HIF1a
- Known as:
- HIF1a
- Catalog number:
- 000019A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- HIF1a
Related genes to: HIF1a
- 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
Anserine Hypoxia Inducible Factor 1, Alpha Elisa Kit (HIF1a)Anserine anti - Hypoxia Inducible Factor 1, Alpha Elisa Kit (HIF1a)anti-HIF1A (1A3)anti-HIF1A, Rabbit polyclonal to HIF1A, Isotype IgG, Host RabbitAntibody to Hypoxia Inducible Factor 1 Alpha (HIF1a) Organism: Bos taurus; Bovine (Cattle) Type: Polyclonal Source: RabbitAntibody to Hypoxia Inducible Factor 1 Alpha (HIF1a) Organism: Bos taurus; Bovine (Cattle) Type: Polyclonal Source: RabbitAntibody to Hypoxia Inducible Factor 1 Alpha (HIF1a) Organism: Chicken (Gallus) Type: Polyclonal Source: RabbitAntibody to Hypoxia Inducible Factor 1 Alpha (HIF1a) Organism: Chicken (Gallus) Type: Polyclonal Source: RabbitAntibody to Hypoxia Inducible Factor 1 Alpha (HIF1a) Organism: Homo sapiens (Human) Type: Polyclonal Source: RabbitAntibody to Hypoxia Inducible Factor 1 Alpha (HIF1a) Organism: Homo sapiens (Human) Type: Polyclonal Source: RabbitAntibody to Hypoxia Inducible Factor 1 Alpha (HIF1a) Organism: Mus musculus (Mouse) Type: Polyclonal Source: RabbitAntibody to Hypoxia Inducible Factor 1 Alpha (HIF1a) Organism: Mus musculus (Mouse) Type: Polyclonal Source: RabbitAntibody to Hypoxia Inducible Factor 1 Alpha (HIF1a) Organism: Rattus norvegicus (Rat) Type: Polyclonal Source: RabbitAntibody to Hypoxia Inducible Factor 1 Alpha (HIF1a) Organism: Rattus norvegicus (Rat) Type: Polyclonal Source: RabbitAntigens HIF1A, 576-785aa, Human, His tag, E.coli, Recombinant Related articles to: HIF1a
- Our previous study verified that lipid nephrotoxicity mediated by hypoxia-inducible factor-1 alpha (HIF-1α) activation aggravates diabetic tubular injury. This study investigated whether emodin, an inhibitor of HIF-1α, improves tubular injury by reducing lipid accumulation in diabetic tubules, and examined its underlying mechanism. - Source: PubMed
Wang YingDeng XueZhu Qian-WenZhang JingQian Zhi-WeiGao FangZhan Shu-QinWu ChaoWang LinLi ShuHu Ze-Bo - Regulatory T (Treg) cells play crucial roles in myocardial fibrosis, a key pathological feature of diabetic cardiomyopathy (DCM). Deleted in breast cancer 1 (DBC1) has emerged as an inhibitor of the immunosuppressive function of Treg cells in inflammatory states. Here, we studied the subpopulation differentiation and function of Treg cells in the myocardium of DCM and explored the role of DBC1 in Treg cell differentiation. - Source: PubMed
Publication date: 2026/04/13
Lu LinheXu YifeiWen ChangnuanZhao QiancongLi ZhihangLiu JiaqiXu FujieLiu JinchengTang Jiayou - Disease progression in multiple sclerosis (MS) remains a major unmet clinical challenge, as it is driven by pathogenic mechanisms that are poorly targeted by currently available disease-modifying treatments. Whereas acute focal inflammation characterizes the relapsing-remitting phase, converging neuropathological, imaging and experimental evidence identifies a chronic low-grade compartmentalized inflammatory process, the so-called "smoldering" inflammation, as a central driver of disease progression in MS. Recent findings suggest that both tissue hypoxia (primarily resulting from vascular dysfunction) and virtual hypoxia (a state of metabolic supply-demand mismatch culminating in bioenergetic failure) may critically contribute to the onset, persistence and compartmentalization of smoldering inflammation. In this review, we first delineate the pathological mechanisms underlying smoldering inflammation, distinguishing between lesional and extra-lesional features. We then examine the processes leading to tissue and virtual hypoxia in MS. As a key link between smoldering inflammation and hypoxia, we focused on the Hypoxia-Inducible Factor (HIF) signaling, the master regulator of cellular responses to hypoxia. Particularly, we reviewed recent evidence supporting its role as a central immunometabolic hub shaping immune and glial cell function within the hypoxic microenvironment of smoldering inflammation in MS. Finally, we critically evaluate the potential of the HIF signaling as a therapeutic target to hamper smoldering inflammation and disease progression in MS. - Source: PubMed
Publication date: 2026/04/28
Missaglia MFilippi MEsposito FGiordano A - This study aims to investigate the therapeutic effect of ethanol extract from fermented broth of Acanthopanacis senticosi Radix et Rhizoma seu Caulis-Ganoderma applanatum (EEA-GF) on IM and clarify its active material basis and mechanism of action. Insomnia (IM) model mice were established by induction with p-chlorophenylalanine (PCPA). The IM status was evaluated through a pentobarbital sodium-induced righting reflex test, hematoxylin-eosin (H&E) staining, and biochemical index detection. The composition of EEA-GF and its blood-migrating components were analyzed based on ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) technology. Core active components were screened by combining weighted gene co-expression network analysis (WGCNA), network pharmacology, and molecular docking technology. Animal experiments have shown that EEA-GF exhibits excellent therapeutic efficacy in the treatment of IM. A total of 19 compounds were identified from the serum of mice administered with EEA-GF via gavage using UPLC-MS/MS technology. Through WGCNA, HIF1A, REN, NFE2L2, and PARP1 were determined as core targets. Gene Ontology (GO) enrichment analysis yielded 87 results. In addition to cancer-related pathways, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis mainly included pathways such as the thyroid hormone signaling pathway and neuroactive ligand-receptor interaction. Molecular docking results showed that five components including kaempferol exhibited good binding activity with the aforementioned core targets, indicating that they may be the key material basis for EEA-GF to exert its anti-IM effect. This study is the first to confirm the therapeutic effect of EEA-GF on IM. This finding and the research on its related mechanisms provide a new theoretical basis for the clinical treatment and management of IM, as well as a candidate target with great development prospects. - Source: PubMed
Zhao Ying-YingXu Hao-DongJin Song-LinLv Yin-DeGao Si-YuWang Li-HongLi Yan-Cui - Hypertrophied adenoids in children can impair breathing and lead to obstructive sleep apnea (OSA), often accompanied by abnormal growth and weakened stamina and immunity. However, the cause of the pathological transformation in these originally immune-enhancing lymphoid tissues remains unclear. Our study provides the first single cell transcriptomic and immune repertoire atlas of adenoids from normal snoring to mild, moderate, and severe OSA, and identified markedly asynchronous functional modules, transcriptional regulatory networks and intercellular communications during the progression of OSA. Children with severe OSA exhibited exhibit active Hippo, Notch, and Wnt signaling, alongside significant downregulation of energy synthesis. Analysis revealed compromised T-cell and B-cell immunity, as well as reduced antigen processing by innate immune cells, coupled with diminished cell-cell communication in severe OSA group. T-cell receptor and B-cell receptor sequencing results also support more infection imprints and abnormal germinal centers and antibody class switching. Mechanistically, HIF1A-mediated hypoxic signaling likely drives the downregulation of key immune components (including HLA and interferon molecules), positioning it as a promising therapeutic target for OSA. - Source: PubMed
Publication date: 2026/04/27
Yang QinCui YunfeiHuang XiaoLiu JunlinMa XiaopengGao George FuPan HongguangQin Shijie