PPM1D encodes WIP1, a serine-threonine phosphatase that had previously been shown to be the driver oncogene of a 17q23 amplicon that is present in approximately 15% of human breast tumors. However, it is unknown whether it has any role in the remaining 85% of breast tumors. A recent study using Wip1-deficient mice revealed that blocking its function significantly impaired RAS and ERBB2-induced breast tumor formation, suggesting that the inhibition of Wip1 could be a broad-spectrum treatment for breast cancer. However, because of the structure of Wip1, the development of small molecule inhibitors is a significant challenge.
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Wip1 Deficiency Promotes Neutrophil Recruitment to the Infection Site and Improves Sepsis Outcome.
Front Immunol
August 2017
Department of General Surgery, PLA Army General Hospital, Beijing, China.
Sepsis is defined as an uncontrolled host response to infection, and no specific therapy or drugs have been used in clinical trials currently. Discovering new therapeutic targets for sepsis treatment has always been a central problem in the field of sepsis research. Neutrophils stand at the first line in controlling infection and have been identified to be dysregulated with impaired migration and antimicrobial function during sepsis.
View Article and Find Full Text PDFPhosphatase wild-type p53-induced phosphatase 1 controls the development of T9 cells and allergic airway inflammation.
J Allergy Clin Immunol
June 2018
State Key Laboratory of Membrane Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China. Electronic address:
Background: Allergic asthma is one of the most common diseases worldwide, resulting in a burden of diseases. No available therapeutic regimens can cure asthma thus far.
Objective: We sought to identify new molecular targets for T9 cell-mediated allergic airway inflammation.
Wild-type p53-induced Phosphatase 1 Deficiency Exacerbates Myocardial Infarction-induced Ischemic Injury.
Chin Med J (Engl)
June 2017
Department of Coronary Artery Disease, State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China.
Background: Myocardial infarction (MI) is a major disease burden. Wild-type p53-induced phosphatase 1 (Wip1) has been studied extensively in the context of cancer and the regulation of different types of stem cells, but the role of Wip1 in cardiac adaptation to MI is unknown. We investigated the significance of Wip1 in a mouse model of MI.
View Article and Find Full Text PDFWIP1 phosphatase is a critical regulator of adipogenesis through dephosphorylating PPARγ serine 112.
Cell Mol Life Sci
June 2017
Department of Cognitive Science, Institute of Basic Medical Sciences, Beijing, 100850, China.
WIP1, as a critical phosphatase, plays many important roles in various physiological and pathological processes through dephosphorylating different substrate proteins. However, the functions of WIP1 in adipogenesis and fat accumulation are not clear. Here, we report that WIP1-deficient mice show impaired body weight growth, dramatically decreased fat mass, and significantly reduced triglyceride and leptin levels in circulation.
View Article and Find Full Text PDFThe use of histone deacetylase inhibitors and inhibitors of MEK/ERK-pathway is proposed as a novel potential approach in cancer treatment. Here we studied the effects of histone deacetylase inhibitor, sodium butyrate, and MEK/ERK-pathway inhibitor, PD0325901, on cells with modifications in genes involved in anti-cancer therapy response, Wip1 phosphatase and p53. We have investigated the effect of these agents on cell cycle of wild-type cells, Wip1 knockout cells and cells with double deletion of Wip1 and p53.
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