Ask about this productRelated genes to: TRIB1 Blocking Peptide
- Gene:
- TRIB1 NIH gene
- Name:
- tribbles pseudokinase 1
- Previous symbol:
- -
- Synonyms:
- C8FW, GIG2, TRB1
- Chromosome:
- 8q24.13
- Locus Type:
- gene with protein product
- Date approved:
- 2004-05-10
- Date modifiied:
- 2016-11-01
Related products to: TRIB1 Blocking Peptide
Related articles to: TRIB1 Blocking Peptide
- Recent reports have shown that polymorphisms in the and genes are associated with plasma lipid levels and the risk of cardiovascular disease. This study evaluates the associations of and polymorphisms with subclinical atherosclerosis (SA) and plasma lipid levels in Mexican individuals. This study included 1406 Mexican mestizo individuals (417 individuals with SA and 989 healthy controls). Genotyping of and polymorphisms was performed using TaqMan assays in a real-time PCR system. To analyze whether these polymorphisms are associated with SA and plasma lipid levels, we used logistic regression (OR [95% CI]), adjusted for confounding factors. The genotype of the rs2737229 / polymorphism showed a significant association with the risk of developing SA under multiple genetic models [codominant: OR = 1.61 (95% CI: 1.10-2.36), = 0.048; recessive: OR = 1.42 (1.02-1.99), = 0.039; additive: OR = 1.26 (1.05-1.53), = 0.015]. Similarly, the genotype of the rs2954029 / polymorphism was also significantly associated with the risk of developing SA [codominant: OR = 1.63 (1.10-2.43), = 0.033; recessive: OR = 1.64 (1.13-2.37), = 0.009]. In a sub-analysis of SA individuals, individuals with homozygous for the rs2737229 polymorphism had higher LDL cholesterol levels [135 mg/dL (110-148)] than those with homozygous [118 mg/dL (99-139)] ( < 0.003). The analysis of the rs2954029 polymorphism showed that carriers of the genotype had increased glucose levels [97 mg/dL (87-118)] compared to carriers of the genotype [91 mg/dL (84-99)] ( < 0.002). In summary, our findings showed that, in Mexican Mestizos, the genotype of the rs2737229 / SNP and the genotype of the rs2954029 / polymorphism are associated with a higher risk of developing SA and elevated levels of glucose and LDL cholesterol. - Source: PubMed
Publication date: 2026/04/05
Vargas-Alarcón GilbertoPosadas-Sánchez RosalindaPérez-Méndez OscarArellano-González MarvaFragoso José Manuel - Diabetes-related vascular complications are characterized by impaired ischemia-driven angiogenesis and delayed wound healing. MicroRNAs (miRNAs) are emerging as powerful targets for multifaceted diseases. We previously identified that miRNA-181c-5p has anti-angiogenic properties, but its role in diabetes is unknown. In a hindlimb ischemia model, streptozotocin-rendered diabetic mice treated with an miRNA-181c-5p inhibitor (anti-miR-181c-5p) exhibited improved blood flow reperfusion and increased arteriolar density, compared with diabetic anti-miR-negative (anti-miR-Neg) control mice. Diabetic anti-miR-Neg mice had reduced perfusion relative to nondiabetic control mice. In a murine wound-healing model, inhibition of miRNA-181c-5p rescued diabetes-impaired wound closure rate and increased capillary density, whereas diabetic anti-miR-Neg wounds healed more slowly than nondiabetic anti-miR-Neg wounds. In vitro, inhibition of miRNA-181c-5p increased endothelial tubule formation and cell migration under high-glucose conditions. Mechanistically, anti-miR-181c-5p elevated VEGFA and VEGFR2 protein expression, ERK2 phosphorylation, and Bcl2 mRNA levels. Whole-transcriptome sequencing identified two genes (Elmo3 and Trib1) that were upregulated in anti-miR-181c-5p-treated hindlimbs and wounds. Luciferase assays confirmed VEGFA as a likely direct target of miR-181c-5p, whereas ERK2, ELMO3, and TRIB1 are indirectly regulated. These findings demonstrate that miRNA-181c-5p inhibition promotes angiogenesis and improves vascular repair in diabetes, identifying miRNA-181c-5p as a potential therapeutic target for preventing diabetic vascular complications. - Source: PubMed
Publication date: 2026/03/31
Solly Emma LLuo YingjunPrimer Khalia RMulangala JocelyneDi Bartolo Belinda ANicholls Stephen JPsaltis Peter JBouman Chen ZhenBursill Christina ATan Joanne T M - Atherosclerosis represents a chronic inflammatory disease of the arterial wall and remains a principal cause of cardiovascular morbidity and mortality. Macrophages critically govern lesion initiation, progression, and destabilization, and accumulating evidence indicates that protein kinases are key regulators of their phenotype and function. This systematic review synthesizes data from 162 publications encompassing 76 kinases to delineate the contribution of macrophage-associated kinase signaling to atherogenesis. The identified kinases span major families, including AGC, CaMK, CMGC, Ste20, and tyrosine kinases, each exerting distinct regulatory effects on macrophage survival, polarization, lipid handling, efferocytosis, and inflammatory activation. Several kinases, such as CaMK2γ, CaMK4, DCLK1, Trib1, and STK25, exhibit pro-atherogenic activity by promoting foam cell formation, expanding the necrotic core, and propagating inflammatory pathways. Conversely, kinases, including STK11 and the context-dependent mediator Akt1, exhibit protective or dual functions that contribute to metabolic homeostasis and reparative macrophage states. Despite substantial mechanistic insights and the established therapeutic utility of kinase inhibitors in oncology, clinical translation in the context of atherosclerosis remains limited. This review consolidates current knowledge, identifies critical gaps, and outlines prospective avenues to target macrophage-specific kinase pathways as novel therapeutic strategies for atherosclerosis. - Source: PubMed
Publication date: 2026/03/27
Müller Jana Svan der Vorst Emiel P C - Cardiovascular disease (CVD) represents a significant global public health challenge, with its high incidence and mortality rates imposing a substantial socioeconomic burden. Tribbles family proteins (TRIB1, TRIB2, and TRIB3), functioning as pseudokinases, play a pivotal role in the pathogenesis and progression of various CVDs, including coronary heart disease, heart failure, hypertension, cardiomyopathy, and pulmonary hypertension. The progression of CVD is modulated by the tribbles family proteins through key mechanisms such as the regulation of inflammatory responses, apoptosis, endoplasmic reticulum stress, and insulin signaling pathways. Furthermore, polymorphisms within the tribbles family genes are strongly associated with genetic susceptibility to CVDs, thereby influencing disease risk and clinical manifestations. Multiple therapeutic strategies targeting the tribbles family have demonstrated potential in improving cardiac and vascular function, offering novel avenues for CVD treatment. This review provides an in-depth analysis of the structural characteristics of tribbles family proteins and elucidates the mechanisms of tribbles in CVDs and their potential as therapeutic targets. - Source: PubMed
Publication date: 2026/03/19
Zhang WenkangZhang MinhaoSha ZiqiYan GaoliangTang ChengchunLi Mingkang - Metabolic reprogramming, particularly the dysregulation of cholesterol metabolism, is a hallmark of pancreatic ductal adenocarcinoma (PDAC). However, the underlying molecular drivers remain largely elusive. In this study, we demonstrate that Tribbles homolog 1 (TRIB1) is elevated in PDAC tissues and is significantly associated with poor prognosis. Functionally, TRIB1 mRNA knockdown suppresses PDAC cell growth and tumor formation, while its overexpression promotes both. Mechanistically, TRIB1 protein binds to the DNA-binding domain of PPARγ and inhibits its transcriptional activity. This interaction relieves the PPARγ-mediated repression of HMGCR, the rate-limiting enzyme in the mevalonate pathway, thereby fueling de novo cholesterol biosynthesis. Furthermore, in vivo experiments indicate that PDAC tumors with high TRIB1 expression were more sensitive to the HMGCR inhibitor atorvastatin. Collectively, our findings highlight the critical role of the TRIB1-PPARγ-HMGCR axis in the metabolic rewiring of PDAC and suggest that TRIB1 may serve as a predictive biomarker for optimizing statin-based metabolic therapies. - Source: PubMed
Sun RuiQin HenanZhang WenheGuo XinTeng YibinXu MengyuanLiu JiweiNing ZhenWang Aman