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TAX1BP1 Antibody (Center) Blocking Peptide
Synthetic peptide
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
| Primary Accession | Q86VP1 |
|---|---|
| Clone Names | 100528067 |
| Gene ID | 8887 |
|---|---|
| Other Names | Tax1-binding protein 1, TRAF6-binding protein, TAX1BP1, T6BP |
| Format | Peptides are lyophilized in a solid powder format. Peptides can be reconstituted in solution using the appropriate buffer as needed. |
| Storage | Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C. |
| Precautions | This product is for research use only. Not for use in diagnostic or therapeutic procedures. |
| Name | TAX1BP1 |
|---|---|
| Synonyms | T6BP |
| Function | Ubiquitin-binding adapter that participates in inflammatory, antiviral and innate immune processes as well as selective autophagy regulation (PubMed:30459273, PubMed:29940186, PubMed:30909570). Plays a key role in the negative regulation of NF-kappa-B and IRF3 signalings by acting as an adapter for the ubiquitin-editing enzyme A20/TNFAIP3 to bind and inactivate its substrates (PubMed:17703191). Disrupts the interactions between the E3 ubiquitin ligase TRAF3 and TBK1/IKBKE to attenuate 'Lys63'-linked polyubiquitination of TBK1 and thereby IFN- beta production (PubMed:21885437). Recruits also A20/TNFAIP3 to ubiquitinated signaling proteins TRAF6 and RIPK1, leading to their deubiquitination and disruption of IL-1 and TNF-induced NF-kappa-B signaling pathways (PubMed:17703191). Inhibits virus-induced apoptosis by inducing the 'Lys-48'-linked polyubiquitination and degradation of MAVS via recruitment of the E3 ligase ITCH, thereby attenuating MAVS- mediated apoptosis signaling (PubMed:27736772). As a macroautophagy/autophagy receptor, facilitates the xenophagic clearance of pathogenic bacteria such as Salmonella typhimurium and Mycobacterium tuberculosis (PubMed:26451915). Upon NBR1 recruitment to the SQSTM1- ubiquitin condensates, acts as the major recruiter of RB1CC1 to these ubiquitin condensates to promote their autophagic degradation (PubMed:33226137, PubMed:34471133). Mediates the autophagic degradation of other substrates including TICAM1 (PubMed:28898289). |
| Cellular Location | Cytoplasm. Mitochondrion. Preautophagosomal structure Cytoplasmic vesicle, autophagosome |
| Tissue Location | Expressed in all tissues tested. |
Thousands of laboratories across the world have published research that depended on the performance of antibodies from Abcepta to advance their research. Check out links to articles that cite our products in major peer-reviewed journals, organized by research category.
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Provided below are standard protocols that you may find useful for product applications.
Background
The HTLV-1 Tax protein transcriptionally activates theHTLV-1 promoter. Tax also binds to and stimulates the expression ofcellular genes, including transcription factors and other proteins(Gachon et al., 1998 [PubMed 9733879]).
References
Parvatiyar, K., et al. J. Biol. Chem. 285(20):14999-15009(2010)Ruiz, M.T., et al. Braz J Otorhinolaryngol 76(2):193-198(2010)Shembade, N., et al. Science 327(5969):1135-1139(2010)Dieguez-Gonzalez, R., et al. Ann. Rheum. Dis. 68(4):579-583(2009)Shembade, N., et al. EMBO J. 28(5):513-522(2009)
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