Ask about this productRelated genes to: Hif1a protein
- 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 protein
Related articles to: Hif1a protein
- Oral lichen planus (OLP), known as a common and chronic mucosal inflammatory disease. Due to its potential for cancerous transformation, this disease has long been a subject of significant concern. Its pathogenesis is that an unknown antigen activates oral keratinocytes and antigen-presenting cells (APCs) in the epithelium, leading to a T cell-mediated immune response. This study investigates the regulatory role of HIF-1α transcription factor and the potential role of autophagy in a simulated OLP inflammatory cell model. In this study, by comparing the control group with the model group, we observed a notable up-regulation of mRNA expression. Additionally, both the autophagy marker protein LC3-II and its substrate p62 exhibited abnormal accumulation, suggesting that autophagy is impaired at the lysosomal degradation stage. Furthermore, mechanistic studies have shown that HIF-1α leads to dysfunction of the autophagy-lysosomal pathway by inhibiting the expression of lysosomal-related genes, while knockdown of HIF-1α alleviates the disruption of autophagic and promotes the improvement of cell activity. In experiments with , stimulation with lipopolysaccharide ( LPS) shortens worms' lifespan, but knocking down the gene reverses this effect. Similarly, deletion of the key autophagy genes and reduces worm survival rates. Results indicate that HIF-1α plays a vital role in regulating autophagy-lysosomal function and cellular homeostasis. In summary, the excessively high expression of HIF-1α aggravates cellular and systemic damage by impairing autophagy-lysosomal function in OLP. Conversely, the targeted inhibition of HIF-1α restores autophagy function, suggesting a potential therapeutic strategy. - Source: PubMed
Publication date: 2026/04/14
Li XieHan ChaoYao YuemeiShi YuanxinChen BinXiao YiBai Guohui - Carbon nanodots were synthesized from Chaenomeles speciosa flowers and comprehensively characterized. UV-Vis analysis revealed a broad absorption band from 200 to 400 nm, attributed to π→π* (200-250 nm) and n→π* (250-350 nm) transitions, while fluorescence under 365 nm excitation showed bright blue emission. HRTEM images indicated spherical nanoparticles forming clustered aggregates, with lattice fringes exhibiting interplanar spacings of 0.091-0.093 nm, confirming a partially graphitic structure. XRD analysis showed a broad amorphous baseline in the 10-40° 2θ range, indicating low crystallinity. FTIR and XPS analyses identified abundant surface -OH, C = O, and C-O groups, with elemental composition of C 68.28%, O 23.03%, N 6.70%, S 0.40%, and Si 1.59%, resulting in a C/O ratio of 2.97. Chaenomeles speciosa quantum dots (CS-CQDs) exhibited dose-dependent cytotoxicity in MDA-MB-231 cells (viability: 70% at 2.5 mg/mL, 60% at 5 mg/mL) and HeLa cells (approximately 50% at 2.5-5 mg/mL), with minimal effects on hTERT-HME1 cells (viability greater than 85% at 0.6 mg/mL). Apoptosis increased from 25% to 55% in MDA-MB-231, from 24% to 65% in HeLa, and from 5.9% to 25% in HME1, with negligible necrosis. Gene expression analyses showed NF-κB upregulation (3-fold in MDA-MB-231; 6-fold in HeLa), BAX and BCL-2 upregulation in HeLa (approximately 2.5-fold), and downregulation of HIF1A, IL-6, MMP2, and MMP9. Wound healing assays indicated reduced migration in MDA-MB-231 (44% to 21%), increased migration in HeLa (18.7% to 30%), and minimal change in HME1 (73.5% to 71.5%). These results demonstrate that CS-CQDs possess favorable optical and structural properties and selectively induce apoptosis in cancer cells, with minimal impact on non-cancerous cells, highlighting their potential as targeted anticancer nanomaterials. - Source: PubMed
Publication date: 2026/04/29
Sarı Zeynep BetülGümrükçüoğlu AbidinTorunoğlu Emine İncilaySarı Muhammet EminAytar Erdi Can - Neuroinflammation and pyroptosis driven by excessive microglial activation play key roles in cerebral ischemia-reperfusion injury (CIRI). Hyperbaric oxygen preconditioning (HBO-PC) exhibits neuroprotective effects, but its mechanisms remain unclear. Leucine-rich α-2-glycoprotein 1 (LRG1) is implicated in CIRI pathology, yet whether HBO-PC modulates neuroinflammation and pyroptosis via LRG1 is unknown. - Source: PubMed
Lv WenyingLv JunzheXiong KexinYuan ShunshunYang JingyaoGuo Dazhi - 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