HIF1A polyclonal antibody
- Known as:
- HIF1A pab (anti-)
- Catalog number:
- PAB9946
- Product Quantity:
- 100 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- HIF1A polyclonal antibody
Related genes to: HIF1A polyclonal antibody
- Gene:
- HIF1A NIH gene
- Name:
- hypoxia inducible factor 1 subunit alpha
- Previous symbol:
- -
- Synonyms:
- MOP1, HIF-1alpha, PASD8, HIF1, bHLHe78
- Chromosome:
- 14q23.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-03-27
- Date modifiied:
- 2018-04-23
Related products to: HIF1A polyclonal antibody
Related articles to: HIF1A polyclonal antibody
- Cerebrovascular damage is increasingly recognized as an early event in the dementia continuum, occurring before typical Alzheimer's disease (AD) pathological changes. Hypoxia-inducible factor 1 (HIF-1) is a transcription factor composed of HIF-1α and HIF-1β subunits which, under hypoxic conditions, dimerize and activate hypoxia response element (HRE)-containing genes. HIF-1α has been reported to be implicated in neuroinflammation, a key feature of AD. - Source: PubMed
Publication date: 2026/06/03
Arosio BeatriceFerri EvelynRossi Paolo DionigiAiello JacopoCaponetto SimoneOlivieri FabiolaFenoglio ChiaraGalimberti DanielaLucchi Tiziano AngeloMontano Nicola - To investigate the molecular mechanism by which gemcitabine (GEM) inhibits ovarian cancer (OC) progression, focusing on the hypoxia-inducible factor 1-alpha (HIF1A)/UBR5/LATS2 axis and Hippo pathway. Bioinformatics analysis of gene expression omnibus datasets identified HIF1A-associated modules. Transcriptional regulation of UBR5 by HIF1A was validated via ChIP-PCR and dual-luciferase assays. Anti-tumor effects of GEM were assessed in OC cell lines and an orthotopic mouse model using functional assays (CCK-8, transwell), Western blot, Co-IP, and ubiquitination analysis. HIF1A transcriptionally upregulates UBR5 in OC. GEM downregulated the HIF1A/UBR5 axis, suppressing OC cell proliferation, migration, and invasion. Mechanistically, UBR5 promoted LATS2 ubiquitination and degradation. GEM inhibited this interaction, stabilizing LATS2, activating the Hippo pathway, and suppressing downstream YAP1/FGFR1 signaling. In vivo, GEM inhibited tumor growth and downregulated HIF1A, UBR5, and FGFR1. GEM suppresses OC progression by targeting the HIF1A/UBR5 axis, which subsequently stabilizes LATS2, activates the Hippo pathway, and inhibits YAP1/FGFR1 signaling, revealing a novel therapeutic mechanism. - Source: PubMed
Publication date: 2026/06/17
Zhang JinXu LixiaGuo KaiDong WeijiaDai XinGu Donghua - Osteoarthritis (OA) is a chronic disease characterized by the degeneration of articular cartilage and secondary hyperosteogeny, typically located in weight-bearing joints. - Source: PubMed
Publication date: 2026/06/18
Yang JiapengQin HuilingHao XintongWang GanggangNi Shufang - Adaptation to chronic hypoxia (CH) enhances myocardial tolerance to ischemia/reperfusion injury and is closely associated with stabilization of hypoxia-inducible factor-1 alpha (HIF-1α), a central transcription factor in hypoxic response. Given the central role of mitochondria in cardiac pathophysiology, we investigated the contribution of HIF-1α to cellular mechanisms underlying CH-induced cardioprotection, with a focus on proteomic remodeling, antioxidant defense, and regulation of the mitochondrial permeability transition pore (mPTP). Adult male wild-type and heterozygous Hif1a knockout mice were exposed to intermittent CH (7000 m, 8 h/day, 4 weeks) or kept under normoxia. Isolated perfused hearts treated with cyclosporine A, an inhibitor of mPTP opening, were subjected to global ischemia/reperfusion insult for infarct size determination. Quantitative label-free proteomics was conducted to assess HIF-1α-dependent changes. We evaluated oxidative stress, measured levels of proteins associated with antioxidant defense and mPTP regulation. In parallel, a proof-of-concept study was performed in transfected AC16 cardiomyocytes exposed to HO-induced oxidative stress. CH induced HIF-1α-dependent cardioprotection by limiting infarct size through regulation of mPTP opening. Moreover, CH attenuated oxidative stress and promoted the protective translocation of hexokinase-2 to mitochondria in an HIF-1α-dependent manner. Consistently, HIF-1α overexpression enhanced cardiomyocyte survival under oxidative stress, whereas HIF-1α inhibition by acriflavine reduced cell viability. These findings identify HIF-1α as a key mediator of CH-induced adaptive response and cardioprotection during I/R injury in the mouse heart, acting through mPTP regulation. - Source: PubMed
Publication date: 2026/06/18
Opletalova BarboraAlan LukasFerko MiroslavAndelova NataliaJanko DavidEckhardt AdamHolzerova KristynaBohuslavova RomanaPavlinkova GabrielaKolar FrantisekHlavackova MarketaAlanova Petra - Cardiovascular diseases, which are non-communicable diseases, are among the leading causes of death worldwide. - Source: PubMed
Publication date: 2026/02/20
Bağış Murat ZiyaAmaç BişarHacanli YaseminErsöz EzharGüldür Muhammet EminKoyuncu İsmailEgi Kadir