期刊
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH
卷 1866, 期 1, 页码 124-143出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.bbamcr.2018.09.002
关键词
MAP kinase; MAP kinase phosphatase; Diabetes; Obesity; Neuropathology; Oncogenic signalling
资金
- Cancer Research UK Program [C8227/A12053]
- MRC [MR/N020790/1]
- Norwegian Cancer Society
- Northern Norway Regional Health Authority/Helse Nord RHF [SFP1170-14]
- Aakre foundation
- Astex Pharmaceuticals through the Milner Therapeutics Consortium
- MRC [MR/N020790/1] Funding Source: UKRI
It is well established that a family of dual-specificity MAP kinase phosphatases (MKPs) play key roles in the regulated dephosphorylation and inactivation of MAP kinase isoforms in mammalian cells and tissues. MKPs provide a mechanism of spatiotemporal feedback control of these key signalling pathways, but can also mediate crosstalk between distinct MAP kinase cascades and facilitate interactions between MAP kinase pathways and other key signalling modules. As our knowledge of the regulation, substrate specificity and catalytic mechanisms of MKPs has matured, more recent work using genetic models has revealed key physiological functions for MKPs and also uncovered potentially important roles in regulating the pathophysiological outcome of signalling with relevance to human diseases. These include cancer, diabetes, inflammatory and neurodegenerative disorders. It is hoped that this understanding will reveal novel therapeutic targets and biomarkers for disease, thus contributing to more effective diagnosis and treatment for these debilitating and often fatal conditions.
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