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
- The mitochondrial permeability transition pore (mPTP) opening is a phenomenon in which the inner mitochondrial membrane abruptly becomes permeable when matrix calcium reaches a critical threshold. Despite 5 decades of intensive research, no protein has been universally accepted as essential for mPTP opening, limiting mechanistic understanding and raising questions about the validity of mPTP-targeted strategies to mitigate cardiac ischemia-reperfusion (I/R) injury. Here, we discuss convergent findings from two independent laboratories identifying the innate immune receptor NLRX1 as an unexpected, essential requirement for mPTP activity. NLRX1 is the only NOD-like receptor (NLR) that is targeted to the mitochondrion. NLRX1 deficiency abolishes (1) calcium-induced mPTP opening, (2) cyclosporine A sensitivity of the pore, and (3) mitochondrial calcium release following cardiac I/R. To test whether loss of mPTP function aligns with loss of NLRX1 across evolution, we performed forward and reciprocal bioinformatic (Blastp) searches and found that species reported to lack an mPTP (e.g., Artemia franciscana and Drosophila melanogaster) also lack NLRX1, further supporting a mandatory role for NLRX1 in mPTP occurrence. Notably, NLRX1-deficient hearts can exhibit increased, rather than decreased, I/R injury at specific ischemia durations. This mirrors reports that deletion of established mPTP regulators (e.g., Ppif) may also worsen injury under defined conditions, consistent with context-dependent, potentially protective roles for transient mPTP activity (e.g., mitochondrial calcium release, PI3K/Akt signaling). In summary, we propose that NLRX1 is the only currently identified protein that is strictly required for mPTP opening, and that indiscriminate inhibition of the mPTP is unlikely to represent a universally effective cardioprotective strategy against I/R injury. - Source: PubMed
Publication date: 2026/08/19
Zuurbier Kielen RZuurbier Coert J - 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 - Mitochondrial dysfunction is considered a hallmark of the aging brain, and this organelle can be affected by several neurodegenerative conditions, leading to slowed bioenergetics and reduced energy production. These processes will affect neuronal communication and synaptic plasticity, generating cognitive decline during aging. Interestingly, we previously observed that mitochondrial dysfunction can be influenced by pathological forms of tau, which are posttranslational modifications of this protein implicated in neurodegeneration and aging. In this context, accumulating evidence indicates that mitochondrial impairment may be associated with activation of the mitochondrial permeability transition pore (mPTP). mPTP has been described as a critical regulator of mitochondrial function, and its pathological activation by cyclophilin D (CypD) induces neurodegeneration and reduces brain function. However, the role of CypD/mPTP on cognitive decline and its implications on tau pathology and neurodegeneration during aging has not been studied. Therefore, we evaluated the contribution of CypD/mPTP in mitochondrial dysfunction, cognitive decline, and tau pathology observed in aging animals. Aging mice lacking CypD expression (CypD-/-) (24-month-old) showed better cognitive performance, improved mitochondrial bioenergetics, increased ATP production, and mPTP closure compared with age-matched wild-type mice (24-month-old) with endogenous expression of CypD. Consequently, hippocampal tissue from aged wild-type animals showed a significant decrease in presynaptic protein levels (SV2) compared to aged CypD-/- animals. More importantly, CypD ablation prevented caspase-3 cleaved tau accumulation in the cytosolic and mitochondrial fractions of hippocampal tissue from 24-month-old mice, in contrast with wild-type aged mice that expressed endogenous CypD. These novel results indicate that CypD acts as a neurodegenerative promoter, inducing synaptic defects and cognitive decline by opening mPTP and mitochondrial dysfunction. More importantly, CypD contributes to the neurodegenerative effects of caspase-3-cleaved tau during aging, suggesting a novel neurodegenerative target induced by tau pathology. - Source: PubMed
Publication date: 2026/07/09
Olesen Margrethe AIsla EduardoJohnson Gail V WPorter George AQuintanilla Rodrigo A - 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