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Mouse Anti-KEAP1 Recombinant Antibody (CBLY1-073) (CBMAB-K0753-LY)

This product is antibody recognizes KEAP1. The antibody CBLY1-073 immunoassay techniques such as: WB, IHC-P, IF, IP, ELISA.
See all KEAP1 antibodies

Summary

Host Animal
Mouse
Specificity
Human
Clone
CBLY1-073
Antibody Isotype
IgG
Application
WB, IHC-P, IF, IP, ELISA

Basic Information

Specificity
Human
Antibody Isotype
IgG
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Purity
> 95% Purity determined by SDS-PAGE.
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freezethaw cycles.

Target

Full Name
Kelch Like ECH Associated Protein 1
Introduction
This gene encodes a protein containing KELCH-1 like domains, as well as a BTB/POZ domain. Kelch-like ECH-associated protein 1 interacts with NF-E2-related factor 2 in a redox-sensitive manner and the dissociation of the proteins in the cytoplasm is followed by transportation of NF-E2-related factor 2 to the nucleus. This interaction results in the expression of the catalytic subunit of gamma-glutamylcysteine synthetase. Two alternatively spliced transcript variants encoding the same isoform have been found for this gene. [provided by RefSeq, Jul 2008]
Entrez Gene ID
9817
UniProt ID
Q14145
Alternative Names
Kelch Like ECH Associated Protein 1; Kelch-Like Family Member 19; Cytosolic Inhibitor Of Nrf2; Kelch-Like Protein 19; KLHL19; INrf2; Kelch-Like ECH-Associated Protein 1; KIAA0132;
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:15983046, PubMed:15601839).
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:19489739, PubMed:16006525, PubMed:17127771, PubMed:18251510, 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).
Biological Process
Cellular response to interleukin-4IEA:Ensembl
Cellular response to oxidative stressManual Assertion Based On ExperimentIDA:UniProtKB
Cytoplasmic sequestering of transcription factorManual Assertion Based On ExperimentIBA:GO_Central
In utero embryonic developmentIEA:Ensembl
Negative regulation of DNA-binding transcription factor activityManual Assertion Based On ExperimentTAS:ParkinsonsUK-UCL
Positive regulation of proteasomal ubiquitin-dependent protein catabolic processManual Assertion Based On ExperimentTAS:ParkinsonsUK-UCL
Protein ubiquitinationManual Assertion Based On ExperimentIDA:UniProtKB
Regulation of autophagyManual Assertion Based On ExperimentIDA:UniProtKB
Regulation of epidermal cell differentiationIEA:Ensembl
Ubiquitin-dependent protein catabolic processManual Assertion Based On ExperimentIDA:UniProtKB
Cellular Location
Cytoplasm; Nucleus. Mainly cytoplasmic (PubMed:15601839).
In response to selective autophagy, relocalizes to inclusion bodies following interaction with SQSTM1/p62 (PubMed:20452972).
PTM
Non-enzymatic covalent modifications of reactive cysteines by electrophile metabolites inactivate the BCR(KEAP1) complex (PubMed:17127771, PubMed:18251510, PubMed:29590092, PubMed:30323285).
Accumulation of fumarate promotes the formation of cysteine S-succination (S-(2-succinyl)cysteine), leading to inactivate the BCR(KEAP1) complex and promote NFE2L2/NRF2 nuclear accumulation and activation (By similarity).
Nitric oxide-dependent 8-Nitro-cGMP formation promotes cysteine guanylation (S-cGMP-cysteine), leading to NFE2L2/NRF2 nuclear accumulation and activation (By similarity).
Itaconate, an anti-inflammatory metabolite generated in response to lipopolysaccharide, alkylates cysteines, activating NFE2L2/NRF2 (PubMed:29590092).
Methylglyoxal, a reactive metabolite that accumulates when the glycolytic enzyme PGK1 is inhibited, promotes formation of a methylimidazole cross-link between proximal Cys-151 and Arg-135 on another KEAP1 molecule, resulting in an inactive dimer that inactivates the BCR(KEAP1) complex (PubMed:30323285).
Degraded via a proteasomal-independent process during selective autophagy: interaction with phosphorylated SQSTM1/p62 sequesters KEAP1 in inclusion bodies, leading to its degradation.
Auto-ubiquitinated by the BCR(KEAP1) complex (PubMed:15572695, PubMed:15983046).
Quinone-induced oxidative stress, but not sulforaphane, increases its ubiquitination (PubMed:15572695, PubMed:15983046).
Ubiquitination and subsequent degradation is most pronounced following prolonged exposure of cells to oxidative stress, particularly in glutathione-deficient cells that are highly susceptible to oxidative stress (PubMed:15572695, PubMed:15983046).

Ulasov, A. V., Rosenkranz, A. A., Georgiev, G. P., & Sobolev, A. S. (2022). Nrf2/Keap1/ARE signaling: Towards specific regulation. Life Sciences, 291, 120111.

Yu, C., & Xiao, J. H. (2021). The Keap1-Nrf2 system: a mediator between oxidative stress and aging. Oxidative Medicine and Cellular Longevity, 2021, 1-16.

Kopacz, A., Kloska, D., Forman, H. J., Jozkowicz, A., & Grochot-Przeczek, A. (2020). Beyond repression of Nrf2: An update on Keap1. Free Radical Biology and Medicine, 157, 63-74.

Baird, L., & Yamamoto, M. (2020). The molecular mechanisms regulating the KEAP1-NRF2 pathway. Molecular and cellular biology, 40(13), e00099-20.

Taguchi, K., & Yamamoto, M. (2020). The KEAP1–NRF2 system as a molecular target of cancer treatment. Cancers, 13(1), 46.

Suzuki, T., Muramatsu, A., Saito, R., Iso, T., Shibata, T., Kuwata, K., ... & Yamamoto, M. (2019). Molecular mechanism of cellular oxidative stress sensing by Keap1. Cell reports, 28(3), 746-758.

Cuadrado, A., Rojo, A. I., Wells, G., Hayes, J. D., Cousin, S. P., Rumsey, W. L., ... & Dinkova-Kostova, A. T. (2019). Therapeutic targeting of the NRF2 and KEAP1 partnership in chronic diseases. Nature reviews Drug discovery, 18(4), 295-317.

Tu, W., Wang, H., Li, S., Liu, Q., & Sha, H. (2019). The anti-inflammatory and anti-oxidant mechanisms of the Keap1/Nrf2/ARE signaling pathway in chronic diseases. Aging and disease, 10(3), 637.

Bellezza, I., Giambanco, I., Minelli, A., & Donato, R. (2018). Nrf2-Keap1 signaling in oxidative and reductive stress. Biochimica et Biophysica Acta (BBA)-Molecular Cell Research, 1865(5), 721-733.

Yamamoto, M., Kensler, T. W., & Motohashi, H. (2018). The KEAP1-NRF2 system: a thiol-based sensor-effector apparatus for maintaining redox homeostasis. Physiological reviews, 98(3), 1169-1203.

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For research use only. Not intended for any clinical use.

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