Ask about this productRelated genes to: RB1CC1 antibody
- Gene:
- RB1CC1 NIH gene
- Name:
- RB1 inducible coiled-coil 1
- Previous symbol:
- -
- Synonyms:
- KIAA0203, Cc1, DRAGOU14, FIP200, ATG17, PPP1R131
- Chromosome:
- 8q11.23
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-01
- Date modifiied:
- 2016-11-01
Related products to: RB1CC1 antibody
Related articles to: RB1CC1 antibody
- Macroautophagy/autophagy is a critical cellular process that maintains the cellular homeostasis by degrading and recycling cytotoxic material. Despite its importance, the intricate mechanisms governing this process remain partially elusive. Here, we designed and performed a genome-wide loss-of-function screen on a mouse haploid ESC mutant library and identified the actin-binding protein CORO1C (coronin 1C) as a previously unrecognized regulator of mammalian autophagy. Interactions between CORO1C and the ACTR2/ARP2 (actin related protein 2)-ACTR3/ARP3 complex are essential for branched actin network assembly, SQSTM1/p62 body formation, and maintaining autophagosome structural integrity. Unlike CORO1A and CORO1B, CORO1C possesses a unique second actin-binding site involved in regulating the branched actin network and autophagic process. Notably, newborn mice died earlier in starvation than wild-type littermates and multiple tissues showed autophagy-deficient phenotypes. Moreover, the adult -deficient mice exhibit severe spatial learning memory impairment. Collectively, our research uncovered the surprising role of CORO1C in promoting the formation of branched actin network and its central role in the assembly of structures vital to autophagy.: ACTR2/ARP2: actin related protein 2; ACTR3/ARP3: actin related protein 3; ARPC2: actin related protein 2/3 complex, subunit 2; ATG: autophagy related; ATG5: autophagy related 5; BafA1: bafilomycin A; CQ: chloroquine; FACS: fluorescence-activated cell sorting; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; haESC: haploid embryonic stem cell; HML: haploid-mutant library; IF: immunofluorescence; KO: knockout; MAP1LC3B/LC3: microtubule-associated protein 1 light chain 3B; RB1CC1/FIP200: RB1-inducible coiled-coil 1; SQSTM1/p62: sequestosome 1; STX17: syntaxin 17; TEM: transmission electron microscopy; WB: western blotting; WT: wild type. - Source: PubMed
Publication date: 2026/04/20
Zhang GuozhongYu NingqingSun YiLi XiaowenSun LihongLiu GuangHuang Yue - Climate change creates major challenges in livestock industry, making chickens vulnerable to heat stress because they can tolerate a narrow range of temperatures. Heat stress disrupts metabolic and physiological homeostasis, leading to reduced growth, productivity, reproduction, and immune function, thereby threatening the economic viability of poultry farming. This review explores the multifaceted impacts of heat stress on poultry, including physiological responses, production performance, and immune function. Recent advances in transcriptomic and genomic research have shed light on the molecular mechanisms underlying heat stress resilience in poultry. Key genes such as HSP70, HSP90, HSP27, and HSP47 are significantly upregulated under heat stress, playing vital roles in protein folding, preventing aggregation, and protecting cellular integrity. Additionally, genes like SOD and CAT enhance antioxidant defenses, mitigating oxidative damage. Genes such as RB1CC1, BAG3, and TRMT1L regulate apoptosis and oxidative stress, promoting cell survival. In the liver, CCK, DIO3, and ANGPTL4 improve energy homeostasis and reduce metabolism-related heat production, while BMP10 and MYH7 in the heart contribute to cardiac adaptation during thermal stress. Genetic adaptations such as the Naked neck, Frizzle, and Dwarf gene provide intrinsic thermotolerance by reducing feather mass, altering feather structure, and minimizing body size, thereby improving heat dissipation. These genetic traits, combined with transcriptomic insights into heat resilience genes, offer opportunities for developing heat-tolerant chicken breeds. By integrating molecular genetics, transcriptomics, and management strategies, this review highlights the importance of selective breeding programs to enhance poultry thermotolerance. Future research should focus on leveraging indigenous breeds, advanced molecular tools, and nutritional interventions to mitigate the effects of rising global temperatures. Enhancing heat stress resilience in poultry is imperative to ensure sustainable production and global food security in this climate change. - Source: PubMed
Publication date: 2026/03/09
Hossain Md MortuzaAhn JinhyunChoi Soo-YounHur Sung-PyoLim DajeongShin DonghyunLee SanghoonPark Jong-Eun - Methyl protodioscin (MPD), a furostanol saponin found in the rhizomes of Dioscorea plants, has been shown to effectively inhibit proliferation of prostate cancer cells in vitro and in vivo. However, the mechanism underlying this inhibitory action remains unclear. To elucidate the mechanism, we used mass spectrometry to analyze protein rearrangements in detergent-resistant membranes (DRMs). Ferroptosis-related factors were identified in cells in vitro and in vivo. MPD induced the expression of acyl-CoA synthetase long chain family member 4 and reduced expression levels of glutathione peroxidase 4 and solute carrier family 7 member 11. Following MPD treatment, RB1-inducible coiled-coil 1 (RB1CC1) dissociated from DRMs and translocated from the cytoplasm to the nucleus. This translocation induced the expression of ferroptosis-related protein coiled-coil-helix-coiled-coil-helix domain containing 3, promoting ferroptosis in prostate cancer cells. As the nuclear translocation of RB1CC1 was promoted by the JNK signaling pathway, SP600125, a JNK inhibitor, prevented the MPD-induced RB1CC1 nuclear translocation. In summary, MPD induced the dissociation of RB1CC1 from DRMs and its subsequent nuclear translocation, contributing to ferroptosis of prostate cancer cells. - Source: PubMed
Publication date: 2025/12/25
Wang RuonanHu ChaoyuZhao YiWu ShuhanCao ShujuanXu LeimingYin DengkeTan Song - Histone modifications play an important role in intestinal homeostasis and regeneration. Here, we identify histone H3 lysine 9 di-methylation (H3K9me2) as an epigenetic regulator of intestinal epithelial repair through mass spectrometry-based screening of histone modifications. We then find that H3K9me2 and its methyltransferase G9a levels are reduced during acute injury and progressively increase during regeneration in both mouse models and human clinical samples. Genetic ablation of G9a in intestinal epithelial cells or pharmacological inhibition of its enzymatic activity substantially impairs intestinal regeneration and reduces survival following irradiation. Mechanistically, integrative genomic analyses reveal that G9a-mediated H3K9me2 suppresses chromatin accessibility and transcriptional activity of cell cycle arrest genes, including Rb1cc1, Rb1, Cdkn1a, and Pten, thereby promoting intestinal stem cell proliferation. Furthermore, we elucidate that IL-4-STAT6 signaling controls G9a expression during regeneration, i.e., IL-4 upregulation leads to STAT6 phosphorylation and subsequent transcriptional activation of G9a. These findings establish the IL-4-STAT6-G9a-H3K9me2 regulatory axis as a critical epigenetic mechanism controlling intestinal regeneration with therapeutic potential for gastrointestinal disorders. - Source: PubMed
Publication date: 2026/01/19
Chen JingzhouShi XiaoliangZhou XinyiHuang JuXia LinghaoHu ZhenGu JiajiSheng XiaoleGe XiaolongFu XudongXiao QianZhou WeiBai RongpanXu ZhengpingSheng Jinghao - This study aimed to investigate the expression of infl ammatory bowel disease (IBD)-associated genes in oral cancer and to elucidate the cellular and molecular pathways that may serve as potential therapeutic targets. - Source: PubMed
Publication date: 2025/12/15
Cheng YongweiLiu ZhenyinXie ShifengZhang NingyiGuo LiangWu YujinLiao YuanDai Yunkai