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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Protein phosphatase, Mg2+/Mn2+ dependent, 1D

Wip1, PPM1D, WIPI, PP2Cdelta
The protein encoded by this gene is a member of the PP2C family of Ser/Thr protein phosphatases. PP2C family members are known to be negative regulators of cell stress response pathways. The expression of this gene is induced in a p53-dependent manner in response to various environmental stresses. While being induced by tumor suppressor protein TP53/p53, this phosphatase 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. This phosphatase thus mediates a feedback regulation of p38-p53 signaling that contributes to growth inhibition and the suppression of stress induced apoptosis. This gene is located in a chromosomal region known to be amplified in breast cancer. The amplification of this gene has been detected in both breast cancer cell line and primary breast tumors, which suggests a role of this gene in cancer development. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: p53, CAN, p38, Atm, Atg18
Papers on Wip1
PPM1D exerts its oncogenic properties in human pancreatic cancer through multiple mechanisms.
Ai et al., Shanghai, China. In Apoptosis, Jan 2016
UNASSIGNED: Protein phosphatase, Mg(2+)/Mn(2+) dependent, 1D (PPM1D) is emerging as an oncogene by virtue of its negative control on several tumor suppressor pathways.
Biallelic FANCD1/BRCA2 mutations predisposing to glioblastoma multiforme with multiple oncogenic amplifications.
Sullivan et al., Melbourne, Australia. In Cancer Genet, Jan 2016
This revealed strong clustering with the K27 mutation subgroup and copy number analysis showed gains of chromosomes 1q, 4q, part of 7q, part of 8q and 17q with resultant amplifications of MDM4, CDK6, MET, MYC and PPM1D (WIP1).
The Pro-apoptotic STK38 Kinase Is a New Beclin1 Partner Positively Regulating Autophagy.
Camonis et al., Paris, France. In Curr Biol, Nov 2015
Upon autophagy induction, STK38-depleted cells display impaired LC3B-II conversion; reduced ATG14L, ATG12, and WIPI-1 puncta formation; and significantly decreased Vps34 activity, as judged by PI3P formation.
SUN anchors pollen WIP-WIT complexes at the vegetative nuclear envelope and is necessary for pollen tube targeting and fertility.
Meier et al., Columbus, United States. In J Exp Bot, Oct 2015
The observed pollen defects are similar to phenotypes observed in a wip1-1 wip2-1 wip3-1 wit1-1 wit2-1 mutant.
Function of human WIPI proteins in autophagosomal rejuvenation of endomembranes?
Proikas-Cezanne et al., Tübingen, Germany. In Febs Lett, Jul 2015
Earlier, we identified the human WD-repeat protein interacting with phosphoinositides (WIPI) family and showed that WIPI proteins function as essential phosphatidylinositol 3-phosphate (PtdIns3P) effectors at the nascent autophagosome.
Immunohistochemistry-based prognostic biomarkers in NSCLC: novel findings on the road to clinical use?
Micke et al., Uppsala, Sweden. In Expert Rev Mol Diagn, Apr 2015
Only 26 proteins first described after 2008 (ALDH1A1, ANXA1, BCAR1, CLDN1, EIF4E, EZH2, FOLR1, FOXM1, IL7R, IL12RB2, KIAA1524, CRMP1, LOX, MCM7, MTA1, MTDH, NCOA3, NDRG2, NEDD9, NES, PBK, PPM1D, SIRT1, SLC7A5, SQSTM1 and WNT1) demonstrated a consistent prognostic association in two or more independent patient cohorts, thus qualifying as promising candidates for diagnostic use.
WIPI proteins: essential PtdIns3P effectors at the nascent autophagosome.
Kohlbacher et al., Tübingen, Germany. In J Cell Sci, Feb 2015
Members of the human WD-repeat protein interacting with phosphoinositides (WIPI) family play an important role in recognizing and decoding the PtdIns3P signal at the nascent autophagosome, and hence function as autophagy-specific PtdIns3P-binding effectors, similar to their ancestral yeast Atg18 homolog.
Age-related mutations associated with clonal hematopoietic expansion and malignancies.
Ding et al., Saint Louis, United States. In Nat Med, 2014
Remarkably, 83% of these mutations were from 19 leukemia and/or lymphoma-associated genes, and nine were recurrently mutated (DNMT3A, TET2, JAK2, ASXL1, TP53, GNAS, PPM1D, BCORL1 and SF3B1).
WIPI-Mediated Autophagy and Longevity.
Proikas-Cezanne et al., Tübingen, Germany. In Cells, 2014
Central to the regulatory relationship between autophagy and longevity is the control of insulin/insulin-like growth factor receptor-driven activation of mTOR (mechanistic target of rapamycin), which inhibits WIPI (WD repeat protein interacting with phosphoinositides)-mediated autophagosome formation.
Marker-assisted selection of Fusarium wilt-resistant and gynoecious melon (Cucumis melo L.).
Luan et al., Harbin, China. In Genet Mol Res, 2014
In this study, molecular markers were designed based on the sex determination genes ACS7 (A) and WIP1 (G) and the domain in the Fusarium oxysporum-resistant gene Fom-2 (F) in order to achieve selection of F. oxysporum-resistant gynoecious melon plants.
Integrated genomic characterization of papillary thyroid carcinoma.
Cancer Genome Atlas Research Network, Bethesda, United States. In Cell, 2014
We observed a low frequency of somatic alterations (relative to other carcinomas) and extended the set of known PTC driver alterations to include EIF1AX, PPM1D, and CHEK2 and diverse gene fusions.
Exome sequencing identifies somatic gain-of-function PPM1D mutations in brainstem gliomas.
Yan et al., Beijing, China. In Nat Genet, 2014
This study led to the discovery of tumor-specific mutations in PPM1D, encoding wild-type p53-induced protein phosphatase 1D (WIP1), in 37.5% of the BSGs that harbored hallmark H3F3A mutations encoding p.Lys27Met substitutions.
Mosaic PPM1D mutations are associated with predisposition to breast and ovarian cancer.
Rahman et al., United Kingdom. In Nature, 2013
Using pooled next-generation sequencing of 507 genes implicated in the repair of DNA in 1,150 samples, an analytical strategy focused on protein-truncating variants (PTVs) and a large-scale sequencing case-control replication experiment in 13,642 individuals, here we show that rare PTVs in the p53-inducible protein phosphatase PPM1D are associated with predisposition to breast cancer and ovarian cancer.
Ionizing radiation-induced responses in human cells with differing TP53 status.
Murray et al., Edmonton, Canada. In Int J Mol Sci, 2012
In addition, we discuss the important role of WIP1, a p53-regulated oncogene, in the temporal regulation of the DNA damage response and its contribution to p53 dynamics post-irradiation.
Wip1-dependent regulation of autophagy, obesity, and atherosclerosis.
Bulavin et al., Singapore, Singapore. In Cell Metab, 2012
Wip1 phosphatase, a known negative regulator of Atm-dependent signaling, plays a major role in controlling fat accumulation and atherosclerosis in mice.
HDM2 promotes WIP1-mediated medulloblastoma growth.
Castellino et al., Atlanta, United States. In Neuro Oncol, 2012
Combined WIP1 and HDM2 inhibition is more effective than WIP1 inhibition alone in blocking growth of WIP1 high-expressing medulloblastoma cells.
Over-expression of wild-type p53-induced phosphatase 1 confers poor prognosis of patients with gliomas.
Jiao et al., China. In Brain Res, 2012
The results of this study suggested that Wip1 may be related to pathological diagnosis and prognosis evaluation for malignant gliomas.
Regulation of the Wip1 phosphatase and its effects on the stress response.
Fornace et al., United States. In Front Biosci, 2011
Wip1 functions to abrogate cell cycle checkpoints and inhibit senescence, apoptosis, DNA repair, and the production of inflammatory cytokines
Wip1-dependent signaling pathways in health and diseases.
Bulavin et al., Singapore, Singapore. In Prog Mol Biol Transl Sci, 2011
The tumor-resistant phenotype of Wip1-deficient mice provides a model for Wip1's role in tumorigenesis. Wip1 also regulates neurogenesis from adult stem cells. Review.
WIP1 phosphatase is a negative regulator of NF-kappaB signalling.
Tergaonkar et al., Singapore, Singapore. In Nat Cell Biol, 2009
WIP1 is a direct phosphatase of Ser 536 of the p65 subunit of NF-kappaB and negatively regulates NF-kappaB signalling.
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