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anti-Human TRIB1 Antibodies:
anti-Mouse (Murine) TRIB1 Antibodies:
anti-Rat (Rattus) TRIB1 Antibodies:
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Human Polyclonal TRIB1 Primary Antibody for ELISA, WB - ABIN544404
Wilkin, Suarez-Huerta, Robaye, Peetermans, Libert, Dumont, Maenhaut: Characterization of a phosphoprotein whose mRNA is regulated by the mitogenic pathways in dog thyroid cells. in European journal of biochemistry / FEBS 1997
Show all 3 Pubmed References
Cow (Bovine) Polyclonal TRIB1 Primary Antibody for ELISA - ABIN451704
Sung, Guan, Czibula, King, Eder, Heath, Suvarna, Dower, Wilson, Francis, Crossman, Kiss-Toth: Human tribbles-1 controls proliferation and chemotaxis of smooth muscle cells via MAPK signaling pathways. in The Journal of biological chemistry 2007
Human Monoclonal TRIB1 Primary Antibody for ELISA, WB - ABIN564425
Ji, Bian, Yu, Yuan, Liu, Yu, Li, Zhu, Jia, Guan, Zhang, Meng, Jin, Bai, Yu, Lee, Sun, Fu: Expulsion of micronuclei containing amplified genes contributes to a decrease in double minute chromosomes from malignant tumor cells. in International journal of cancer. Journal international du cancer 2014
Mouse (Murine) Polyclonal TRIB1 Primary Antibody for ELISA, WB - ABIN4362341
Yokoyama, Kanno, Yamazaki, Takahara, Miyata, Nakamura: Trib1 links the MEK1/ERK pathway in myeloid leukemogenesis. in Blood 2010
Associations for BCO2, PCSK9, and TR1B1 Polymorphism and Lifestyle Factors with Ischemic Stroke
These results suggest that TRB1 suppresses the expression of G6Pase and PEPCK by attenuating FOXO1 transcriptional activity and negatively regulates gluconeogenesis.
TRIB1 single nucleotide polymorphims rs17321515 and rs2954029 were significant associated with the risk of non-alcoholic fatty liver disease in Chinese Han population.
Acute knockdown of TRIB1 in human primary hepatocytes resulted in decreased expression of MTTP and APOB, required for very low density lipoprotein (VLDL) assembly although particle secretion was not significantly affected.
this study shows that Trib1 is overexpressed in Systemic Lupus Erythematosus, while it regulates immunoglobulin production in murine B cells
High expression of TRbeta1 is associated with longer breast cancer-specific survival independent of other prognostic factors. Given that low TRbeta expression is associated with chemotherapy resistance in-vitro, TRbeta1 may also serve as a predictive biomarker or even a therapeutic target given the availability of TRbeta agonists.
Study demonstrates that TRIB1 suppression and TRIB1 overexpression respectively reduce and increase HNF4A activity. TRIB1 and HNF4A partially colocalize and form complexes in vivo. Mapping of the interaction interfaces identified two distinct regions within TRIB1 which associated with the N-terminal region of HNF4A. These findings establish that TRIB is required for HNF4A function.
The expression profiles of TRIB1, TRIB2, and TRIB3 in human and murine hematopoietic stem, progenitor and mature cells, and in human leukemia datasets have been mapped.
findings support the hypothesis that TRIB1 gene expression in human umbilical vein endothelial cells depends on the duration of intrauterine exposure to hyperglycaemia
our study reveals that TRIB1 promotes CRC cell migration and invasion by up-regulating the expression of MMP-2 via the activation of FAK/Src and ERK pathways, knockdown of TRIB1 expression in CRC cells abolishes these effects.
role of TRIB1 in cell cycle and survival that is mediated via the modulation of NFkappaB signaling.
the co-operativity observed between MYC and TRIB1 in the absence of PML/RARA show that, outside of acute promyelocytic leukemia, gain of both genes may drive selection for trisomy 8.
The crucial role of TRIB1 in cisplatin-induced enrichment of CSC and drug resistance was verified by knockdown TRIB1. Interestingly, cisplatin treatment also contributed to the increasement of HDAC, the interaction of TRIB1 with HDAC, and inactivation of p53.
Trib1 formed a complex with pHDAC1.
Studies indicate that tribbles homolog 1 (Drosophila) protein appear to be involved in some of the most common diseases, such as cancer, metabolic disease and hyperlipidaemia.
Studies suggest that pseudo-kinase family of tribbles (TRIB) proteins TRIB1, TRIB2 and TRIB3 play roles in pathogenesis of rheumatoid arthritis (RA) and osteoarthritis.
Studies indicate that the minor allele of a single nucleotide polymorphism (SNP, rs6982502) in the regulatory sequence reduces the activity of the tribbles homolog 1 (Drosophila) protein (TRIB1) promoter.
Studies suggest that pseudo-kinase family of tribbles (TRIB) proteins TRIB1, TRIB2 and TRIB3 were involved in the pathogenesis of inflammation.
Studies indicate that tribbles homolog 1 (Drosophila) protein (TRIB1) interacts with the master molecule of Tregs, forkhead box P3 (FOXP3), a transcription factor essential for Treg suppressive activity.
Studies indicate that tribbles homolog 1 (Drosophila) protein (tribbles-1; TRIB1) is an important modulator of human energy metabolism and metabolic syndromes.
These findings suggest that Trib1 extensively controls macrophage M1/M2 polarization via the JAK/STAT signaling pathway.
The Liver Clock Controls Cholesterol Homeostasis through Trib1 Protein-mediated Regulation of PCSK9/Low Density Lipoprotein Receptor (LDLR) Axis.
Deletion of hepatic Trib1 leads to increased C/EBPalpha binding near upregulated lipogenic genes, as well as Trib1 itself.
TRIB1 and TRIB3 are more strongly expressed than TRIB2 in cumulus cells (CC) surrounding oocytes from preovulatory follicles than in CC of immature ones.
These data suggested that the modulation of TRIB1 expression affects hepatic lipogenesis and glycogenesis through multiple molecular interactions.
In gene knock-down experiments in macrophages using small interfering RNAs targeted to Trib1, it was observed that TNF-alpha production was increased following treatment with IFN-gamma and/or TLR2 ligands.
These results indicate that COP1 and Trib1 act as an oncoprotein complex functioning upstream of C/EBPalpha, and its ligase activity is crucial for leukemogenesis.
tribbles-1 is a novel binding partner of Foxp3 in regulatory T cells
results demonstrate that Trib1 is critical for adipose tissue maintenance and suppression of metabolic disorders by controlling the differentiation of tissue-resident M2-like macrophages
Trib1-knockout mice showed elevated levels of plasma TG and cholesterol due to increased VLDL production.
Trib1 transduced hematopoietic stem cells developed acute myeloid leukemia.
Dual role of TRB1 as both a target and a (co) activator of inflammatory signaling might provide a molecular rationale for the amplification of proinflammatory responses of adipose tissue.
describe suppression of adipocyte differentiation by TRBs Trib1, Trib2, Trib3
These results demonstrate that Trib1 is a negative regulator of NF-IL6 protein expression and modulates NF-IL6-dependent gene expression in toll-like receptors-mediated signaling.
a nuclear factor\; gene expression induced by m1-acetylcholine receptor
tribbles homolog 1 (Drosophila)
, G-protein-coupled receptor induced protein
, phosphoprotein C8FW
, tribbles homolog 1
, G-protein-coupled receptor-induced gene 2 protein
, G-protein-coupled receptor-induced protein 2
, phosphoprotein regulated by mitogenic pathways
, tribbles-like protein 1
, G-protein-coupled receptor induced protein GIG2