PPIF Antibody
- Known as:
- PPIF Antibody
- Catalog number:
- GWB-BSP856
- Product Quantity:
- 20ug
- Category:
- -
- Supplier:
- GenWay
- Gene target:
- PPIF Antibody
Related genes to: PPIF Antibody
- Gene:
- PPIF NIH gene
- Name:
- peptidylprolyl isomerase F
- Previous symbol:
- -
- Synonyms:
- hCyP3, Cyp-D
- Chromosome:
- 10q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-06-02
- Date modifiied:
- 2015-09-07
Related products to: PPIF Antibody
Related articles to: PPIF Antibody
- Ppif (Cyclophilin D, CypD) is a key regulator of mitochondrial permeability transition pore (mPTP) opening and plays an important role in maintaining mitochondrial homeostasis by regulating mitochondrial calcium dynamics and redox balance. Although Ppif deficiency has been reported to alter basal mitochondrial function, its impact on hepatocyte responses to carcinogenic stress and hepatocarcinogenesis remains poorly understood. Here, we investigated how Ppif deficiency influences acute cellular responses to diethylnitrosamine (DEN) and the subsequent development of liver tumors. Primary hepatocytes isolated from Ppif -knockout mice exhibited increased basal oxygen consumption and elevated mitochondrial and cellular ROS levels compared with wild-type hepatocytes. Following DEN challenge, Ppif-deficient hepatocytes showed enhanced ROS, increased DNA damage, and greater HIF1α accumulation. Despite these enhanced stress responses, caspase-3 activation and hepatocyte death were attenuated in Ppif-deficient hepatocytes, suggesting altered cellular adaptation to DEN-induced injury. Consistent with these acute responses, chronic DEN treatment resulted in increased oxidative DNA damage, elevated Ki67-positive proliferating cells, and significantly enhanced liver tumor burden in Ppif-deficient mice. Collectively, our findings demonstrate that Ppif deficiency alters hepatocyte responses to carcinogenic stress by promoting the survival of damaged hepatocytes, thereby facilitating DEN-induced hepatocarcinogenesis. These findings identify Ppif as a critical regulator of hepatocyte responses to carcinogenic stress during liver tumor development. - Source: PubMed
Publication date: 2026/07/22
Park Hye-KyungHu SungSong HanaKang Byoung HeonChoi Soo Youn - During the staged progression of chronic obstructive pulmonary disease (COPD), mitophagy homeostasis is disrupted and exhibits a typical dual role. Mitophagy is tightly regulated by ion channel-controlled mitochondrial membrane potential (ΔΨm) and may associate with mitochondrial permeability transition pore (mPTP) dynamics. However, this regulatory mechanism remains largely unknown, and the stage-specific requirements of mitophagy in COPD progression have yet to be established. - Source: PubMed
Publication date: 2026/06/29
Xu AnranLv YapingLi ShaobinZhang XinhuiZhang JirongZhan ChengyanCheng YanqiTang LingZhang ChenXiang SiyangFang HongZhou Donghua - Acute myeloid leukemia (AML) remains challenging to treat due to clinical heterogeneity and a lack of prognostic biomarkers. To address this, we developed a prognostic signature based on platelet-related genes (PRGs). By analyzing transcriptomic data from TCGA-LAML, GSE146173, and Beat AML 2.0 cohorts, we identified and validated an 11-gene signature (PSME2, PPIF, SYTL4, S100A4, CCND3, SMIM15, PARVB, STXBP5, KCNMB1, GABRE, SLC50A1) using LASSO-Cox regression. This model effectively stratified patients into high- and low-risk groups with distinct survival outcomes (p < 0.001) and demonstrated high predictive accuracy (1-/3-/5-year AUC: 0.832/0.782/0.880). High-risk patients exhibited immunosuppressive features, including upregulated immune checkpoints (CD274, CTLA4, HAVCR2, LAG3, PDCD1LG2, PDCD1), prominent monocyte infiltration, and reduced dendritic`11 cell activity. Drug sensitivity analysis suggested gefitinib, zebularine, and simvastatin as potential therapies for high-risk AML (p < 0.05). We further validated the signature's prognostic value using qPCR and clinical grouping. Notably, in vitro studies indicated that KCNMB1 facilitates AML progression. In conclusion, our robust PRG-based model elucidates the link between platelet biology, immune dysregulation, and therapeutic vulnerability in AML, offering clinical utility for risk stratification and treatment decisions. - Source: PubMed
Wu YiChen WanjiaGong SiqiWang JiajiaZhai Zhimin - Despite prevalent gender discrimination in medical education, its influence on personal and professional development, foundational competencies in medical training per the Association of American Medical Colleges (AAMC), remains unclear. This retrospective cross-sectional study assesses how experiences of gender discrimination in medical school influence personal and professional identity formation (PPIF) among males and females. - Source: PubMed
Publication date: 2026/06/22
Venkataraman ShruthiNguyen MytienChaudhry Sarwat IDesai Mayur MFancher Tonya LHajduk Alexandra MMason Hyacinth R CWebber AlexisBoatright Dowin - Acute myeloid leukemia (AML) is a hematologic malignancy characterized by heterogeneity, poor prognosis, and limited biomarkers for risk prediction. Mitochondria pathway related genes (MPRGs), as central regulators of cellular metabolism and immune microenvironment dynamics, may provide useful information for prognostic assessment and biological characterization in AML. - Source: PubMed
Publication date: 2026/05/19
Dou RuiLi WeiZhang LeiLi DanCheng WeiZhu Zunmin