Ask about this productRelated genes to: CHAC2 Blocking Peptide
- Gene:
- CHAC2 NIH gene
- Name:
- ChaC cation transport regulator homolog 2
- Previous symbol:
- -
- Synonyms:
- GCG1
- Chromosome:
- 2p16.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-10-25
- Date modifiied:
- 2017-05-16
Related products to: CHAC2 Blocking Peptide
Related articles to: CHAC2 Blocking Peptide
- Highly metastatic cancer cells depend on polyunsaturated fatty acids (PUFAs) to enhance membrane fluidity, yet this adaptive advantage concurrently renders them more susceptible to ferroptosis. However, the adaptation and survival strategies of metastatic gastric cancer (GC) cells under severe stress conditions remain unclear. To identify driver genes underlying peritoneal metastasis (PM) in GC, we performed integrated multi-omics analyses of GC tissues, followed by validation using a large cohort of clinical samples (n = 124) and corresponding prognostic data. Both in vitro and in vivo functional studies confirmed that ChaC2 is a critical driver of PM from GC. Mechanistic investigations revealed that ChaC2 attenuates ferroptosis sensitivity caused by elevated PUFAs levels in metastatic GC cells. Under hypoxic conditions, HIF-1α transcriptionally upregulates eIF4B and promotes cytoplasmic translocation of PABP1, leading to liquid-liquid phase separation (LLPS) of the PABP1/eIF4B complex. This phase-separated structure recruits G3BP1 to nucleate stress granules (SGs), within which ChaC2 mRNA is selectively sequestered, thereby enhancing its stability and translational efficiency. Collectively, our findings demonstrate that hypoxia-induced PABP1/eIF4B LLPS specifically upregulates ChaC2 expression, enabling metastatic cancer cells to evade ferroptosis triggered by their own metastatic demands and ultimately facilitating tumor dissemination. This study uncovers a critical adaptive regulatory mechanism employed by metastatic GC cells to cope with stress challenges during PM, thereby offering novel therapeutic targets and strategic insights for intervention. - Source: PubMed
Publication date: 2026/03/02
Lin ZaihuanGao YukeZhang QiYang SaixuanChen YabangDing HanluPeng WenxuZhang XinyinNurzat YeltaiHu JulongLiao WenjingXiong BinXiao MangZhang Xiaowen - This review explores the critical function of the evolutionarily conserved ChaC-like enzyme family as central regulators of intracellular glutathione (GSH) homeostasis, focusing on the mammalian isoforms CHAC1 and CHAC2. We detail how these γ-glutamylcyclotransferases degrade GSH, thereby modulating cellular redox balance and integrating diverse stress signaling pathways. CHAC1 emerges as a key stress-responsive effector, transcriptionally upregulated the ATF4-CHOP axis during endoplasmic reticulum stress and amino acid deprivation. Its role is especially crucial in the induction of ferroptosis, an iron-dependent cell death pathway, positioning it as a context-dependent modulator of cancer progression, neurotoxicity and neurodegeneration. Furthermore, we examine the opposing roles of CHAC1 and CHAC2 in stem cell fate decisions NOTCH1 signaling and development. The complex duality of CHAC1 in oncology, acting as both a tumor suppressor by promoting ferroptosis and a potential oncogene in -mutant backgrounds, alongside its functions in neuroprotection and immunity, underscores its therapeutic potential. - Source: PubMed
Publication date: 2025/12/18
Schröder EmmaJalilvand Tida VKahl JaninaKaiser Charlotte SLiebau Eva - The goal of this study was to evaluate effects of short-term acute salinity challenges on the hemocyte physiology in northern quahogs, Mercenaria mercenaria, an important aquaculture species in the U.S. The objectives were to: 1) challenge adult northern quahogs with salinities of 5, 15, 25 (control), 35, and 45 ppt; 2) evaluate cellular responses, including hemocyte concentration, viability, phagocytosis rate, ROS production, and lysosomal presence at 12 h, 24 h, 48 h, 72 h, 144 h, and 21 days post-challenge; and 3) evaluate the molecular response of hemocytes after 72 h challenge. M. mercenaria at 5, 15, 25, 35 ppt exposure showed no mortality, while at 45 ppt showed a 100 % mortality at day 7, reflecting better tolerance to hyposalinity. Changes of hemolymph osmolality at different salinities and exposure periods indicated M. mercenaria equilibrates with the environmental seawater within its tolerance range (15-35 ppt) as an osmoconformer. Hemocyte concentration increased significantly at 5, 15, and 45 ppt stress. Hemocyte immune functions exhibited a varied pattern in response to different salinity levels, enabling them to resolve stresses. The RNAseq of hemocytes revealed DEGs in response to salinity challenges, specifically enrichment of amino acid transporters (SLC2A5, SLC6A1, SLC5A8, SLC1A3, SLC25A38), immune response (CHAC2, MGST3, IRF1, and IRFD2) and cell signaling (Wnt, TRAIL-activated and Toll) pathway in hyper/hypo salinity groups, indicated their importance in salinity stress responses. This study provided critical insights into the cellular and molecular responses of M. mercenaria hemocytes to salinity challenges. - Source: PubMed
Publication date: 2025/07/31
Zeng YangqingZeng XianyuanYee Jayme CYang Huiping - Patients with schizophrenia (SCZ) experience constipation at significantly higher rates compared with the general population. This relationship suggests a potential genetic overlap between these two conditions. - Source: PubMed
Publication date: 2025/03/03
Luo QinghuaAn MingweiWu YunxiangWang JiawenMao YuantingZhang LeichangWang Chen - Legg-Calvé-Perthes disease (LCPD) involves femoral head osteonecrosis caused by disrupted blood supply, leading to joint deformity and early osteoarthritis. This study investigates the role of miRNA-223-5p in regulating hypoxia-induced apoptosis and enhancing osteogenesis in bone marrow mesenchymal stem cells (BMSCs). Utilizing a juvenile New Zealand white rabbit model of LCPD established through femoral neck ligation, we transfected BMSCs with miR-223-5p mimics, inhibitors, and controls, followed by hypoxic exposure. The impact of miR-223-5p on BMSC apoptosis was assessed using qPCR, Western blotting, and dual-luciferase reporter assays, focusing on the Wnt/β-catenin signaling pathway. In vivo, we evaluated the effects of transplanting miR-223-5p-overexpressing BMSCs into the LCPD model. Our results indicate that miR-223-5p is downregulated under hypoxic conditions. Overexpression of miR-223-5p in BMSCs inhibited hypoxia-induced apoptosis and activated the Wnt/β-catenin pathway by directly targeting CHAC2. In vivo, miR-223-5p-overexpressing BMSCs enhanced femoral head osteogenesis and reduced necrosis in the LCPD model. These findings suggest that miR-223-5p inhibits hypoxia-induced apoptosis in BMSCs by targeting CHAC2 and activating the Wnt/β-catenin pathway, proposing miR-223-5p as a promising target for improving bone repair in ischemic conditions. - Source: PubMed
Publication date: 2025/01/24
Yang JiafeiZhang TianjiuZhu XingtaoHe ZhexiJiang XuYu SongGu Huajian