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The observations suggest a novel role of ATR kinase in mediating its own signal attenuation via PPM1D recruitment to chromatin as an essential mechanism for restarting the stalled forks, cell cycle re-entry and cellular recovery from replication stress.
NF-kappaB served as a positive transcriptional regulator of WIP1 to activate its expression and affect its function in colorectal cancer cells.
ese results enhance our understanding of the molecular mechanisms that govern nucleoli formation by demonstrating that PPM1D regulates nucleolar formation by regulating NPM phosphorylation status through a novel signalling pathway, PPM1D-CDC25C-CDK1-PLK1
These data support the notion that Wip1 contributes to the formation of the ERMs in PDR membranes via NF-kappaB signaling.
In an in vitro model of the blood-brain barrier, LPS raised Wip1 expression. Wip1 knockdown increased permeability and decreased transepithelial electrical resistance, protein expression of ZO-1, and occluding. Wip1 silencing augmented TNF-alpha, IL-1beta, IL-12, and IL-6. Sonic hedgehog signaling was activated by Wip1 overexpression and inhibited by silencing. Wip1 may protect the BBB against LPS damage via SHH signal...
Studies suugest Wip1 role in tumorigenesis through regulation of p53 and p38MAPK pathways.
The inhibition of Wip1 might fortify p53-mediated tumor suppression by Mdm2 antagonists.
Wip1 suppressed ovarian cancer cell invasion, migration, epithelial to mesenchymal transition (EMT), and ovarian cancer metastasis in xenograft animal models.
model reproduces the observed cellular phenotypes in experiments: oscillatory (for low DNA damage) regulated by negative feedback loops involving mainly p53 and Mdm2 and apoptotic or senescent (for high DNA damage) regulated by the positive p53/Wip1/miR-16 feedback loop
This suggests an important cross-talk between SHH and WIP1 pathways that accelerates tumorigenesis and supports WIP1 inhibition as a potential treatment strategy for MB.
Wip1 activity and its relevance to cancer as an oncoprotein is reviewed
The authors show that a global spread of ATM activity on chromatin and phosphorylation of ATM targets including KAP1 control Plk1 re-activation. These phosphorylations are rapidly counteracted by the chromatin-bound phosphatase Wip1, allowing cell cycle restart despite persistent ATM activity present at DNA lesions.
Truncating and missense PPM1D mutations are associated with prostate cancer.
this study shows that expression of Wip1 is decreased in patients with active inflammatory bowel disease
Wip1 is frequently overexpressed in nonsmall cell lung cancer, which may serve an essential role in the p38MAPK/p53/p16 signaling pathway.
Study identified 14 individuals with mild to severe Intellectual Disability (ID) and/or developmental delay and de novo truncating PPM1D mutations; all mutations were located in the last or penultimate exon, suggesting escape from nonsense-mediated mRNA decay.
PPM1D gene silencing combined with TMZ eradicates glioma cells through cell apoptosis and cell cycle arrest
High PPM1D expression is associated with breast cancer.
PPM1D in the chromosomal location 17q22-24 might be the most relevant candidate gene with respect to a potential functional implication in meningioma progression.
potential prognostic marker and therapeutic target for hepatocellular carcinoma
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.
protein phosphatase 1D
, protein phosphatase 1D magnesium-dependent, delta isoform
, protein phosphatase 2C delta isoform
, protein phosphatase Wip1
, wild-type p53-induced phosphatase 1
, p53-induced protein phosphatase 1
, protein phosphatase 2C isoform delta
, protein phosphatase magnesium-dependent 1 delta
, protein phosphatase, Mg2+/Mn2+ dependent 1D L homeolog
, protein phosphatase, Mg2+/Mn2+ dependent, 1D
, protein phosphatase 1D magnesium-dependent, delta