Difference between revisions of "Phosphatase Subfamily PPM1D"

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[[Phosphatase classification|Phosphatase Classification]]: [[Phosphatase_Fold_PPM|Fold PPM (PP2C)]]: [[Phosphatase_Superfamily_PPM|Superfamily PPM (PP2C)]]: [[Phosphatase_Family_PPM|Family PPM (PP2C)]]: [[Phosphatase_Subfamily_PPM1D|Subfamily PPM1D]] (WIP1)
 
[[Phosphatase classification|Phosphatase Classification]]: [[Phosphatase_Fold_PPM|Fold PPM (PP2C)]]: [[Phosphatase_Superfamily_PPM|Superfamily PPM (PP2C)]]: [[Phosphatase_Family_PPM|Family PPM (PP2C)]]: [[Phosphatase_Subfamily_PPM1D|Subfamily PPM1D]] (WIP1)
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=== Evolution ===
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PPM1D (WIP1) most likely emerged in holozoa. It is single copy in most genomes, including human genome. See [http://resdev.gene.com/gOrtholog/view/cluster/MC0005181/overview internal gOrtholog database].
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=== Domain ===
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PPM1D (WIP1) has a single structure domain, the phosphatase domain of PPM (PP2C) fold.
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=== Function ===
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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:
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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>.
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=== References ===
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<biblio>
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#Chen15 pmid=25879755
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</biblio>

Revision as of 17:40, 17 April 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) 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 [1].

References

  1. Chen Z, Yi W, Morita Y, Wang H, Cong Y, Liu JP, Xiao Z, Rudolph KL, Cheng T, and Ju Z. Wip1 deficiency impairs haematopoietic stem cell function via p53 and mTORC1 pathways. Nat Commun. 2015 Apr 16;6:6808. DOI:10.1038/ncomms7808 | PubMed ID:25879755 | HubMed [Chen15]