DUSP13 antibody Polyclonal Antibodies Primary antibodies
- Known as:
- DUSP13 (anti-) Polyclonal Antibodies Primary antibodies
- Catalog number:
- orb101406
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- DUSP13 antibody Polyclonal Antibodies Primary antibodies
Related genes to: DUSP13 antibody Polyclonal Antibodies Primary antibodies
- Gene:
- DUSP13 NIH gene
- Name:
- dual specificity phosphatase 13
- Previous symbol:
- -
- Synonyms:
- BEDP, TMDP, FLJ32450, DUSP13A, DUSP13B
- Chromosome:
- 10q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-11-11
- Date modifiied:
- 2016-10-05
Related products to: DUSP13 antibody Polyclonal Antibodies Primary antibodies
Related articles to: DUSP13 antibody Polyclonal Antibodies Primary antibodies
- Atherosclerosis and arteriosclerosis are major contributors to cardiovascular disease (CVD), yet their shared and distinct molecular underpinnings remain incompletely understood. This study integrates proteomics, Bayesian colocalization, and Mendelian randomization (MR), and structural modelling to explore the shared and distinct plasma proteome associated with arteriosclerosis and atherosclerosis across different vascular beds. - Source: PubMed
Publication date: 2026/05/14
Huang JingxianMeena DevendraAchtari MargauxSmith AlexanderJudy RenaeMimouni NourBis Joshua CFranceschini NoraFung KennethMunroe Patricia BDamrauer Scott MTzoulaki IoannaDehghan Abbas - Centrosome amplification (CA) contributes to cancer but remains poorly characterized in non-neoplastic conditions such as pressure injuries (PI). This study investigated CA-related genes (CARGs) in PI to identify potential therapeutic targets. - Source: PubMed
Publication date: 2026/04/09
Li SenShen HaoweiLi KunlinWang XinSun ZhaofeiLi YanpingYuan Yuhuan - Hypertensive heart disease (HHD) and hypertrophic cardiomyopathy (HCM) are characterized by left ventricular hypertrophy and diastolic dysfunction. Despite overlapping remodeling features, their distinct mechanisms and therapeutic responses remain unclear. This study integrated genetic, imaging, and proteomic data to identify key mediators underlying β1-adrenergic receptor blockers (β1-blockers)-related therapeutic heterogeneity between HHD and HCM. - Source: PubMed
Publication date: 2026/02/09
Chen ZheTang YifanLi ShuangPan LiangbinWu JiaxuanLiu JiangjiangMa HaitaoWang BinXie Kai - Sepsis is a life-threatening condition with high mortality, underscoring the urgent need for effective therapeutic targets. We conducted a proteome-wide Mendelian randomization (MR) analysis using plasma protein data from the FinnGen, UKB-PPP, and deCODE cohorts to identify proteins causally associated with sepsis. The analysis included 16,074 cases and 363,227 controls in FinnGen and 11,643 cases and 474,841 controls in the UK Biobank, spanning four exposure-outcome combinations. Proteins were prioritized based on a false discovery rate <0.05 in one combination and < 0.05 in another. Colocalization and phenome-wide association studies (PheWAS) were performed to evaluate causality and potential off-target effects. Three proteins─dual specificity phosphatase 13 (DUSP13), inhibin beta C chain (INHBC), and toll-like receptor 1 (TLR1)─showed strong evidence of colocalization with sepsis risk. PheWAS confirmed broader disease associations for DUSP13 and TLR1, while INHBC showed no significant adverse associations and is considered druggable. TLR1 is currently under clinical investigation. ELISA-based experimental validation in 20 sepsis patients and 20 controls demonstrated elevated serum levels of DUSP13 and INHBC and reduced levels of TLR1 in sepsis. These findings identify DUSP13, INHBC, and TLR1 as promising therapeutic targets for sepsis, supported by genetic, phenotypic, and experimental evidence. - Source: PubMed
Publication date: 2025/06/03
Liu BingyangJin YuhongDing YiGu YiZhou JianqingLuo Chun - Proteomics has been scarcely explored for predicting treatment outcomes in major depressive disorder (MDD), due to methodological challenges and costs. Predicting protein levels from genetic scores provides opportunities for exploratory studies and the selection of targeted panels. In this study, we examined the association between genetically predicted plasma proteins and treatment outcomes - including non-response, non-remission, and treatment-resistant depression (TRD) - in 3559 patients with MDD from four clinical samples. Protein levels were predicted from individual-level genotypes using genetic scores from the publicly available OmicsPred database, which estimated genetic scores based on genome-wide genotypes and proteomic measurements from the Olink and SomaScan platforms. Associations between predicted protein levels and treatment outcomes were assessed using logistic regression models, adjusted for potential confounders including population stratification. Results were meta-analysed using a random-effects model. The Bonferroni correction was applied. We analysed 257 proteins for Olink and 1502 for SomaScan; 111 proteins overlapped between the two platforms. Despite no association was significant after multiple-testing correction, many top results were consistent across phenotypes, in particular seven proteins were nominally associated with all the analysed outcomes (CHL1, DUSP13, EVA1C, FCRL2, KITLG, SMAP1, and TIM3/HAVCR2). Additionally, three proteins (CXCL6, IL5RA, and RARRES2) showed consistent nominal associations across both the Olink and SomaScan platforms. The convergence of results across phenotypes is in line with the hypothesis of the involvement of immune-inflammatory mechanisms and neuroplasticity in treatment response. These results can provide hints for guiding the selection of protein panels in future proteomic studies. - Source: PubMed
Publication date: 2025/05/22
Oliva VincenzoPossidente ChiaraFanelli GiuseppeDomschke KatharinaMinelli AlessandraGennarelli MassimoMartini PaoloBortolomasi MarcoSquassina AlessioPisanu ClaudiaKasper SiegfriedZohar JosephSouery DanielMontgomery StuartAlbani DiegoForloni GianluigiFerentinos PanagiotisRujescu DanMendlewicz JulienBaune Bernhard T Vieta EduardSerretti AlessandroFabbri Chiara