Ask about this productRelated genes to: PPM1D antibody
- Gene:
- PPM1D NIH gene
- Name:
- protein phosphatase, Mg2+/Mn2+ dependent 1D
- Previous symbol:
- -
- Synonyms:
- Wip1, PP2C-DELTA
- Chromosome:
- 17q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-10-14
- Date modifiied:
- 2019-04-23
Related products to: PPM1D antibody
Related articles to: PPM1D antibody
- Clonal hematopoiesis driven by somatic mutations is an emerging cardiovascular risk factor, and the DNA damage response gene is among the most frequently mutated genes. Mutations in are enriched in cancer patients and survivors, where cytotoxic therapies promote the expansion of mutant clones, a condition termed therapy-related clonal hematopoiesis. Although -mutant clonal hematopoiesis has been associated with increased risk and poorer prognosis of atherosclerotic cardiovascular disease in humans, it remains unclear whether these mutations, or their expansion under cytotoxic stress, causally contribute to atherosclerosis. - Source: PubMed
Publication date: 2026/05/28
Amorós-Pérez MartaZuriaga María AZorita VirginiaRamos-Neble Beatriz LMatesanz NuriaPlötner ClaraDi Carli MilenaMol Eline L CMoro RosaCuevas DiegoAndrés VicenteFuster José J - Astrocyte-mediated neuroinflammation has recently been implicated as a key contributor to neurodegeneration following retinal ischemia-reperfusion (IR) injury. However, the role of miR‑16‑5p in this process remains unclear. This study aimed to investigate the function and mechanism of miR‑16‑5p. TargetScan was used to predict miR-16-5p targets, which were validated by RNA pull-down. miR‑16‑5p expression was assessed by RT‑qPCR in IR retinas and in astrocytes after oxygen-glucose deprivation/reoxygenation (OGD/R). Astrocyte activation, inflammatory cytokine, and Wip1/nuclear factor kappa B (NF‑κB) signaling were examined following miR-16-5p modulation with mimics or inhibitors in vitro and in vivo. Retinal ganglion cell (RGC) apoptosis, retinal function, and morphology were evaluated. miR‑16‑5p was found to potentially target wild-type p53-induced phosphatase 1 (Wip1) and decreased Wip1 expression. In IR-injured mouse retinas and OGD/R-treated astrocytes, miR‑16‑5p expression was significantly downregulated. This decrease was accompanied by astrocyte activation, increased TNF-α and IL-1β levels, and upregulation of Wip1 and phosphorylated NF-κB p65 (p-p65). These retinal changes indicated retinal injury, characterized by increased TUNEL-positive RGCs, elevated cleaved caspase-3 levels, retinal thinning, and reduced electroretinography (ERG) amplitudes. Treatment with miR-16-5p mimics ameliorated these molecular, cellular, structural, and functional alterations, whereas miR‑16‑5p inhibitors exacerbated them. Collectively, miR-16-5p may protect RGCs from IR-induced apoptosis by suppressing astrocyte-mediated inflammation via the Wip1/NF-κB signaling axis. - Source: PubMed
Publication date: 2026/05/21
Hu WenHe WenjingHuang GuangyiZhou YuchenLi YueTao ShuyaLei DaizaiTang FenTang NingningJiang LiLan QiangqiangHuang HuiChen QiZhang ShaoyangFu HongranHuang RongXu Fan - Clonal hematopoiesis (CH) is an age-associated condition common in the elderly that arises when hematopoietic stem cells acquire somatic mutations in an assortment of genes, most commonly , , , , and CH is associated with increased coronary artery disease and all-cause mortality. Epidemiological studies have revealed that different CH driver mutations are associated with unique outcomes. CH is more prevalent in patients following radiation and cytotoxic therapy. CH has been strongly associated with coronary artery disease, peripheral artery disease, and all-cause mortality. However, it is unclear if this relationship is causative. - Source: PubMed
Publication date: 2026/05/21
De Jeronimo Diaz CesarLiao HuajunHardaway BrianLi LinkeGan Anna LuLiu MandyKim AliceQian GraceAbramowicz SandraLam EditheTseng Zian HDevine W PatrickTall Alan RYu ZhiMiller Peter GEbert Benjamin LFidler Trevor P - Cyclin-dependent kinase 4/6 (CDK4/6) inhibitors such as palbociclib have improved the treatment of hormone receptor-positive, luminal A breast cancer; however, therapeutic resistance remains a major challenge. Wild-type p53-induced phosphatase 1 (Wip1) is a negative regulator of the p53 pathway and is often over-expressed in luminal breast cancers. This study aimed to determine whether Wip1 inhibition enhances the anti-proliferative and pro-apoptotic effects of the CDK4/6 inhibitor palbociclib in luminal A breast cancer cells and to elucidate the underlying cell cycle-related mechanisms. MCF-7 cells were treated with palbociclib and Wip1 inhibitor GSK2830371, alone or in combination. Cell viability was assessed using the WST-1 assay, cell cycle distribution was analysed by flow cytometry, and apoptosis was evaluated using Annexin V/7-aminoactinomycin D staining. Expression of cell cycle regulators (CDK2, CDK4, CDK6, cyclin D1/D3, Rb, phospho-Rb) and p53-related proteins (p53, phospho-p53 Ser15, p21, p27) was determined by Western blot analysis. The combined treatment produced a concentration-dependent reduction in cell viability and a marked increase in both early and late apoptotic populations compared with monotherapies. While palbociclib alone induced G1 arrest, co-treatment with GSK2830371 shifted cells toward G2 accumulation. This was accompanied by enhanced phosphorylation of p53, up-regulation of p21 and p27, and dephosphorylation of Rb, indicating dual checkpoint engagement. These findings demonstrate that Wip1 inhibition augments palbociclib-mediated cell cycle arrest and apoptosis through modulation of the p53-Rb axis. The dual blockade of Wip1 and CDK4/6 may represent a promising therapeutic strategy for p53-proficient luminal A breast cancer. - Source: PubMed
Çolak GökhanKaygusuz NazllcanMeydan NezihOktay EsinKılıc Eren Mehtap - Leukemia cutis (LC) is characterized by dermal infiltration of leukemic blasts and typically occurs in patients with known leukemia. Rarely, LC is identified at the time of initial diagnosis of systemic disease, especially acute myeloid leukemia (AML). We describe a case of LC identified at the initial diagnosis of AML consistent with therapy-related disease in a patient with metastatic non-small-cell lung cancer (NSCLC) previously treated with cytotoxic chemotherapy and immunotherapy. - Source: PubMed
Publication date: 2026/05/09
Bowen AdamDiLoreto NicholasBayya MahaMcDonald RobertIsaac Daniel