fasting blood glucose (FBG), Fasting serum insulin,Hepatic Insulin Gene Expression, pancreas Insulin Gene Expression ,Hepatic Insulin Receptors Gene expression and histological sections of pancrease and liver.54 Rattus rattus male rats weighting(180 -200g) were divided into 3 groups: A normal control daily administrated with Dw, B Diabetic control daily administrated with Dw and C diabetic group daily administrated with 400 mg/Kg body weight of C. chinesis Lam. methanolic extract, each group consisted of 18 rats and further divided into (3) sub- groups 1 ,2 and 3. According to the period of administration 30, 60 and 90 days respectively. The results showing the daily administration of 400 mg/Kg body weight of C. chinesis Lam. methanolic extract for 60 day causing significance decrease in FBG and In the other hand each of fasting serum insulin, hepatic Insulin gene expression,pancreas Insulin gene expression and hepatic Insulin receptor gene expression was increased in group C in compare to B group and return all studied parameters involving pancrease and liver texture to the normal state ,which were statically morphologically not appeared any significant difference from A group .this study concluded that the daily administration type 1 diabetic rats with 400 mg/Kg body weight of C. chinesis Lam. extract for 60 day was return fasting serum insulin and FBG to normal value by upregulated the gene expression of hepatic INS Gene ,INSR gene , pancreas INS Gene ,regenerate pancreatic beta- cell and returnthe texture of both liver and pancrease to the normal state

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Krook, A., S. Kumar, I. Laing, A. J. M. Boulton, J. A. H. Wass i S. O'Rahilly. "Molecular Scanning of the Insulin Receptor Gene in Syndromes of Insulin Resistance". Diabetes 43, nr 3 (1.03.1994): 357–68. http://dx.doi.org/10.2337/diab.43.3.357.

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Krook, A., S. Kumar, I. Laing, A. J. Boulton, J. A. Wass i S. O'Rahilly. "Molecular scanning of the insulin receptor gene in syndromes of insulin resistance". Diabetes 43, nr 3 (1.03.1994): 357–68. http://dx.doi.org/10.2337/diabetes.43.3.357.

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Accili, D., A. Cama, F. Barbetti, H. Kadowaki, T. Kadowaki i S. I. Taylor. "Insulin resistance due to mutations of the insulin receptor gene: An overview". Journal of Endocrinological Investigation 15, nr 11 (grudzień 1992): 857–64. http://dx.doi.org/10.1007/bf03348820.

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Oelbaum, R. S., P. M. G. Bouloux, S. R. Li, M. G. Baroni, J. Stocks i D. J. Galton. "Insulin receptor gene polymorphisms in Type 2 (non-insulin-dependent) diabetes mellitus". Diabetologia 34, nr 4 (kwiecień 1991): 260–64. http://dx.doi.org/10.1007/bf00405085.

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