Difference between revisions of "Phosphatase Subfamily PPM1D"
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* PPM1D (WIP1) is highly expressed in HSCs but decreases with age, and WIP1-deficient (Wip1-/-) mice exhibited multifaceted HSC aging phenotypes, including the increased pool size and impaired repopulating activity <cite>Chen15</cite>. | * PPM1D (WIP1) is highly expressed in HSCs but decreases with age, and WIP1-deficient (Wip1-/-) mice exhibited multifaceted HSC aging phenotypes, including the increased pool size and impaired repopulating activity <cite>Chen15</cite>. | ||
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| + | * PPM1D (WIP1) controls antigen-independent B cell development in a p53-dependent manner <cite>Yi15</cite>. | ||
=== References === | === References === | ||
Revision as of 19:05, 28 May 2015
Phosphatase Classification: Fold PPM (PP2C): Superfamily PPM (PP2C): Family PPM (PP2C): Subfamily PPM1D (WIP1)
Evolution
PPM1D (WIP1) most likely emerged in holozoa. It is single copy in most genomes, including human genome. See internal gOrtholog database.
Domain
PPM1D (WIP1) has a single structure domain, the phosphatase domain of PPM (PP2C) fold.
Function
PPM1D is also known as WIP1 (Wild-type p53-induced phosphatase 1). It negatively regulates the activity of p38 MAP kinase (MAPK/p38) through which it reduces the phosphorylation of p53, and in turn suppresses p53-mediated transcription and apoptosis. It is therefore involved in diverse pathways. Below are some examples of its functions:
- PPM1D (WIP1) oncogene promotes progression and invasion of aggressive medulloblastoma variants [1].
- PPM1D (WIP1) is highly expressed in HSCs but decreases with age, and WIP1-deficient (Wip1-/-) mice exhibited multifaceted HSC aging phenotypes, including the increased pool size and impaired repopulating activity [2].
- PPM1D (WIP1) controls antigen-independent B cell development in a p53-dependent manner [3].
References
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