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acanthosis nigricans/tyrosine
L'enllaç es desa al porta-retalls
Pàgina 1 des de 42 resultats
Defect in tyrosine kinase activity of the insulin receptor from a patient with insulin resistance and acanthosis nigricans.
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We report here a defect in tyrosine kinase activity of the insulin receptor from an insulin-resistant patient with acanthosis nigricans using cultured Ebstein-Barr virus (EBV)-transformed B-lymphocytes. As judged by affinity labeling and immunoblotting, the alpha- and beta-subunits of insulin
Analysis of the insulin receptor gene tyrosine kinase domain in obese patients with hyperandrogenism, insulin resistance and acanthosis nigricans (type C insulin resistance).
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OBJECTIVE
To test the hypothesis that the triad of hyperandrogenism, insulin resistance and acanthosis nigricans (HAIR-AN syndrome) in the presence of obesity, also known as type C insulin resistance (type C), is caused by mutations at the tyrosine kinase domain of the insulin receptor
Autoantibodies to the insulin receptor (B-10) can stimulate tyrosine phosphorylation of the beta-subunit of the insulin receptor and a 185,000 molecular weight protein in rat hepatoma cells.
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The immunoglobulin G (IgG) fraction obtained from the serum of a patient (B-10) with type B insulin resistance and acanthosis nigricans stimulated both glucose oxidation in rat adipocytes and autophosphorylation of tyrosine residues in the beta-subunit of insulin receptors in H-35 hepatoma cells.
Autophosphorylation of cultured skin fibroblast insulin receptors from patients with severe insulin resistance and acanthosis nigricans.
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The severe insulin resistance with acanthosis nigricans seen in young women without insulin-receptor autoantibodies is characterized by hyperinsulinemia and decreased in vivo responsiveness to insulin. We evaluated the potential cellular defects in insulin-receptor binding and autophosphorylation in
Production of inhibitor of insulin-receptor tyrosine kinase in fibroblasts from patient with insulin resistance and NIDDM.
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Although non-insulin-dependent diabetes mellitus (NIDDM) is associated with defects in insulin action, the molecular basis of this resistance is unknown. We studied fibroblasts from a markedly insulin-resistant patient with NIDDM but without acanthosis nigricans. Her fibroblasts were resistant to
Tyrosine kinase activity of the insulin receptor of patients with type A extreme insulin resistance: studies with circulating mononuclear cells and cultured lymphocytes.
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The syndrome of type A insulin resistance in nonobese women is characterized by hyperinsulinemia, resistance to exogenous insulin, acanthosis nigricans, polycystic ovaries, and masculinization. Insulin binding to intact circulating monocytes and cultured Epstein-Barr virus-transformed B-lymphocytes
Reevaluation of the evidence that an antibody to the insulin receptor is insulinmimetic without activating the protein tyrosine kinase activity of the receptor.
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The immunoglobulin fraction of a polyclonal anti-insulin receptor antibody (B-10) derived from a patient with severe insulin resistance and acanthosis nigricans was tested for its ability to activate the protein kinase activity of the insulin receptor and to mimic insulin action in Chinese hamster
Arg1201Gln mutation of insulin receptor impairs tyrosine kinase activity and causes insulin resistance: a case report.
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Type A insulin resistance syndrome (TAIRS) is a rare subtype of congenital insulin resistance (IR), which is characterized by specific clinical manifestations without clear diagnostic criteria and is easily misdiagnosed or overlooked. Herein we present a case of TAIRS with acanthosis nigricans (AN),
Insulin resistance and diabetes due to different mutations in the tyrosine kinase domain of both insulin receptor gene alleles.
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Mutations in the insulin receptor gene can lead to in vivo and in vitro insulin resistance and can be the cause of diabetes mellitus in selected patients. We have studied a 22-year-old diabetic woman with Type A insulin resistance and acanthosis nigricans. Insulin binding to the patient's
Suppression of severe achondroplasia with developmental delay and acanthosis nigricans by the p.Thr651Pro mutation.
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Severe achondroplasia with developmental delay and acanthosis nigricans (SADDAN) is an extremely rare severe skeletal dysplasia characterized by significant developmental delay, brain structural abnormalities, hearing loss, and acanthosis nigricans. The disorder is the result of a single missense
Transmembrane domain sequence requirements for activation of the p185c-neu receptor tyrosine kinase.
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The receptor tyrosine kinase p185c-neu can be constitutively activated by the transmembrane domain mutation Val664-->Glu, found in the oncogenic mutant p185neu. This mutation is predicted to allow intermolecular hydrogen bonding and receptor dimerization. Understanding the activation of p185c-neu
Activating mutations of the tyrosine kinase receptor FGFR3 are associated with benign skin tumors in mice and humans.
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Specific germline activating point mutations in the gene encoding the tyrosine kinase receptor FGFR3 (fibroblast growth factor receptor 3) result in autosomal dominant human skeletal dysplasias. The identification in multiple myeloma and in two epithelial cancers-bladder and cervical carcinomas-of
Acanthosis nigricans in the setting of niacin therapy.
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We report the case of a 63-year-old obese man with a rapid-onset of widespread acanthosis nigricans (AN) in the setting of having recently initiated treatment with niacin for dyslipidemia. Although obesity and insulin-resistance are risk factors for AN, AN associated with endocrine dysfunction tends
A mutation in the tyrosine kinase domain of the insulin receptor associated with insulin resistance in an obese woman.
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Insulin resistance is frequently associated with acanthosis nigricans and hyperandrogenism. In patients with type A insulin resistance, this has been shown to be due to genetic defects in insulin receptor function. However, other patients with a similar clinical syndrome have been reported to have a
Human diabetes associated with a deletion of the tyrosine kinase domain of the insulin receptor.
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The insulin receptor has an intrinsic tyrosine kinase activity that is essential for signal transduction. A mutant insulin receptor gene lacking almost the entire kinase domain has been identified in an individual with type A insulin resistance and acanthosis nigricans. Insulin binding to the
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