Receptor tyrosine kinases (RTKs) consociate in regulatory clusters in Alzheimer's disease and type 2 diabetes

被引：9

作者：

Majumder, Piyali ^{[1
]}

Roy, Kasturi ^{[1
]}

Bagh, Sangram ^{[1
]}

Mukhopadhyay, Debashis ^{[1
]}

机构：

[1] HBNI, Saha Inst Nucl Phys, Biophys & Struct Genom Div, Block AF,Sect 1, Kolkata 700064, WB, India

来源：

MOLECULAR AND CELLULAR BIOCHEMISTRY | 2019年 / 459卷 / 1-2期

关键词：

Alzheimer's disease; Type; 2; diabetes; RTKs; Regulatory clusters; ENDOPLASMIC-RETICULUM STRESS; INDUCED INSULIN-RESISTANCE; GROWTH-FACTOR RECEPTOR; HEPG2; CELLS; DOWN-REGULATION; PROTEIN; DOMAIN; PHOSPHORYLATION; EXPRESSION; APOPTOSIS;

D O I：

10.1007/s11010-019-03560-5

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Alzheimer's disease (AD) and type 2 diabetes (T2D) share the common hallmark of insulin resistance. It is conjectured that receptor tyrosine kinases (RTKs) play definitive roles in the process. To decipher the signaling overlap behind this phenotypic resemblance, the activity status of RTKs is probed in post-mortem AD and T2D tissues and cell models. Activities of only about one-third changed in a similar fashion, whereas about half of them showed opposite outcomes when exposed to contrasting signals akin to AD and T2D. Interestingly, irrespective of disease type, RTKs with enhanced and compromised activities clustered distinctly, indicating separate levels of regulations. Similar regulatory mechanisms within an activity cluster could be inferred, which have potential to impact future therapeutic developments.

引用

页码：171 / 182

页数：12

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