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https://www.readbyqxmd.com/read/28105167/cisplatin-induces-hepg2-cell-cycle-arrest-through-targeting-specific-long-noncoding-rnas-and-the-p53-signaling-pathway
#1
Ping Wang, Jiayue Cui, Jihong Wen, Yunhui Guo, Liangzi Zhang, Xia Chen
Cisplatin has been used effectively in the treatment of hepatocellular carcinoma (HCC). Long noncoding RNAs (lncRNAs) were recently reported to contribute to the pathogenesis and progression of HCC. Their molecular mechanism related to cisplatin treatment remains unclear. The purpose of this study is to identify specific lncRNAs and to clarify their functions in HCC after cisplatin exposure. Reannotation and identification of differentially expressed lncRNAs were performed using the microarray data set GSE38122 in the Gene Expression Omnibus database...
December 2016: Oncology Letters
https://www.readbyqxmd.com/read/28097612/wip1-phosphatase-plays-a-critical-neuroprotective-role-in-brain-injury-induced-by-high-altitude-hypoxic-inflammation
#2
Dahu Li, Lijun Zhang, Xin Huang, Lili Liu, Yunling He, Lun Xu, Yiyao Zhang, Tong Zhao, Liying Wu, Yongqi Zhao, Kuiwu Wu, Yan Wu, Ming Fan, Lingling Zhu
The hypobaric hypoxic environment in high-altitude areas often aggravates the severity of inflammation and induces brain injury as a consequence. However, the critical genes regulating this process remain largely unknown. The phosphatase wild-type p53-induced phosphatase 1 (WIP1) plays important roles in various physiological and pathological processes, including the regulation of inflammation in normoxia, but its functions in hypoxic inflammation-induced brain injury remain unclear. Here, we established a mouse model of this type of injury and found that WIP1 deficiency augmented the release of inflammatory cytokines in the peripheral circulation and brain tissue, increased the numbers of activated microglia/macrophages in the brain, aggravated cerebral histological lesions, and exacerbated the impairment of motor and cognitive abilities...
January 17, 2017: Neuroscience Bulletin
https://www.readbyqxmd.com/read/28027003/lzap-is-a-novel-wip1-binding-partner-and-positive-regulator-of-its-phosphatase-activity-in-vitro
#3
J Jacob Wamsley, Natalia Issaeva, Hanbing An, Xinyuan Lu, Lawrence A Donehower, Wendell G Yarbrough
The phosphatase Wip1 attenuates the DNA damage response (DDR) by removing phosphorylation marks from a number of DDR proteins (p53, MDM2, Chk1/2, p38). Wip1 also dephosphorylates and inactivates RelA. Notably, LZAP, a putative tumor suppressor, has been linked to dephosphorylation of several of these substrates, including RelA, p38, Chk1, and Chk2. LZAP has no known catalytic activity or functional motifs, suggesting that it exerts its effects through interaction with other proteins. Here we show that LZAP binds Wip1 and stimulates its phosphatase activity...
December 27, 2016: Cell Cycle
https://www.readbyqxmd.com/read/27991505/wip1-inhibitor-gsk2830371-inhibits-neuroblastoma-growth-by-inducing-chk2-p53-mediated-apoptosis
#4
Zhenghu Chen, Long Wang, Dayong Yao, Tianshu Yang, Wen-Ming Cao, Jun Dou, Jonathan C Pang, Shan Guan, Huiyuan Zhang, Yang Yu, Yanling Zhao, Yongfeng Wang, Xin Xu, Yan Shi, Roma Patel, Hong Zhang, Sanjeev A Vasudevan, Shangfeng Liu, Jianhua Yang, Jed G Nuchtern
Neuroblastoma (NB) is the most common extracranial tumor in children. Unlike in most adult tumors, tumor suppressor protein 53 (p53) mutations occur with a relatively low frequency in NB and the downstream function of p53 is intact in NB cell lines. Wip1 is a negative regulator of p53 and hindrance of Wip1 activity by novel inhibitor GSK2830371 is a potential strategy to activate p53's tumor suppressing function in NB. Yet, the in vivo efficacy and the possible mechanisms of GSK2830371 in NB have not yet been elucidated...
December 19, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27959454/clinical-significance-of-wip1-overexpression-and-its-association-with-the-p38mapk-p53-p16-pathway-in-nsclc
#5
Shize Yang, Siyuan Dong, Xiaohan Qu, Xinwen Zhong, Qigang Zhang
Wip1 is deregulated in numerous human malignancies. However, its roles in non‑small cell lung cancer (NSCLC) remain unclear. In the current study, the expression of Wip1 was investigated in NSCLC and its clinical significance was detected. Immunohistochemical staining was used to measure the expression of (wild‑type p53 induced phosphatase 1) Wip1, p38 mitogen‑activated protein kinase (MAPK), p53, p16 protein in a group of 60 NSCLC and 20 normal lung tissues. In addition, western blotting was performed to detect the Wip1 protein in fresh tissues...
February 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/27713908/ppm1d-wip1-in-medulloblastoma
#6
EDITORIAL
Mwangala P Akamandisa, Rita Nahta, Robert C Castellino
No abstract text is available yet for this article.
2016: Oncoscience
https://www.readbyqxmd.com/read/27687530/wip-1-inhibits-intestinal-inflammation-in-inflammatory-bowel-disease
#7
Qi Zhang, Cuiping Zhang, Fangzhi Chang, Kun Liang, Xiaoyan Yin, Xiaoyu Li, Kun Zhao, Qinghui Niu, Zibin Tian
Inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn's disease (CD), is a chronically intestinal autoimmune disease, the pathological mechanisms of which are not very clear. Wild type p-53 induced phosphatase 1 (Wip1), a serine/threonine protein phosphatase, has been reported to negatively regulate the inflammation in sepsis. However, the role of Wip1 in IBD is not very clear. Therefore, colonic tissues and peripheral blood from patients with IBD and healthy controls were collected to analyzed mRNA and protein expression of Wip1 using the method of qPCR and immunohistochemistry...
July 25, 2016: Cellular Immunology
https://www.readbyqxmd.com/read/27686532/gamma-h2ax-upregulation-caused-by-wip1-deficiency-increases-depression-related-cellular-senescence-in-hippocampus
#8
Zhi-Yong He, Wen-Yue Wang, Wei-Yan Hu, Lu Yang, Yan Li, Wei-Yuan Zhang, Ya-Shu Yang, Si-Cheng Liu, Feng-Lan Zhang, Rong Mei, Da Xing, Zhi-Cheng Xiao, Ming Zhang
The PP2C family member Wild-type p53-induced phosphatase 1 (Wip1) critically regulates DNA damage response (DDR) under stressful situations. In the present study, we investigated whether Wip1 expression was involved in the regulation of DDR-induced and depression-related cellular senescence in mouse hippocampus. We found that Wip1 gene knockout (KO) mice showed aberrant elevation of hippocampal cellular senescence and of γ-H2AX activity, which is known as a biomarker of DDR and cellular senescence, indicating that the lack of Wip1-mediated γ-H2AX dephosphorylation facilitates cellular senescence in hippocampus...
September 30, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27526774/a-novel-mathematical-model-of-atm-p53-nf-%C3%AE%C2%BAb-pathways-points-to-the-importance-of-the-ddr-switch-off-mechanisms
#9
Katarzyna Jonak, Monika Kurpas, Katarzyna Szoltysek, Patryk Janus, Agata Abramowicz, Krzysztof Puszynski
BACKGROUND: Ataxia telangiectasia mutated (ATM) is a detector of double-strand breaks (DSBs) and a crucial component of the DNA damage response (DDR) along with p53 and NF- κB transcription factors and Wip1 phosphatase. Despite the recent advances in studying the DDR, the mechanisms of cell fate determination after DNA damage induction is still poorly understood. RESULTS: To investigate the importance of various DDR elements with particular emphasis on Wip1, we developed a novel mathematical model of ATM/p53/NF- κB pathways...
August 15, 2016: BMC Systems Biology
https://www.readbyqxmd.com/read/27524485/ccan-assembly-configures-composite-binding-interfaces-to-promote-cross-linking-of-ndc80-complexes-at-the-kinetochore
#10
Gülsah Pekgöz Altunkaya, Francesca Malvezzi, Zuzana Demianova, Tomasz Zimniak, Gabriele Litos, Florian Weissmann, Karl Mechtler, Franz Herzog, Stefan Westermann
Partitioning of the genome requires kinetochores, large protein complexes that mediate dynamic attachment of chromosomes to the spindle. Kinetochores contain two supramolecular protein assemblies. The ten-protein KMN network harbors key microtubule-binding sites in the Ndc80 complex and mediates assembly of checkpoint complexes via the KNL-1/Spc105 protein [1, 2]. As KMN does not contact DNA directly, it relies on different centromere-binding proteins for recruitment and cell-cycle-dependent assembly. These proteins are collectively referred to as the CCAN (constitutive centromere-associated network) [2-4]...
September 12, 2016: Current Biology: CB
https://www.readbyqxmd.com/read/27505679/wip1-controls-global-heterochromatin-silencing-via-atm-brca1-dependent-dna-methylation
#11
Doria Filipponi, Julius Muller, Alexander Emelyanov, Dmitry V Bulavin
No abstract text is available yet for this article.
August 8, 2016: Cancer Cell
https://www.readbyqxmd.com/read/27207279/up-regulation-of-wip1-involves-in-neuroinflammation-of-retinal-astrocytes-after-optic-nerve-crush-via-nf-%C3%AE%C2%BAb-signaling-pathway
#12
Haibin Zhong, Ling Cui, Fan Xu, Lifei Chen, Li Jiang, Hui Huang, Jiping Xu, Xin Zhao, Li Li, Siming Zeng, Min Li
OBJECTIVE: To evaluate the expression and possible roles of Wip1 in retinal astrocytes after optic nerve crush (ONC). METHODS: Expressions of Wip1, GFAP, and p-p65 in ONC model were analyzed by Western blot and immunofluorescence. The mRNA expressions of the pro-inflammatory cytokines (IL-8, TNF-α, IL-6 and IL-1β) were analyzed by RT-PCR. RESULTS: Wip1 was up-regulated at 14 days after ONC by Western blot and immunofluorescence. The changes of Wip1 were striking in astrocytes...
September 2016: Inflammation Research: Official Journal of the European Histamine Research Society ... [et Al.]
https://www.readbyqxmd.com/read/27183917/cooperation-of-nutlin-3a-and-a-wip1-inhibitor-to-induce-p53-activity
#13
Anusha Sriraman, Marija Radovanovic, Magdalena Wienken, Zeynab Najafova, Yizhu Li, Matthias Dobbelstein
Targeting the Mdm2 oncoprotein by drugs has the potential of re-establishing p53 function and tumor suppression. However, Mdm2-antagonizing drug candidates, e. g. Nutlin-3a, often fail to abolish cancer cell growth sustainably. To overcome these limitations, we inhibited Mdm2 and simultaneously a second negative regulator of p53, the phosphatase Wip1/PPM1D. When combining Nutlin-3a with the Wip1 inhibitor GSK2830371 in the treatment of p53-proficient but not p53-deficient cells, we observed enhanced phosphorylation (Ser 15) and acetylation (Lys 382) of p53, increased expression of p53 target gene products, and synergistic inhibition of cell proliferation...
May 31, 2016: Oncotarget
https://www.readbyqxmd.com/read/27158969/wip1-phosphatase-modulates-both-long-term-potentiation-and-long-term-depression-through-the-dephosphorylation-of-camkii
#14
Zhi-Yong He, Wei-Yan Hu, Ming Zhang, Zara Zhuyun Yang, Hong-Mei Zhu, Da Xing, Quan-Hong Ma, Zhi-Cheng Xiao
Synaptic plasticity is an important mechanism that underlies learning and cognition. Protein phosphorylation by kinases and dephosphorylation by phosphatases play critical roles in the activity-dependent alteration of synaptic plasticity. In this study, we report that Wip1, a protein phosphatase, is essential for long-term potentiation (LTP) and long-term depression (LTD) processes. Wip1-deletion suppresses LTP and enhances LTD in the hippocampus CA1 area. Wip1 deficiency-induced aberrant elevation of CaMKII T286/287 and T305 phosphorylation underlies these dysfunctions...
May 3, 2016: Cell Adhesion & Migration
https://www.readbyqxmd.com/read/27121065/wip1-suppresses-ovarian-cancer-metastasis-through-the-atm-akt-snail-mediated-signaling
#15
Sheng Yin, Pan Wang, Lina Yang, Yang Liu, Yan Wang, Mingming Liu, Zihao Qi, Jiao Meng, Ting-Yan Shi, Gong Yang, Rongyu Zang
Inactivation of p53 greatly contributes to serous ovarian cancer, while the role of the wild-type p53 induced phosphatase 1 (Wip1) is quite unclear. In this study, by silencing or overexpression of Wip1, we found that Wip1 suppressed ovarian cancer cell invasion, migration, epithelial to mesenchymal transition (EMT), and ovarian cancer metastasis in xenograft animal models. Mechanistic studies showed that Wip1 may block ovarian cancer metastasis through inhibition of Snail and p-Akt expression because silencing or overexpression of Wip1 either upregulated or downregulated the expression of Snail and p-Akt (Ser 473), while further knockdown of Snail by shRNA or inhibition of p-Akt by a chemical compound attenuated cell invasion, migration and EMT in Wip1 silencing cells...
May 17, 2016: Oncotarget
https://www.readbyqxmd.com/read/27086929/wip1-modulates-responsiveness-to-sonic-hedgehog-signaling-in-neuronal-precursor-cells-and-medulloblastoma
#16
J Wen, J Lee, A Malhotra, R Nahta, A R Arnold, M C Buss, B D Brown, C Maier, A M Kenney, M Remke, V Ramaswamy, M D Taylor, R C Castellino
High-level amplification of the protein phosphatase PPM1D (WIP1) is present in a subset of medulloblastomas (MBs) that have an expression profile consistent with active Sonic Hedgehog (SHH) signaling. We found that WIP1 overexpression increased expression of Shh target genes and cell proliferation in response to Shh stimulation in NIH3T3 and cerebellar granule neuron precursor cells in a p53-independent manner. Thus, we developed a mouse in which WIP1 is expressed in the developing brain under control of the Neurod2 promoter (ND2:WIP1)...
April 18, 2016: Oncogene
https://www.readbyqxmd.com/read/27077811/wee1-inhibition-potentiates-wip1-dependent-p53-negative-tumor-cell-death-during-chemotherapy
#17
V Clausse, A R Goloudina, B Uyanik, E Y Kochetkova, S Richaud, O A Fedorova, A Hammann, M Bardou, N A Barlev, C Garrido, O N Demidov
Inactivation of p53 found in more than half of human cancers is often associated with increased tumor resistance to anti-cancer therapy. We have previously shown that overexpression of the phosphatase Wip1 in p53-negative tumors sensitizes them to chemotherapeutic agents, while protecting normal tissues from the side effects of anti-cancer treatment. In this study, we decided to search for kinases that prevent Wip1-mediated sensitization of cancer cells, thereby interfering with efficacy of genotoxic anti-cancer drugs...
April 14, 2016: Cell Death & Disease
https://www.readbyqxmd.com/read/27073481/association-between-overexpression-of-wip1-and-prognosis-of-patients-with-non-small-cell-lung-cancer
#18
Min Zhao, Hongbin Zhang, Guiyun Zhu, Jian Liang, Ning Chen, Yonghui Yang, Xiangcun Liang, Hongmei Cai, Wei Liu
Wild-type p53-induced phosphatase 1 (Wip1), also termed PPM1D, is a member of the protein phosphatase 2C family, which is characterized by distinctive oncogenic properties. Overexpression of Wip1 is observed in certain types of human tumors that are associated with significantly poor prognosis. The present study aimed to detect the expression of Wip1 in non-small cell lung cancer (NSCLC) and to analyze its prognostic value in such patients. The protein expression level of Wip1 was compared between NSCLC and normal lung tissue specimens using by immunohistochemistry, and it was found that Wip1 was highly expressed in NSCLCs but was absent or weakly expressed in normal lung tissues...
April 2016: Oncology Letters
https://www.readbyqxmd.com/read/26950306/phosphatase-wip1-masters-il-17-producing-neutrophil-mediated-colitis-in-mice
#19
Xuelian Hu, Peng Wang, Junfeng Du, Fan Yang, Yuan Tian, Xiaofei Shen, Tao Yang, Lianfeng Zhang, Yong Zhao
Wild-type p53-induced phosphatase 1 (Wip1) is currently believed to be a promising drug target for cancer therapy. Our recent studies showed that deletion of Wip1 remarkably promoted neutrophil inflammatory response. Whether Wip1 is involved in the regulation of inflammatory bowel disease is unknown. In the present study, we found that Wip1 knockout (KO) mice were more susceptible to colitis induced by dextran sulphate sodium (DSS) than wild-type mice as substantiated by the lower mouse survival ratio, rapid bodyweight loss, increased disease activity index, shorter colon length, and more severe pathology of colons in Wip1KO mice...
June 2016: Inflammatory Bowel Diseases
https://www.readbyqxmd.com/read/26928575/feedbacks-bifurcations-and-cell-fate-decision-making-in-the-p53-system
#20
Beata Hat, Marek Kochańczyk, Marta N Bogdał, Tomasz Lipniacki
The p53 transcription factor is a regulator of key cellular processes including DNA repair, cell cycle arrest, and apoptosis. In this theoretical study, we investigate how the complex circuitry of the p53 network allows for stochastic yet unambiguous cell fate decision-making. The proposed Markov chain model consists of the regulatory core and two subordinated bistable modules responsible for cell cycle arrest and apoptosis. The regulatory core is controlled by two negative feedback loops (regulated by Mdm2 and Wip1) responsible for oscillations, and two antagonistic positive feedback loops (regulated by phosphatases Wip1 and PTEN) responsible for bistability...
February 2016: PLoS Computational Biology
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