Anti-TRIB1 polyclonal antibody (DPABH-00761)

Rabbit anti-Human TRIB1 (aa 104-372) polyclonal antibody for WB, IHC-P


Host Species
Antibody Isotype
Species Reactivity
Recombinant fragment, corresponding to a region within amino acids 104-372 of Human TRIB1.


Application Notes
WB: 1/500 - 1/3000; IHC-P: 1/100 - 1/1000.
*Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own experiment using appropriate negative and positive controls.


Alternative Names
TRIB1; tribbles homolog 1 (Drosophila); tribbles homolog 1; C8FW; GIG2; TRB1
Entrez Gene ID
UniProt ID


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Polymorphisms at newly identified lipid-associated loci are associated with blood lipids and cardiovascular disease in an Asian Malay population


Authors: Tai, E. Shyong; Sim, Xue Ling; Ong, Twee Hee; Wong, Tien Yin; Saw, Seang Mei; Aung, Tin; Kathiresan, Sekar; Orho-Melander, Marju; Ordovas, Jose M.; Tan, Jonathan T.; Seielstad, Mark

We conducted a cross-sectional study of Malay articipants aged 40-80 years (n = 2,932) to examine the associations between polymorphisms at newly identified, lipid-associated loci with blood lipid levels and prevalent cardiovascular disease (CVD) in a Malay population in Asia. A polymorphism adjacent to the TRIB1 locus (rs17321515) was associated with elevated total cholesterol and LDL-cholesterol (LDL-C) after adjustment for age and sex (both P values <0.007) and with increased risk of coronary heart disease and CVD [odds ratio (OR) 1.23, 95% confidence interval (95% CI) 1.03-1.46; and OR 1.2, 95% CI 1.02-1.42, respectively] under an additive model of inheritance. In addition, using recessive models of inheritance, polymorphisms on chromosome 19 adjacent to the CILP2 and PBX4 loci (rs16996148) and on chromosome 1 at the GALNT2 locus (rs4846914) were associated with elevated HDL-C (P = 0.005) and lower LDL-C (P = 0.048), respectively. Although novel, the former is consistent with the association between this polymorphism and lower blood triglycerides observed in the initial studies conducted in populations of European ancestry. Neither showed statistically significant association with CVD. These observations should form the basis of further investigation to identify the causative polymorphisms at this locus, and also to understand the mechanistic roles that this protein may play in lipoprotein metabolism in Asians and other populations.-Tai, E. S., X. L. Sim, T. H. Ong, T. Y. Wong, S. M. Saw, T. Aung, S. Kathiresan, M. Orho-Melander, J. M. Ordovas, J. T. Tan, and M. Seielstad. Polymorphisms at newly identified lipid-associated loci are associated with blood lipids and cardiovascular disease in an Asian Malay population. J. Lipid Res. 2009. 50: 514-520.

Clinical utility of an array comparative genomic hybridization analysis for Williams syndrome


Authors: Yagihashi, Tatsuhiko; Torii, Chiharu; Takahashi, Reiko; Omori, Mikimasa; Kosaki, Rika; Yoshihashi, Hiroshi; Ihara, Masahiro; Minagawa-Kawai, Yasuyo; Yamamoto, Junichi; Takahashi, Takao; Kosaki, Kenjiro

Low birthweight resulting from a non-optimal fetal environment is correlated epidemiologically to a higher risk of adult diseases, and which has also been demonstrated using animal models for maternal undernutrition. In this study, we subjected pregnant mice to 50% food restriction (FR), and profiled gene expression and promoter DNA methylation genome-wide using the fetal livers. The fact that effect of food restriction is opposite between before and after birth encouraged us to hunt for genes that are expressed oppositely to adult calorie restriction (CR) using the maternal livers. Among oppositely regulated genes, we identified trib1 (tribbles homolog 1). Using genetically modified mice, trib1 has been shown to have a demonstrable contribution to a risk of hypertriglyceridaemia and insulin resistance. Our data showed that the trib1 expression and its promoter DNA methylation could be affected physiologically (by maternal nutrition), and therefore might be a strong candidate gene for developmental origins of adult diseases. Furthermore, lepr (leptin receptor) gene was downregulated by maternal FR, indicating its potential role in induction of obesity and diabetes. Gene expression as well as promoter DNA methylation profiling revealed that glucocorticoid receptor target genes were regulated by maternal FR. This supports previous studies that suggest an important role of fetal glucocorticoid exposure in the mechanism of developmental origins of diseases. Our transcriptomics profiling data also suggested that maternal FR impaired development of the immune system. An inventory of candidate genes responsible for developmental origins of health and disease is presented and discussed in this study.

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