TRIP10 antibody - N-terminal region (ARP34191_P050)
- Known as:
- TRIP10 (anti-) - N-terminal region (ARP34191_P050)
- Catalog number:
- arp34191_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- TRIP10 antibody - N-terminal region (ARP34191_P050)
Related genes to: TRIP10 antibody - N-terminal region (ARP34191_P050)
- Gene:
- TRIP10 NIH gene
- Name:
- thyroid hormone receptor interactor 10
- Previous symbol:
- STOT
- Synonyms:
- STP, HSTP, CIP4
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-06-14
- Date modifiied:
- 2014-11-18
Related products to: TRIP10 antibody - N-terminal region (ARP34191_P050)
Related articles to: TRIP10 antibody - N-terminal region (ARP34191_P050)
- CaN (calcineurin) promotes pathological cardiac remodeling but also cardioprotection in ischemia-reperfusion injury. CaN inhibitors are also immunosuppressants. This pleiotropy complicates targeting calcineurin in cardiovascular disease. CIP4/TRIP10 (Cdc42-interacting protein 4) is a scaffold protein that binds the CaNAβ (calcineurin Aβ) N-terminal polyproline domain and organizes a calcium and CaNAβ2 signaling compartment independent of contractile calcium. We showed that CIP4-CaNAβ2 signalosomes promote pathological cardiac hypertrophy induced by pressure overload. It is unknown whether CIP4-CaNAβ2 signalosomes contribute to cardioprotection and remodeling in ischemic disease. - Source: PubMed
Publication date: 2025/12/17
Samuelsson Anne-MajBayer Abraham LLi JinliangLi YangLewis DeEsmondTurcotte Moriah GDodge-Kafka Kimberly LAlcaide PilarKapiloff Michael S - Calcineurin in a pleiotropic signaling enzyme that promotes pathological cardiac remodeling but also cardioprotection in ischemia-reperfusion injury. In addition, calcineurin inhibitors are immunosuppressants. This pleiotropy has precluded the use of calcineurin inhibitors as treatments for heart failure. Cdc42-interacting protein 4 (CIP4/TRIP10) is an endosomal scaffold protein that organizes a calcium and calcineurin Aβ2 (CaNAβ2) signaling compartment activated by G-protein coupled receptors independently of contractile calcium. CIP4 binds CaNAβ2 via the CaNAβ-specific N-terminal polyproline (PP) domain. We previously showed that targeting of CIP4-CaNAβ2 signalosomes inhibited pathological cardiac hypertrophy and the development of heart failure induced by chronic pressure overload in mice. It is unknown whether CIP4-CaNAβ2 signalosomes contribute to cardioprotection and/or cardiac remodeling in ischemic heart disease. - Source: PubMed
Publication date: 2025/05/15
Samuelsson Anne-MajBayer Abraham LLi JinliangLi YangLewis DeEsmondTurcotte Moriah GildartDodge-Kafka Kimberly LAlcaide PilarKapiloff Michael S - Studies have established a strong link between erectile dysfunction (ED) and genetic factors. However, the genetic protective genes associated with ED have yet to be identified. In this study, we used Mendelian randomization (MR) analysis to investigate potential genetic protective genes related to ED. - Source: PubMed
Publication date: 2025/02/15
Qu ZejieLi YurongYuan QuangangYang Siming - Collagen VI-related dystrophies (COL6RD) are a group of rare muscle disorders caused by mutations in specific genes responsible for type VI collagen production. It affects muscles, joints, and connective tissues, leading to weakness, joint problems, and structural issues. Currently, there is no effective treatment for COL6RD; its management typically addresses symptoms and complications. Therefore, it is essential to decipher the disease's molecular mechanisms, identify drug targets, and develop effective treatment strategies to treat COL6RD. In this study, we employed differential gene expression analysis, weighted gene co-expression network analysis, and genome-scale metabolic modeling to investigate gene expression patterns in COL6RD patients, uncovering key genes, significant metabolites, and disease-related pathophysiological pathways. First, we performed differential gene expression and weighted gene co-expression network analyses, which led to the identification of 12 genes (, , , , , , , , , , , ) as potential hub genes involved in the disease. Second, we utilized a drug repurposing strategy to identify pharmaceutical candidates that could potentially modulate these genes and be effective in the treatment. Next, we utilized context-specific genome-scale metabolic models to compare metabolic variations between healthy individuals and COL6RD patients. Finally, we conducted reporter metabolite analysis to identify reporter metabolites (e.g., phosphatidates, nicotinate ribonucleotide, ubiquinol, ferricytochrome C). In summary, our analysis revealed critical genes and pathways associated with COL6RD and identified potential targets, reporter metabolites, and candidate drugs for therapeutic interventions. - Source: PubMed
Publication date: 2024/10/29
Ceyhan Atakan BurakKaynar AliAltay OzlemZhang ChengTemel Sehime GulsunTurkez HasanMardinoglu Adil - Overall adiposity and body fat distribution are heritable traits associated with altered risk of cardiometabolic disease and mortality. Performing rare variant (minor allele frequency<1%) association testing using exome-sequencing data from 402,375 participants in the UK Biobank (UKB) for nine overall and tissue-specific fat distribution traits, we identified 19 genes where putatively damaging rare variation associated with at least one trait (Bonferroni-adjusted <1.58×10 ) and 50 additional genes at FDR≤1% ( ≤4.37×10 ). These 69 genes exhibited significantly higher (one-sided -test =3.58×10 ) common variant prioritisation scores than genes not significantly enriched for rare putatively damaging variation, with evidence of monotonic allelic series (dose-response relationships) among ultra-rare variants (minor allele count≤10) in 22 genes. Combining rare and common variation evidence, allelic series and longitudinal analysis, we selected 14 genes for CRISPR knockdown in human white adipose tissue cell lines. In three previously uncharacterised target genes, knockdown increased (two-sided -test <0.05) lipid accumulation, a cellular phenotype relevant for fat mass traits, compared to Cas9-empty negative controls: (fold change [FC]=1.72, =0.0028), (FC=1.35, =0.0096), and (FC=1.39, =0.0157); furthermore, knockdown of (FC=0.25, =5.52×10 ) and (FC=0.51, =1.91×10 ) resulted in reduced lipid accumulation. Integrating across population-based genetic and functional evidence, we highlight therapeutic avenues for altering obesity and body fat distribution by modulating lipid accumulation. - Source: PubMed
Publication date: 2025/03/14
Baya Nikolas AErdem Ilknur SurVenkatesh Samvida SReibe SaskiaCharles Philip DNavarro-Guerrero ElenaHill BarneyLassen Frederik HeymannClaussnitzer MelinaPalmer Duncan SLindgren Cecilia M