Ask about this productRelated genes to: Cyb5r2 antibody
- Gene:
- CYB5R2 NIH gene
- Name:
- cytochrome b5 reductase 2
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 11p15.4
- Locus Type:
- gene with protein product
- Date approved:
- 2005-07-13
- Date modifiied:
- 2014-11-18
Related products to: Cyb5r2 antibody
Related articles to: Cyb5r2 antibody
- Breast ductal carcinoma in situ (DCIS), a common precursor of breast cancer, has poorly understood susceptible driver genes. This study aimed to identify genes influencing DCIS progression by integrating Mendelian randomization (MR) and Gene Expression Omnibus (GEO) datasets. - Source: PubMed
Publication date: 2025/09/11
Mo Cai-QinXie Rui-WangLi Wei-WeiZhong Min-JieLi Yu-YangLin Jun-YuZhang Juan-SiZheng Sheng-KaiLin WeiKong Ling-JunXu Sun-WangChen Xiang-Jin - Ferroptosis, an iron-dependent form of programmed cell death, arises from the accumulation of lipid peroxides at toxic levels. Sorafenib, a first-line treatment for advanced hepatocellular carcinoma, shows limited clinical efficacy due to drug resistance. However, the mechanisms underlying Sorafenib resistance, especially related to ferroptosis, remain poorly understood. In this study, we identify activating transcription factor 7-interacting protein (ATF7IP) as a key inhibitor of ferroptosis. ATF7IP depletion promotes Sorafenib-induced ferroptosis, resulting in decreased cell viability, reduced cellular glutathione (GSH) levels, increased lipid peroxidation, and altered mitochondrial crista structure. Notably, ATF7IP knockdown shows cooperative effects with Sorafenib in inhibiting hepatocellular carcinoma growth in mice. Mechanistically, ATF7IP interacts with SET domain bifurcated histone lysine methyltransferase 1 (SETDB1) to epigenetically silence the transcription of cytochrome b5 reductase 2 (CYB5R2), thereby reducing cellular Fe levels. Meanwhile, ATF7IP stabilizes the antioxidant sensor Parkinsonism-associated deglycase (PARK7) protein which preserves the transsulfuration pathway to produce GSH, also leading to the inhibition of Sorafenib-induced ferroptosis. In conclusion, our findings identify ATF7IP as a critical ferroptosis inhibitor and represent ATF7IP as a novel therapeutic target for Sorafenib-based combination therapies of hepatocellular carcinoma. - Source: PubMed
Publication date: 2025/07/24
Su YijieHuang SiruiDuan YangZhang LiangFeng ShengyunLv YinggeLan BeiXuan Chenghao - Diabetic retinopathy (DR), the leading cause of adult blindness, has its risk increased by excessive endoplasmic reticulum stress (ERS). Nuclear receptor subfamily 2 group f member 2 (NR2F2) is an orphan nuclear receptor with essential roles in angiogenesis. However, its roles in DR remain unknown. Notably, NR2F2 protein expression was upregulated in streptozotocin-induced diabetic mice retina and the retinal endothelial cells characterized by endothelial marker CD31. Retinal NR2F2 expression was knocked down in diabetic mice using adeno-associated virus serotype 2. NR2F2 knockdown increased retinal thickness, decreased acellular capillary formation and FITC-labeled dextran leakage, and increased tight junction (TJ) protein ZO-1 expression in vivo. Additionally, NR2F2 knockdown inhibited reactive oxygen species generation and the ERS marker CHOP expression in vivo. In high glucose (HG)-induced human retinal microvascular endothelial cell (HRMEC) monolayers, NR2F2 knockdown inhibited FITC-dextran flux, increased transendothelial electrical resistance, reduced VEGFA secretion and restored expression and continuous distribution of TJ proteins. NR2F2 knockdown also reduced ERS markers expression and inhibited ERS-related signaling pathways in vitro. mRNA-seq analysis in NR2F2-knockdown HRMECs exposed to HG showed that NR2F2 inhibition upregulated CYB5R2 mRNA level. NR2F2 was bound directly to the CYB5R2 promoter for transcriptional repression in HRMECs. CYB5R2 overexpression inhibited ERS-related protein expressions and barrier dysfunction in HRMEC monolayers, and CYB5R2 knockdown reversed the endothelial protective effect of NR2F2 inhibition. In conclusion, NR2F2 knockdown attenuates vascular dysfunction by alleviating ERS in retinal microvascular endothelial cells and alleviates disease progression in DR mice. This may be achieved by reducing CYB5R2 transcriptional repression. - Source: PubMed
Zhang TaoYang QianhanChen JunJiang JiyuHan JingnanZhou Yun - Prolonged adaptation of ancestors of indigenous peoples of the Far North of Asia and America to extreme natural and climatic conditions of the Arctic has resulted in changes in genes controlling various metabolic processes. However, most genetic variability observed in the Eskimo and Paleoasians (the Chukchi and Koryaks) is related to adaptation to the traditional Arctic diet, which is rich in lipids and proteins but extremely poor in plant carbohydrates. The results of population genetic studies have demonstrated that specific polymorphic variants in genes related to lipid metabolism (, , , and ) and carbohydrate metabolism (, , and ) are prevalent in the Eskimo and Paleoasian peoples. When individuals deviate from their traditional dietary patterns, the aforementioned variants of genetic polymorphism can lead to the development of metabolic disorders. American Eskimo-specific variants in genes related to glucose metabolism ( and ) significantly increase the risk of developing type 2 diabetes. These circumstances indicate the necessity for a large-scale genetic testing of indigenous population of the Far North and the need to study the biochemical and physiological consequences of genetically determined changes in the activity of enzymes of lipid and carbohydrate metabolism. - Source: PubMed
Malyarchuk Boris A - Neoadjuvant chemotherapy (NAC) is the primary preoperative therapy for breast cancer. The luminal subtype of breast cancer shows less NAC response than the basal subtype, with an inefficient NAC treatment effect. Understanding of the molecular and cellular mechanisms responsible for this chemoresistance is an important issue when determining optimal treatment. - Source: PubMed
Publication date: 2023/05/09
Zhu ZhenShen HongyuXu JialinFang ZhengWo GuanqunMa YingYang KaiWang YalinYu QiangTang Jin-Hai