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TRB3 / TRIB3 Antibody (Internal)
Rabbit Polyclonal Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, IHC-P, IF, E |
|---|---|
| Primary Accession | Q96RU7 |
| Reactivity | Human, Mouse, Rat |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 40kDa |
| Dilution | IHC-P (10 µg/ml), WB (1-2 µg/ml), |
| Gene ID | 57761 |
|---|---|
| Other Names | Tribbles homolog 3, TRB-3, Neuronal cell death-inducible putative kinase, SINK, p65-interacting inhibitor of NF-kappa-B, TRIB3, C20orf97, NIPK, SKIP3, TRB3 |
| Target/Specificity | TRB3 antibody is human, mouse and rat reactive. At least two isoforms of TRB3 are known to exist; this antibody will detect both isoforms. |
| Reconstitution & Storage | Long term: -20°C; Short term: +4°C. Avoid repeat freeze-thaw cycles. |
| Precautions | TRB3 / TRIB3 Antibody (Internal) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | TRIB3 |
|---|---|
| Synonyms | C20orf97, NIPK, SKIP3, TRB3 |
| Function | Inactive protein kinase which acts as a regulator of the integrated stress response (ISR), a process for adaptation to various stress (PubMed:15781252, PubMed:15775988). Inhibits the transcriptional activity of DDIT3/CHOP and is involved in DDIT3/CHOP-dependent cell death during ER stress (PubMed:15781252, PubMed:15775988). May play a role in programmed neuronal cell death but does not appear to affect non-neuronal cells (PubMed:15781252, PubMed:15775988). Acts as a negative feedback regulator of the ATF4-dependent transcription during the ISR: while TRIB3 expression is promoted by ATF4, TRIB3 protein interacts with ATF4 and inhibits ATF4 transcription activity (By similarity). Disrupts insulin signaling by binding directly to Akt kinases and blocking their activation (By similarity). May bind directly to and mask the 'Thr-308' phosphorylation site in AKT1 (By similarity). Interacts with the NF-kappa-B transactivator p65 RELA and inhibits its phosphorylation and thus its transcriptional activation activity (PubMed:12736262). Interacts with MAPK kinases and regulates activation of MAP kinases (PubMed:15299019). Can inhibit APOBEC3A editing of nuclear DNA (PubMed:22977230). |
| Cellular Location | Nucleus. |
| Tissue Location | Highest expression in liver, pancreas, peripheral blood leukocytes and bone marrow. Also highly expressed in a number of primary lung, colon and breast tumors. Expressed in spleen, thymus, and prostate and is undetectable in other examined tissues, including testis, ovary, small intestine, colon, leukocyte, heart, brain, placenta, lung, skeletal muscle, and kidney |
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Background
Disrupts insulin signaling by binding directly to Akt kinases and blocking their activation. May bind directly to and mask the 'Thr-308' phosphorylation site in AKT1. Binds to ATF4 and inhibits its transcriptional activation activity. Interacts with the NF-kappa-B transactivator p65 RELA and inhibits its phosphorylation and thus its transcriptional activation activity. Interacts with MAPK kinases and regulates activation of MAP kinases. May play a role in programmed neuronal cell death but does not appear to affect non-neuronal cells. Does not display kinase activity. Inhibits the transcriptional activity of DDIT3/CHOP and is involved in DDIT3/CHOP-dependent cell death during ER stress. Can inhibit APOBEC3A editing of nuclear DNA.
References
Bowers A.J.,et al.Oncogene 22:2823-2835(2003).
Wu M.,et al.J. Biol. Chem. 278:27072-27079(2003).
Kiss-Toth E.,et al.J. Biol. Chem. 279:42703-42708(2004).
Ord D.,et al.Biochem. Biophys. Res. Commun. 330:210-218(2005).
Shan Y.X.,et al.Submitted (MAR-2003) to the EMBL/GenBank/DDBJ databases.
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