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KEAP1 Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, IF, E |
|---|---|
| Primary Accession | Q14145 |
| Other Accession | NP_987096, 45269145 |
| Reactivity | Human, Mouse, Rat |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | IgG |
| Calculated MW | 69 kDa |
| Application Notes | KEAP1 antibody can be used for detection of KEAP1 by Western blot at 1 - 2 µg/mL. For immunofluorescence start at 20 µg/mL. |
| Gene ID | 9817 |
|---|---|
| Target/Specificity | KEAP1; At least two isoforms of KEAP1 are known to exist. |
| Reconstitution & Storage | KEAP1 antibody can be stored at 4℃ for three months and -20℃, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures. |
| Precautions | KEAP1 Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | KEAP1 {ECO:0000303|PubMed:14585973, ECO:0000312|HGNC:HGNC:23177} |
|---|---|
| Function | Substrate-specific adapter of a BCR (BTB-CUL3-RBX1) E3 ubiquitin ligase complex that regulates the response to oxidative stress by targeting NFE2L2/NRF2 for ubiquitination (PubMed:14585973, PubMed:15379550, PubMed:15572695, PubMed:15601839, PubMed:15983046, PubMed:37339955). KEAP1 acts as a key sensor of oxidative and electrophilic stress: in normal conditions, the BCR(KEAP1) complex mediates ubiquitination and degradation of NFE2L2/NRF2, a transcription factor regulating expression of many cytoprotective genes (PubMed:15601839, PubMed:16006525). In response to oxidative stress, different electrophile metabolites trigger non-enzymatic covalent modifications of highly reactive cysteine residues in KEAP1, leading to inactivate the ubiquitin ligase activity of the BCR(KEAP1) complex, promoting NFE2L2/NRF2 nuclear accumulation and expression of phase II detoxifying enzymes (PubMed:16006525, PubMed:17127771, PubMed:18251510, PubMed:19489739, PubMed:29590092). In response to selective autophagy, KEAP1 is sequestered in inclusion bodies following its interaction with SQSTM1/p62, leading to inactivation of the BCR(KEAP1) complex and activation of NFE2L2/NRF2 (PubMed:20452972). The BCR(KEAP1) complex also mediates ubiquitination of SQSTM1/p62, increasing SQSTM1/p62 sequestering activity and degradation (PubMed:28380357). The BCR(KEAP1) complex also targets BPTF and PGAM5 for ubiquitination and degradation by the proteasome (PubMed:15379550, PubMed:17046835). |
| Cellular Location | Cytoplasm. Nucleus. Note=Mainly cytoplasmic (PubMed:15601839). In response to selective autophagy, relocalizes to inclusion bodies following interaction with SQSTM1/p62 (PubMed:20452972). |
| Tissue Location | Broadly expressed, with highest levels in skeletal muscle. |
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Provided below are standard protocols that you may find useful for product applications.
Background
KEAP1 Antibody: KEAP1 (kelch-like ECH-associated protein 1) is a stress sensing adaptor for the Cullin3 (Cul3)-dependent E3 ubiquitin ligase complex that negatively regulates NRF2 (NF-E2-related factor 2) and plays a role in the oxidative stress response. It targets NFE2L2/NRF2 for ubiquitination and degradation by the proteasome. KEAP1 contains an amino terminal BTB/POZ domain and a carboxyl terminal KELCH domain which are required for interaction with NRF2, and in binding Cul3-E3 ubiquitin ligase. Altered expression of NRF2 is associated with chronic obstructive pulmonary disease (COPD). KEAP1 also targets the down regulation of NF-κB activity by targeting IKKβ degradation. Mutation of the KEAP1 gene is found in lung cancer.
References
Zhang DD, Lo SC, Cross JV, et al. Keap1 is a redox-regulated substrate adaptor protein for a Cul3-dependent ubiquitin ligase complex. Mol. Cell. Biol. 2004;24:10941-53.
Kobayashi A, Kang MI, Okawa H, et al. Oxidative stress sensor Keap1 functions as an adaptor for Cul3-based E3 ligase to regulate proteasomal degradation of Nrf2. Mol. Cell. Biol. 2004; 24:7130-9.
Jiang J, Mo ZC, Yin K, et al. Epigallocatechin-3-gallate prevents TNF-α-induced NF-kappaB activation thereby upregulating ABCA1 via the Nrf2/Keap1 pathway in macrophage foam cells. Int. J. Mol. Med. 2012; 29:946-56.
Devling TW, Lindsay CD, McLellan LI, et al. Utility of siRNA against Keap1 as a strategy to stimulate a cancer chemopreventive phenotype. Proc. Natl. Acad. Sci. USA 2005; 102: 7280-5A.
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