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抗Human TRIB1 抗体:
抗Mouse (Murine) TRIB1 抗体:
抗Rat (Rattus) TRIB1 抗体:
Human Polyclonal TRIB1 Primary Antibody for WB - ABIN392118
Dugast, Kiss-Toth, Docherty, Danger, Chesneau, Pichard, Judor, Pettré, Conchon, Soulillou, Brouard, Ashton-Chess: Identification of tribbles-1 as a novel binding partner of Foxp3 in regulatory T cells. in The Journal of biological chemistry 2013
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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
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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
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.
Studies indicate that small molecules can reveal rate-limiting signalling outputs and functions of pseudo-kinase family of tribbles (TRIB) proteins TRIB1, TRIB2 and TRIB3 in cells and intact organisms, serving as guides for the development of new drugs.
Studies indicate that overexpression of the wild-type tribbles homolog 1 (Drosophila) protein (Trib1) gene effectively induces leukaemia.
Studies show that TRIB1 and TRIB2 are highly expressed in molecularly-defined sub-types of acute myeloid leukemia (AML).
Studies show a remarkable reduction in tribbles 2 protein (Trib2) expression during oocyte maturation whereas tribbles 1 protein (Trib1) and tribbles 3 protein (Trib3) expression was significantly increased during this process.
SNP rs17321515 associated with plasma triglycerides level and increasing risk of coronary heart disease in male Chinese Han population
These studies indicated that SAP18 expression enhanced the recruitment of mSin3A in coordination with TRIB1 to MTTP regulatory elements and increased MTTP expression.
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