PPIF Antibody - C-terminal (OAAB18234)
- Known as:
- PPIF Antibody - C-terminal (OAAB18234)
- Catalog number:
- oaab18234
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- PPIF Antibody - C-terminal (OAAB18234)
Related genes to: PPIF Antibody - C-terminal (OAAB18234)
- 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 - C-terminal (OAAB18234)
Related articles to: PPIF Antibody - C-terminal (OAAB18234)
- 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 - Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by systemic inflammation and multi-organ involvement, yet its molecular mechanisms remain incompletely understood. While plasma proteomics provides valuable insights into disease-associated alterations, most studies focus on high-abundance proteins. Low-abundance plasma proteins, which often serve as critical regulators of immune signaling and inflammatory pathways, remain insufficiently characterized in RA. - Source: PubMed
Publication date: 2026/05/12
Zhu FengZhang WeiZheng XuejiaLiu DongzhouZeng ZhipengTao HuihuiZhang YujieLi TianyuanQin YurongTang DongeDai Yong - Diabetic foot ulcers (DFU) are a major complication of diabetes, and its pathogenesis remains incompletely elucidated. Converging evidence indicates that oxidative stress and dysregulated mitochondrial polarization participate in DFU progression, nominating these processes as therapeutically actionable targets. This study integrates bulk and single-cell transcriptomic data with machine learning to reconstruct cross-scale, cell type-resolved molecular atlases and regulatory networks. Macrophages and fibroblasts emerged as communication hubs, dominating pathway enrichment and ligand-receptor programs such as macrophage migration inhibitory factor signaling pathway (MIF), ANNEXIN signaling pathway, and COMPLEMENT signaling pathway. Peptidylprolyl isomerase F (PPIF), which encodes cyclophilin D (CypD) and apolipoprotein E (APOE) were further prioritized as putative drivers within macrophages and fibroblasts, and a five-gene classifier was derived with robust performance (internal/external AUC = 0.833/0.933). Within DFU lesions, under the control of non-coding RNA circuitry, SOX5 may shape the inflammatory microenvironment, APOE may participate in lipid-metabolic remodeling, and PPIF (CypD) likely links reactive oxygen species (ROS) accumulation to a p53-dependent mitochondrial death pathway (necroptosis/apoptosis). Orthogonal validation showed significantly increased CypD in diabetic foot ulcer skin (DFUS) and diabetic foot ulcer tendon (DFUT) relative to diabetic foot skin (DFS) and DFT (Diabetic foot tendon), with up-regulated p53 and Cytc and down-regulated ApoE in DFUS; in primary foot-skin fibroblasts, a high-glucose plus tert-butyl hydroperoxide (HG+TBHP) model reproduced elevated ROS, loss of mitochondrial Δψm (mitochondrial membrane potential), growth restriction, and apoptosis, supporting a ROS-CypD/mPTP (mitochondrial permeability transition pore)-Δψm depolarization-p53/Cytc apoptosis axis. The delineated PPIF-centered regulatory network includes upstream transcription factors CEBPB/REL/SPI1 and a downstream ceRNA axis comprising miR-128-3p/miR-23a-3p-long non-coding RNA OIP5-AS1. Additionally, the significant role of polarization-specific reprogramming in regulating macrophage function highlights therapeutic strategies focused on metabolic reprogramming and inhibition of the PPIF/mPTP pathway. Collectively, a cell type-resolved molecular map of DFU is provided, healing-relevant cell populations and regulatory circuits are prioritized, and a translational, testable intervention framework is proposed. - Source: PubMed
Publication date: 2026/04/01
Guo ZeaoZeng ZhaoyangMa XuepengJing Shuai-ShuaiWu YuShan BinPan HaibangShi YuhongLiu AiJiang HugangLi Ning