IVNS1ABP antibody - N-terminal region (ARP33099_P050)
- Known as:
- IVNS1ABP (anti-) - N-terminal region (ARP33099_P050)
- Catalog number:
- arp33099_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- IVNS1ABP antibody - N-terminal region (ARP33099_P050)
Related genes to: IVNS1ABP antibody - N-terminal region (ARP33099_P050)
- Gene:
- IVNS1ABP NIH gene
- Name:
- influenza virus NS1A binding protein
- Previous symbol:
- -
- Synonyms:
- NS1-BP, HSPC068, NS-1, KIAA0850, ND1, KLHL39, ARA3
- Chromosome:
- 1q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-05-19
- Date modifiied:
- 2018-03-16
Related products to: IVNS1ABP antibody - N-terminal region (ARP33099_P050)
Related articles to: IVNS1ABP antibody - N-terminal region (ARP33099_P050)
- We identified a new progeroid syndrome with severe neuropathy and intellectual deficits but its underlying cellular and molecular mechanism is unknown. Exome sequencing revealed a homozygous mutation in the IVNS1ABP gene, which encodes IVNS1ABP, an influenza virus non-structural protein-1 binding protein. To investigate disease mechanisms, we generated isogenic induced pluripotent stem cells (iPSCs) from patient fibroblasts and differentiated them into neural progenitor cells (NPCs). Mutant IVNS1ABP fibroblasts, iPSCs, and NPCs exhibited defective cytokinesis, increased DNA damage, and premature cellular senescence. Consistent with these findings, cerebral organoids showed early differentiation of NPCs into neurons. Molecular profiling as well as biochemical and cellular analysis revealed altered binding of mutant IVNS1ABP to actin / actin-associated proteins and dysregulated actin dynamics during cytokinesis. Taken together, we propose that mutant IVNS1ABP dysregulates actin polymerization and organization which is at least partly responsible for the cellular senescence phenotypes in this progeroid neuropathy. - Source: PubMed
Publication date: 2026/03/19
Yuan FangTan Ye SingWang HaofeiAli Ain NurYuan QiangChou Shu-MinYen Yu-HsinNarayanan GunaseelanZhou LeiShboul MohammadBonnard CarineReversade BrunoZhang Su-Chun - The influence of genetic variation on alternative splicing (AS) across immune cell types and demographic strata in European populations remains poorly understood. Here, we leveraged the OneK1K cohort, comprising 980 individuals of European ancestry with matched genotyping and single-cell RNA sequencing (scRNA-seq) data, to systematically investigate splicing variation at single-cell resolution. Across 13 immune cell types, we identified extensive cell-type-specific AS events and independent cis-splicing quantitative trait loci (cis-sQTLs), with subsets showing distinct sex- and age-biased patterns. Colocalization analysis identified numerous shared signals between cell-type-specific cis-sQTLs and GWAS loci for 30 polygenic traits, demonstrating that splicing regulation represents an important mechanism through which susceptibility loci influence complex traits. Through trans-sQTL analysis, we found that genetic variants exert distal effects on RPS24 splicing via proximal regulation of IVNS1ABP expression, a splicing regulator that interacts with the splicing factor HNRNPK. Collectively, our findings provide new insights into how genetic variation shapes splicing programs across cellular and demographic contexts in European populations, establishing a mechanistic framework for splicing-mediated regulation of complex traits. - Source: PubMed
Publication date: 2026/02/11
Liang YanXia Yi - Programmed cell death (PCD) pathways with druggable potential represent a promising but still underexplored frontier in heart failure (HF) research for diagnosis, prognosis, and therapy. To address this gap, we developed a Druggable Programmed Cell Death Index (DPCDI) through an integrative machine learning framework. An optimal combination of Lasso and Random Forest algorithms identified 15 pivotal genes (CALCOCO2, VPS13D, CLU, STAT3, OPTN, UBB, CXCL12, PPP1R15A, ATF4, IVNS1ABP, HMGB2, JAK2, EXOC7, ENO1, TPCN1) for DPCDI construction. Non-negative matrix factorization (NMF) analysis stratified HF patients into two distinct subtypes, with Subtype 2 exhibiting elevated apoptosis and mitophagy activity. Single-cell RNA sequencing revealed dynamic JAK2 and IVNS1ABP expression during cardiomyocyte state transitions, while CXCL12 showed stage-specific regulation in endothelial cells. Mendelian randomization analysis indicated that genetic predisposition to elevated JAK2 and STAT3 expression was associated with reduced HF risk, whereas CXCL12 overexpression increased susceptibility. Experimental validation in HF mouse models confirmed increased Cxcl12 and Jak2 expression and decreased Stat3 levels. Furthermore, knockout of Cxcl12, Jak2, and Stat3 induced HF phenotypes. Molecular docking identified pifithrin-α as a potent ligand for CXCL12 and strophanthidin for STAT3. Collectively, DPCDI provides a comprehensive framework for HF diagnosis, risk stratification, and targeted therapeutic development. - Source: PubMed
Publication date: 2026/01/15
Zhang LiliZhu YihaoFang YuanYang YanpingYu YinWang HanshiJiang XiyueZhang XueHuang Dong - Egg quality unpredictability remains a significant challenge in aquaculture, limiting reproductive success and production efficiency. Identifying reliable molecular markers of egg quality is therefore essential for optimizing hatchery protocols and selective breeding strategies. Building upon our previous study that used proteomics to investigate early in vivo post-ovulatory ageing in pikeperch (Sander lucioperca), we employed a complementary transcriptomic approach to further elucidate molecular mechanisms underlying egg quality decline. The in vivo ageing model, enabled by commercially applied species-specific suture technique that prevents spontaneous egg release, provides a controlled and biologically relevant framework for identifying early-stage molecular biomarkers of egg developmental competence. Although eggs retained for 5 h post-ovulation (hPO) exhibited no visible deterioration, they showed significantly reduced fertilization and hatching success compared to eggs collected at 1 hPO. Transcriptomic profiling revealed 202 differentially expressed transcripts, implicating processes such as RNA metabolism, mRNA decay, cytoskeletal organization, and cell cycle regulation. Several hub genes (ago2, ep300, kmt2c) were identified as potential key regulators of egg competence, and ivns1abp and setdb1 emerged as promising candidate conserved markers of egg quality across species. This study advances our previous findings by revealing that transcriptomic changes, rather than proteomic alterations, are early and sensitive indicators of post-ovulatory ageing. Together, these results offer valuable insights for developing transcriptome-based biomarkers to improve broodstock management and reproductive outcomes in aquaculture. - Source: PubMed
Publication date: 2025/11/17
Nynca JoannaRocha de Almeida TaináKlopp ChristophePalińska-Żarska KatarzynaKról JarosławLjubobratović UrošBobe JulienŻarski Daniel - Hyperlipidemia (HLP) exacerbates myocardial cell injury by impairing lipophagy, a crucial lipid metabolic process, thereby increasing the risk of acute myocardial infarction (AMI). This study aims to identify biomarkers associated with HLP and lipophagy that are relevant to AMI risk through a combined transcriptomic and Mendelian randomization (MR) approach. - Source: PubMed
Publication date: 2025/08/07
Zou Jun-HuaWang Hua-WeiLong Jia-ZhiYang Xiao-NaYang Li-HongLi Long-JunChen Li-XingDong LingChen JingMeng Zhao-HuiWan Wen