TRIOBP Antibody
- Known as:
- TRIOBP Antibody
- Catalog number:
- GWB-MN228C
- Product Quantity:
- 50ug
- Category:
- -
- Supplier:
- GenWay
- Gene target:
- TRIOBP Antibody
Related genes to: TRIOBP Antibody
- Gene:
- TRIOBP NIH gene
- Name:
- TRIO and F-actin binding protein
- Previous symbol:
- DFNB28
- Synonyms:
- HRIHFB2122, KIAA1662, Tara, TAP68
- Chromosome:
- 22q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-10-04
- Date modifiied:
- 2014-11-18
Related products to: TRIOBP Antibody
Related articles to: TRIOBP Antibody
- We conducted the first genome-wide association meta-analyses of global and sectoral peripapillary retinal nerve fibre layer (pRNFL) thickness and Bruch's membrane opening-minimum rim width (BMO-MRW), the major optic nerve head structural and neurodegeneration biomarkers, including up to 25,942 and 12,080 participants, respectively, from the International Glaucoma Genetics Consortium. We identified 9 global pRNFL thickness and 9 global BMO-MRW loci, along with 28 and 19 loci for pRNFL and BMO-MRW sectors, respectively, comprising both shared and sector-specific loci. To identify intraocular pressure (IOP)-independent drug targets, global pRNFL thickness and BMO-MRW were conditioned on IOP. IOP-independent loci were then prioritised to identify candidate causal genes using transcriptome-wide association study and colocalization analysis. Several genes, such as and had robust associations with both phenotypes, with potential IOP-independent therapeutic translation for glaucoma. Overall, we identified novel loci for pRNFL thickness and BMO-MRW, highlighting potential drug-target genes acting independently from IOP, and elucidating genetic differences among pRNFL sectors. - Source: PubMed
Publication date: 2026/02/10
Aman Asma MDiaz-Torres SantiagoLee Samantha Sze-YeeDriessen Sjoerd Jde Vries Victor Avan der Heide Frank C TKolovos AntoniaSchmidt Joshua MMarshall Henry NSaleh LaniaSchulze AliciaBlokland Gabriëlla AmWebers Carroll A Bvan der Kallen Carla J HWesselius AnkeArts Iljavan Asten FreekjeGorski MathiasZimmermann Martina EStark Klaus JHeid Iris MYoung Terri LPasquale Louis RSegrè Ayellet VWiggs Janey LKhawaja Anthony PHewitt Alex WSchuster Alexander KBerendschot Tos T J MThiadens Alberta A H Jvan Garderen Karin AKlaver Caroline C WHysi Pirro GHammond Christopher JBrandl CarolineCraig Jamie ERamdas Wishal DMacGregor StuartMackey David AGharahkhani Puya - An emerging area of research into major mental illnesses is to investigate the formation of insoluble aggregates of specific proteins in the brains of patients with these conditions. These studies are normally based on examining insoluble protein in post mortem brain samples, but, for practical reasons, typically consider only one region of the brain per subject. Here, we tested post mortem brain samples from multiple brain regions of various individuals, which included patients with major depressive disorder, schizophrenia and victims of suicide. Samples from patients with Alzheimer's disease and control individuals were used for comparison. Notably, 20 tissue samples were available from across the brain of one individual who had both schizophrenia and Alzheimer's disease. Consistently, while insolubility of DISC1 (Disrupted in Schizophrenia 1), CRMP1 (Collapsin Response Mediator Protein 1) and/or TRIOBP-1 (Trio and F-actin Binding Protein, isoform 1) were often present in multiple brain regions, this was not homogenous across the brain. While this study looks at a relatively small number of subjects, and caution must be taken in over-generalising, it is possible that aggregation of these proteins spreads throughout the brain, in a similar manner to the staging seen in neurodegenerative disease. Previous studies may therefore have underestimated the prevalence of protein aggregation in mental illness, due to this heterogeneity of insoluble protein across the brain. - Source: PubMed
Publication date: 2026/02/11
Samardžija BobanaRenner ÉvaPalkovits MiklósBradshaw Nicholas J - The glymphatic system plays a key role in brain waste clearance, but its genetic regulation remains poorly understood. Diffusion Tensor Image Analysis along the Perivascular Space (DTI-ALPS) index is a non-invasive imaging biomarker to asses glymphatic system activity. We integrated mean DTI-ALPS genome-wide association study (GWAS) data from 31,021 individuals of European ancestry with GTEx v8 multi-tissue eQTL data to perform transcriptome-wide association studies (TWAS) using Unified Test for Molecular Signature (UTMOST) and Functional Summary-based Imputation (FUSION). Gene-level associations were further validated by Multi-marker Analysis of Genomic Annotation (MAGMA). Causal inference was conducted using cis-Mendelian randomization (cis-MR) and summary-data-based Mendelian randomization (SMR), while colocalization was applied to provide evidence of strong associations between two traits within a single genetic region, thereby ensuring the stability of the MR conclusions. TWAS identified 17 candidate genes (AGBL5-IT1, CENPA, CGREF1, DNAJC5G, EMILIN1, GCAT, KHK, MAPRE3, OTOF, PLCL1, PREB, RBM43, RFTN2, SERPIND1, SNAP29, TRIOBP, and UCN), among which six protein-coding genes (TRIOBP, MAPRE3, EMILIN1, KHK, GCAT, and CGREF1) were further validated by MAGMA. Cis-MR provided evidence for the causal effects of these six genes, while colocalization supported that the MR conclusions were stable for four of them (TRIOBP, MAPRE3, EMILIN1, and GCAT). Finally, SMR identified three genes (TRIOBP, GCAT, and MAPRE3) that showed consistent and robust associations with DTI-ALPS across multiple tissues. These findings provide statistical evidence for genetic regulation of glymphatic function. - Source: PubMed
Publication date: 2025/12/05
Zhu XiaoyangWang ShengjieZhang ShuaiqiLiu ZhiyuanWang NaWang ShuYang Nixia - Whole-genome sequencing of sporadic vestibular schwannoma (VS) specimens will reveal novel genetic mutations and molecular pathways involved in the pathogenesis of the disease. - Source: PubMed
Publication date: 2025/11/13
Ostrander Benjamin TLa Monte OliviaLi VivienneVo VivianKumar AshleyTelese FrancescaSchwartz Marc SFriedman Rick A - Retinoic acid (RA), a metabolite of vitamin A, exerts paradoxical effects in tissue repair, promoting regeneration in some contexts while driving fibrosis in others. However, the mechanisms governing this functional switch remain elusive. Here, we identify RA as a key paracrine signal that links tubular epithelial injury to fibroblast activation in renal fibrosis. Spatial metabolomics and single-cell transcriptomics reveal that ALDH1A2-mediated RA synthesis is upregulated in injured renal tubules, while RA receptor signaling is enriched in interstitial fibroblasts. RA stimulation induces fibroblast-to-myofibroblast transition (FMT) by upregulating RAI14, a cytoskeletal adaptor that binds and stabilizes TRIOBP, thereby preventing its HECTD1-mediated ubiquitination and degradation. This stabilization enhances F-actin assembly and cytoskeletal tension, leading to YAP nuclear translocation and activation of profibrotic transcriptional programs. Genetic ablation of RAI14 significantly attenuates renal fibrosis in vivo. Together, our findings uncover a tubule-derived RA-RAI14-TRIOBP-YAP axis that translates epithelial injury into fibroblast mechanotransduction, providing mechanistic insight into epithelial-mesenchymal communication and a potential therapeutic target for fibrotic kidney disease. - Source: PubMed
Publication date: 2025/11/14
Zhu JunWang MeixiaZhang YizhiWang XintaoDai LeiLi ZhuLi YangbingZhang XinxinWang HongjieZhao JieLi XiaozhouWang Hong-Hui