Ask about this productRelated genes to: TIMP4 antibody
- Gene:
- TIMP4 NIH gene
- Name:
- TIMP metallopeptidase inhibitor 4
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 3p25.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-07-07
- Date modifiied:
- 2016-10-05
Related products to: TIMP4 antibody
Related articles to: TIMP4 antibody
- Bothrops envenomation induces extensive local tissue destruction and a robust inflammatory response, largely driven by the host's endogenous molecular pathways. Among these, Matrix Metalloproteinases (MMPs), zinc-dependent endopeptidases responsible for extracellular matrix (ECM) degradation, play a central role. The clinical severity of envenomation is therefore strongly influenced by the balance between MMPs and their specific inhibitors, the TIMPs. This study investigated the contribution of MMP-1, MMP-2, MMP-7, MMP-9, and MMP-10 and TIMP-1, TIMP-2, TIMP-3, and TIMP-4 to the inflammatory response following Bothrops snakebites. - Source: PubMed
Publication date: 2026/04/24
Ferreira Neves Juliana CostaMagalhães-Gama FábioSantos Ibiapina Hiochelson NajibeSeixas Kamille BeltrãoBarbosa Êndila SouzaMalheiro AdrianaGonçalves Sachett Jacqueline AlmeidaCampi-Azevedo Ana CarolinaMartins-Filho Olindo AssisTeixeira-Carvalho AndréaSartim Marco AurélioMonteiro WueltonCosta Allyson Guimarães - Glomerulonephritis (GN) is an immune-mediated kidney disorder that causes glomerular injury, progressive renal dysfunction, and end-stage kidney disease. Traditional treatments such as corticosteroids and immunosuppressants are limited by variable efficacy and severe adverse effects, highlighting the need for novel therapeutic targets and personalized strategies. We performed a systematic multi-omics Mendelian randomization (MR) analysis applying established proteomic and transcriptomic quantitative trait loci (pQTL/eQTL) resources to genome-wide association studies (GWAS) of four GN subtypes: acute, chronic, IgA nephropathy, and membranous nephropathy. Bayesian colocalization was used to strengthen causal inference, while independent replication and meta-analysis were conducted using the FinnGen cohort. Mouse knockout phenotypes, drug reposition, and computational pharmacology algorithm were applied to evaluate translational potential. Proteomic-wide MR revealed MTR as protective in chronic GN and HCK as a risk factor for membranous nephropathy, whereas CD302 and CDKN1B showed protective effects. Transcriptomic-wide MR identified candidate genes across GN subtypes: RECQL, BRSK2, and MGP in acute GN; AFM, CFHR5, and EPHB2 in chronic GN; IL6R, MBL2, and PRSS3 in IgA nephropathy; and TIMP4, HCK, and PEAR1 in membranous nephropathy. Bayesian colocalization analysis provided strong support for shared causal variants (PPH4 > 0.8) for HCK, CD302, TIMP4, PEAR1, PARP1, and FHIT. Replication and meta-analysis in the FinnGen cohort provided additional consistency across datasets, while downstream translational annotations highlighted IL6R, MBL2, C5, and CD55 as potential hub targets within immune and complement-related pathways. This integrative multi-omics study provides novel insights into the genetic architecture and therapeutic landscape of GN, identifying potential therapeutic targets that may inform precision nephrology and drug repurposing. Notably, most targets supported by colocalization, mouse knockout phenotypes, and drug repurposing evidence were predominantly identified in membranous nephropathy, suggesting a particularly tractable genetic and therapeutic architecture for this subtype. - Source: PubMed
Publication date: 2026/04/16
Li GuoqiangJianhan FuGu JiashuWang YinhuaiLiu JiachenYang DongZeng DianjieZhao Pengcheng - To develop a gene expression-based prediction model for periodontitis by identifying a compact set of predictive genes and to validate the model using an independent cohort of patient samples analyzed by reverse transcription quantitative polymerase chain reaction (RT-qPCR). - Source: PubMed
Publication date: 2026/03/16
Lee Shin-KyuOh Jung-MinLee Sae-AJoo Ji-YoungKim Hyun-Joo - Sirtuin 3 (SIRT3), a mitochondrial NAD-dependent deacetylase, plays a central role in regulating mitochondrial metabolism, oxidative stress, and cell survival. Although SIRT3 has been implicated in angiogenesis, apoptosis, and inflammation, its global proteomic impact on the brain remains unclear. This study aimed to systematically characterize alterations in angiogenesis-, apoptosis-, chemokine-, and cytokine-related proteins in the brains of SIRT3 knockout (SIRT3 KO aka SIRT3/) mice compared with wild-type (WT) controls. - Source: PubMed
Publication date: 2026/02/28
He QingpingKhan SamiaWang LinlinIbeanu Gordon CLi P Andy - Diabetic ketoacidosis (DKA) occurs frequently in children with type 1 diabetes (T1D). The inflammatory response to DKA may play a role in complications, but the inflammatory pattern is not well characterized. We aimed to describe the inflammatory profile during and after DKA. - Source: PubMed
Publication date: 2026/03/10
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