کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9002021 | 1118569 | 2005 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Novel regulatory roles for protein phosphatase-2A in the islet β cell
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کلمات کلیدی
GAPPACCCAPPmTORIHPPP2APP2ACCMLOKAacetyl coA carboxylase - استیل کولا کربوکسیلازOkadaic acid - اسید اوکادائیکInsulin secretion - ترشح انسولینPancreatic islet - جزیره پانکراسApoptosis - خزان یاختهایDiabetes mellitus - دیابت قندیceramide - سرامیدmammalian target of rapamycin - هدف پستانداران رپامایسینprotein phosphatases - پروتئین فسفاتازProtein phosphatase-2A - پروتئین فسفاتاز 2Aprotein phosphatase 2A - پروتئین فسفاتاز 2Aceramide-activated protein phosphatase - پروتئین فسفاتاز فعال فعال سرامید
موضوعات مرتبط
علوم پزشکی و سلامت
داروسازی، سم شناسی و علوم دارویی
داروشناسی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Novel regulatory roles for protein phosphatase-2A in the islet β cell Novel regulatory roles for protein phosphatase-2A in the islet β cell](/preview/png/9002021.png)
چکیده انگلیسی
Protein phosphorylation constitutes one of the key signaling steps in physiological insulin secretion. The phosphorylation status of a given protein represents the balance of the activities of protein kinases and phosphatases, which induce the addition and removal of phosphate from that protein, respectively. Although several extant studies were focused on the identification and characterization of protein kinases in islets, relatively little information is available on the localization and regulation of protein phosphatases in β cells. Emerging evidence implicates protein phosphatase 2A (PP2A) in the phenomenon of insulin secretion. The three principal objectives of this commentary are to: (i) review the existing evidence, which suggests regulation, by glucose and other insulin secretagogues, of PP2A in the β cell; (ii) discuss the experimental evidence, which implicates PP2A-like enzymes in the dephosphorylation and inactivation of key β cell phosphoprotein substrates (e.g., Akt and Bcl-2), which may be necessary for β cell proliferation and survival, culminating in the loss of the β cell mass; and (iii) highlight potential avenues for future research, including the development of specific pharmacological and therapeutic interventional modalities for the inhibition of specific PP2A-like phosphatases for the prevention of loss of β cell mass leading to the onset of diabetes.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical Pharmacology - Volume 69, Issue 12, 15 June 2005, Pages 1681-1691
Journal: Biochemical Pharmacology - Volume 69, Issue 12, 15 June 2005, Pages 1681-1691
نویسندگان
Anjaneyulu Kowluru,