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Human KEAP1 Protein expressed in HEK-293 Cells - ABIN2724103
Lieder, Reisen, Geppert, Sollberger, Beer, auf dem Keller, Schäfer, Detmar, Schneider, Werner: Identification of UV-protective activators of nuclear factor erythroid-derived 2-related factor 2 (Nrf2) by combining a chemical library screen with computer-based virtual screening. in The Journal of biological chemistry 2012
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KEAP1 acts as a cysteine thiol-rich sensor of redox insults. KEAP1 represses NRF2 activity under quiescent conditions, whereas NRF2 is liberated from KEAP1-mediated repression on exposure to stresses. [review]
the ability of porphyra-334 and shinorine to dissociate Nrf2 from Keap1 was confirmed also by measurement of increased mRNA expression of Nrf2 targeted genes encoding oxidative stress defense proteins in primary skin fibroblasts prior and post UVR exposure.
Aberrant Nrf2/Keap1 system integrity may affect self-defence mechanisms against oxidative stress in primary biliary cholangitis.
this study shows changes of KEAP1 expression levels induced by cell-free DNA in different cell types
Here we present a proof-of-concept application for the rational design of an epitope-specific antibody binding with the target protein Keap1, by grafting pre-defined structural interaction patterns from the native binding partner protein, Nrf2, onto geometrically matched positions of a set of antibody scaffolds. The designed antibodies bind to Keap1 and block the Keap1-Nrf2 interaction in an epitope-specific way
our study emphasizes the discovery of a gene signature regulated by the KEAP1-NRF2-CUL3 axis which is strongly associated with tumorigenesis and drug resistance in head and neck squamous cell cancer .
In the present review we briefly introduce the Nrf2-Keap1 system and describe Nrf2 functions, illustrate the Nrf2-NF-kappaB cross-talk, and highlight the effects of the Nrf2-Keap1 system in the physiology and pathophysiology of striated muscle tissue taking into account its role(s) in oxidative stress and reductive stress
Results show that KEAP1 expression in esophageal squamous cell carcinoma is regulated by miR-432-3p that binds directly its 3'UTR.
An intact complex of PGAM5-KEAP1-Nrf2 preserves mitochondrial motility by suppressing dominant-negative KEAP1 activity.
Hydrogen sulfide attenuates vascular smooth muscle cell calcification in vitro via the KEAP1-NRF2 redox sensing/stress response system by enhancing NQO1 expression.
Keap1 silencing in melanocytes induced melanogenesis and the expression of melanogenesis-associated molecules through HO-1-associated beta-catenin activation. Keap1 downregulation in melanocytes is important for cell proliferation and survival.
itaconate alkylates cysteine residues 151, 257, 288, 273 and 297 on the protein KEAP1, enabling Nrf2 to increase the expression of downstream genes with anti-oxidant and anti-inflammatory capacities
ESI induces protective autophagy of lung cancer cells through Nrf2-p62-keap1 feedback loop
results demonstrate a multifaceted protective potential of KEAP1-NRF2 signaling in key cell types relevant to Huntington disease pathology
Curcumin Protects Skin against UVB-Induced Cytotoxicity via the Keap1-Nrf2 Pathway: The Use of a Microemulsion Delivery System.
The research demonstrated that Keap1 should be a promising E3 ligase adaptor to be used in the design of novel PROTACs.
High cytoplasmic Keap1 expression, which might prevent nuclear translocation of Nrf2 in ovarian cancer cells, was associated with lower disease recurrence and death rate.
The ratio of thioredoxin/Keap1 protein level may be useful for suggesting distant metastasis in colorectal cancer.
our study pinpoints that PAQR3 functions as an adaptor protein to promote Nrf2-Keap1 complex formation, thereby modulating the Nrf2-Keap2 pathway and playing an important role in controlling antioxidant response of the cell
provide a rationale for stratification of human patients with lung cancer harboring KRAS/KEAP1- or KRAS/NRF2-mutant lung tumors as likely to respond to glutaminase inhibition
Nrf2/Keap1 system regulates VSMC apoptosis during neointimal formation, thereby inhibiting neointimal hyperplasia after a vascular injury.
Renal tubular deletion of Keap1 promotes nephrogenic diabetes insipidus features, confirming that Nrf2 activation in developing tubular cells causes a water reabsorption defect.
By inhibiting binding of Keap1 to Nrf2.
these studies are the first to demonstrate that Brain ischemic preconditioning protects the blood-brain barrier against ischemic injury by generation of endogenous electrophiles and activation of the Nrf2 pathway through inhibition of Keap1- and GSK3beta-dependent Nrf2 degradation.
these results suggested that trehalose can function as a novel activator of the p62-Keap1/Nrf2 pathway, in addition to inducing autophagy. Therefore, trehalose may be useful to treat many chronic diseases involving oxidative stress and dysfunction of autophagy.
While injury tended to suppress these genes in wild-type mice, the suppression was attenuated or reversed in Keap1 hypomorphs, suggesting that protection in these mice was mediated by increased Nrf2 transcriptional activity.
These findings suggest that Keap1-Nrf2 system plays a key role in depression and that dietary intake of sulforaphane-rich food during juvenile stages and adolescence can confer stress resilience in adulthood.
these results indicated that inactivation of KEAP1 protein by epigallocatechin gallate may mediate epigallocatechin gallate function in activating NRF2
the incidence, multiplicity and burden of Cutaneous squamous cell carcinomas that form in Keap1(flox/flox)/Nrf2(-/-) mice are much greater than in their Keap1(flox/flox)/Nrf2(+/+) counterparts, establishing Nrf2 activation as the protection mediator.
The p62-keap1-Nrf2 antioxidant pathway was primarily activated in the early stage of APAP hepatotoxicity.
Keap1 deletion in renal tubular cells results in an abnormal kidney development consistent with hydronephrosis.
serine 351 phosphorylation of p62 did not enhance its binding to Keap1 or stabilise the nuclear factor erythroid 2-related factor 2 (Nrf2) transcription factor in this neuronal context. Nrf2 protein levels were markedly decreased despite transcriptional activation of the Nrf2 gene
These results suggest that the Keap1/Nrf2 axis plays a critical role in NFATc1 expression and osteoclastogenic progression.
Results show that Keap1 deficiency in long-term hematopoietic stem cells increases the number of multipotent progenitor cells in steady-state hematopoiesis, and impairs their hematopoietic regeneration capacity .
During cellular stress or electrolytic imbalance, cysteine residue modification in Keap1 induces Nrf2 release from the Nrf2-Keap1 complex, which stabilizes Nrf2 and causes its nuclear translocation.
Results showed that in the basal state, the amount of Keap1 and Cul3 proteins were maintained at higher levels than that of Nrf2, and remained the same even under oxidative and electrophilic stimuli.
This study found that under oxidative stress induced by experimental periodontitis, the Nrf2/antioxidant defense pathway was activated and could be visualized from the luciferase activity in the in Keap1-dependent oxidative stress detector-luciferase mice model.
Caffeic acid induces Nrf2 activation by decreasing the expression of its inhibitor protein Keap1 and blocking the binding of Nrf2 with Keap1.
Hepatocyte-specific deletion of Keap1 triggering constitutive Nrf2 activation shifts hepatic metabolism towards increased lipid catabolism, reduced liponeogenesis and activation of the pentose phosphate pathway.
findings reveal that Keap1 regulates cell migration by affecting the subcellular localization and activity of cortactin independently of its role in oxidant stress responses.
These results suggest that alpha,beta-unsaturated carbonyl entity and catechol moiety of 6S derivatives may react with the cysteine residues of Keap1, disrupting the Keap1-Nrf2 complex, thereby liberating and activating Nrf2. Our findings of natural product-derived Nrf2 activators lead to design options of potent Nrf2 activators for further optimization.
mutation of either residual cysteine residue in Keap1a and Keap1b disrupted the ability of Keap1 to repress Nrf2, indicating that the presence of either Cys-273 or Cys-288 is sufficient for fish Keap1 molecules to fully function
study reports that the Keap1-Nrf2 system comprises discrete sensor sites, including the Keap1 cysteines Cys-151 and Cys-273, for a variety of Nrf2-activating compounds
the potency of 15d-PGJ2 as a signalling molecule in endothelial cells is significantly enhanced by the accumulation of the covalent adduct with 15d-PGJ2 and endogenous Keap1 over the time of exposure to the prostaglandin
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.
cytosolic inhibitor of Nrf2
, kelch-like family member 19
, kelch-like protein 19
, NRF2 cytosolic inhibitor
, ring canal protein
, kelch-like ECH-associated protein 1
, LOW QUALITY PROTEIN: kelch-like ECH-associated protein 1