RINT1 antibody
- Known as:
- RINT1 (anti-)
- Catalog number:
- orb101603
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- RINT1 antibody
Related genes to: RINT1 antibody
- Gene:
- RINT1 NIH gene
- Name:
- RAD50 interactor 1
- Previous symbol:
- -
- Synonyms:
- FLJ11785, RINT-1
- Chromosome:
- 7q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2006-03-02
- Date modifiied:
- 2016-10-05
Related products to: RINT1 antibody
Related articles to: RINT1 antibody
- Infection of the large yellow croaker () embryo cell line YCE1 with megalocytivirus strain FD201807 leads to accumulation of capsid-deficient viral intermediates within intracellular vesicles at 48 h post-infection (a phenotype associated with non-lytic egress), which coincides with the initial peak of viral genomic copies. To characterize the host molecular response during this critical stage, we performed time-course RNA sequencing at 24, 48, 96, and 144 hpi. Integrated analysis identified 6661 differentially expressed genes (DEGs) and 1138 differential alternative splicing (DAS) events affecting 892 genes, with DAS event abundance peaking at 48 h. DAS genes in autophagy and Golgi vesicle transport pathways, both integral to animal innate immunity, were significantly enriched exclusively at this timepoint, featuring novel mutually exclusive exon (MXE) isoforms in (Golgi-associated PDZ and coiled-coil motif containing) and (RAD50 interactor 1). Weighted gene co-expression network analysis (WGCNA) of DEGs identified (mitogen-activated protein kinase 9) and (microtubule-associated protein 1 light chain 3 alpha) as hub genes within modules enriched for autophagy-related functions. Separate co-expression analysis of DAS genes revealed , , and as hub genes, with exhibiting only a single linkage to . These findings implied concurrent transcriptional and virus-induced host splicing regulation of vesicle-associated innate defense pathways and suggest that splicing-derived features may serve as potential candidates for diagnostics or prevention against megalocytivirus disease in . - Source: PubMed
Publication date: 2026/04/20
Zheng ZaiyuChi HongshuLiu XiaodongChen XiuxiaPan YingGong Hui - Immune evasion remains a major obstacle to effective therapy in lung adenocarcinoma (LUAD), and accumulating evidence suggests that DNA damage repair programs actively shape tumor immunity. Here, we identify the Fanconi anemia pathway helicase BRIP1 as a critical coordinator of DNA repair competence and innate immune suppression in LUAD. BRIP1 is significantly upregulated in tumor tissues and correlates with advanced clinical stage and poor prognosis. Functional assays demonstrate that BRIP1 promotes LUAD cell proliferation, invasion, epithelial-mesenchymal transition, and homologous recombination (HR) repair capacity. Mechanistically, BRIP1 drives tumor progression through two interconnected pathways. First, BRIP1 associates with the histone variant macroH2A1 to enhance acetylation of RINT1 at lysine 728, thereby strengthening RINT1-RAD50 interaction, facilitating MRE11-RAD50-NBS1 complex assembly, and augmenting HR-mediated DNA repair. Enhanced repair efficiency limits cytosolic DNA accumulation and suppresses cGAS-STING-dependent innate immune activation. Second, BRIP1 interacts with the RNA demethylase ALKBH5, leading to activation of NF-κB signaling, upregulation of PD-L1, and promotion of metastatic potential. Spatial transcriptomics, single-cell RNA sequencing, and multiplex immunohistochemistry reveal that BRIP1-high tumors exhibit an immune-cold microenvironment characterized by regulatory T-cell enrichment, cytotoxic T-cell exclusion, and impaired immune communication. In vivo, BRIP1 overexpression accelerates tumor growth and metastasis while conferring resistance to PD-L1 blockade, which is effectively reversed by combining anti-PD-L1 therapy with STING activation. Collectively, our findings establish BRIP1 as a molecular link between DNA repair proficiency and immune suppression in LUAD, highlighting BRIP1-associated pathways as actionable targets for rational combination immunotherapy. - Source: PubMed
Publication date: 2026/02/23
Wu HaixiaZhang JiguangYu YilinWang WeiHuang JianyuanLin ZhaoxianHuang HailunLin YingPan XiaojieLin Xing - Lipid droplets (LDs), originating from the ER, play critical roles in lipid metabolism. ER-LD contacts enable lipid exchange and support essential cellular processes. However, how viruses utilize ER-LD coordination remains elusive. Here, we demonstrate that hepatitis C virus (HCV) infection markedly increases LDs abundance and enhances ER-LD contacts. Through a targeted screen of ER-LD tethering proteins, we identified that the NRZ complex, composed of nonsteroidal anti-inflammatory drug-activated gene (NAG), RAD50 interactor 1 (RINT1) and zeste white 10 (ZW10), is essential for HCV-induced ER-LD association and viral infection. Mechanistically, RINT1 and ZW10 interact with the HCV envelope protein E1. Ectopic E1 expression is sufficient to promote ER-LD contacts, which are abolished upon NRZ depletion. NRZ depletion also impairs Dengue virus (DENV) and Zika virus (ZIKV) infection, suggesting its conserved proviral function. Together, this work uncovers a critical mechanism by which host inter-organelle tethering complexes regulate viral infection, offering new insights into virus-host interactions and potential antiviral targets. - Source: PubMed
Publication date: 2026/02/03
Li ZhifangXing YifanHuang XinyiTian BuyunMei JieFu XinyueHuang YuhanZhang QianDing BinbinCao XiaobaoXue YanhongLi ZonghongXu TaoJiu Yaming - Colorectal adenocarcinoma (COAD) cells exploit stress-adaptation programs, such as the unfolded protein response (UPR), to survive in hostile tumour microenvironments. However, the role of specific E3 ubiquitin ligases in regulating these survival pathways remains poorly understood. We investigated Ring Finger Protein 39 (RNF39), an E3 ligase previously implicated in immune signalling, as a potential regulator of COAD progression. - Source: PubMed
Chen LuYuan ChunluanYu TengHui KaiyuanLi XiumingShen XiaozhuJiang XiaodongLiu Bin - Recurrent acute liver failure (RALF) in children is defined as two or more episodes of acute liver failure with complete recovery in between. Several genetic mutations are associated with this condition, including NBAS, RINT1, LARS1 and SCYL1. We have reported liver transplant and mortality rates to help providers make informed management decisions. - Source: PubMed
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