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Diabetes Pathway Assay (CAT#: STEM-MB-0364-WXH)

Introduction

As the most serious microvascular complication, diabetes mellitus, caused by chronic hyperglycemia, leads to the dysfunction of many cells of the kidney and eventually to the development of renal failure.
The main pathophysiological alteration of diabetes signaling is insulin resistance in target tissues with insufficient insulin secretion. Among them, impaired insulin signaling plays an important role in the pathogenesis. Therefore, insulin signaling in diabetes is of great importance.




Principle

In both type 1 and type 2 diabetes, the lack of insulin also affects downstream insulin signaling. The phosphorylation of IRS proteins on tyrosine residues activates insulin signaling and stimulates glucose transport through the downstream activation of PI3-K. The PI3-K-dependent signaling pathway, which is critical for the metabolic effects of insulin, is usually affected in people with diabetes. IRS proteins are abnormally phosphorylated at serine residues during diabetes. In general, the serine phosphorylation of the insulin receptor inhibits insulin signaling (even though it can act as a positive regulator in certain situations).

Applications

Study the regulatory mechanism of diabetes signaling pathway in clinical diseases
Study the influence of various human viruses on the diabetes signaling pathway
Study the influence of carcinogenic drugs or therapies on the signal pathway of diabetes

Procedure

• Luminex Multiplex Assay
• Enzyme-linked immunosorbent assay (ELISA)
• Flow cytometry (FACS analysis) technology

Notes

Detectable targets: PTP, c-Myc, ULK1, PFK, PHGDH, Erk1, Shc, LKB1, LDHA, ANT, VDAC, Bax, Grb2, PDHK, LC3I, PROLC3, ULK, FIP200, PI3K, VPS34, UYRAG, NFκB, RIG-1, , TRAF3, CAP, ISGF3, MSK2, mTOR, TBK1, Vav, CrkII, IRF9, AMBRA1, p38, RIP1, TRAF5, Gab-1, IRS2, MSK1, p65, Tak1, TLR3, Shp-2, IRF5, MEK3, p38MAPK, SH2, TRAF6, IRSI-4, IRS1, MEK6, p50, p53, TRAM, TRIF, IRAK1, ISRE, PKR

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