TRIB1 Antibody
Purified Rabbit Polyclonal Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application
| WB |
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Primary Accession | Q96RU8 |
Reactivity | Human, Mouse |
Host | Rabbit |
Clonality | Polyclonal |
Isotype | Rabbit Ig |
Calculated MW | 41009 Da |
Gene ID | 10221 |
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Other Names | Tribbles homolog 1, TRB-1, G-protein-coupled receptor-induced gene 2 protein, GIG-2, SKIP1, TRIB1 |
Target/Specificity | TRIB1 |
Formulation | In PBS with 0.09% (W/V) sodium azide |
Handling | The antibody solution should be gently mixed before use. |
Background Descriptions | |
Precautions | TRIB1 Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | TRIB1 (HGNC:16891) |
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Function | Adapter protein involved in protein degradation by interacting with COP1 ubiquitin ligase (PubMed:27041596). The COP1- binding motif is masked by autoinhibitory interactions with the protein kinase domain (PubMed:26455797). Serves to alter COP1 substrate specificity by directing the activity of COP1 toward CEBPA (PubMed:27041596). Binds selectively the recognition sequence of CEBPA (PubMed:26455797). Regulates myeloid cell differentiation by altering the expression of CEBPA in a COP1-dependent manner (By similarity). Controls macrophage, eosinophil and neutrophil differentiation via the COP1-binding domain (By similarity). Interacts with MAPK kinases and regulates activation of MAP kinases, but has no kinase activity (PubMed:15299019, PubMed:26455797). |
Tissue Location | Expressed in most human tissues with the highest levels in skeletal muscle, thyroid gland, pancreas, peripheral blood leukocytes, and bone marrow. |
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Provided below are standard protocols that you may find useful for product applications.
Background
TRIB1 antibody, also called gprotein coupled receptor induced, skip1, gig2, c8fwATP, functions in protein binding, protein kinase inhibitor activity, and protein serine/threonine kinase activities. Overexpression of TRIB1 in HeLa cells repressed the basal activity of the IL8 promoter by inhibiting AP1 activity. Overexpression of TRIB1 inhibited oncogenic Ras -driven AP1 activation and MEKK1-mediated AP1 activation. ERK activation was enhanced by TRIB1. Coimmunoprecipitation and yeast 2-hybrid assays showed that MEK1 interacted with both TRIB1 and TRIB3, and MKK4 interacted specifically with TRIB1. Cotransfection of MKK4 enhanced the level of TRIB1, indicating that the TRIB-MAPKK interaction stabilized TRIB1
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