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Keap1 orchestrates the antioxidant response; the system can be targeted for therapy [review]
Keap1 is the main negative regulator of Nrf2 (show GABPA ELISA Kits) [review]
Results show that GSTP (show GSTP1 ELISA Kits) potentiates S-glutathionylation of Keap1, which leads to Nrf2 (show GABPA ELISA Kits) activation and subsequently increases expression of GSTP (show GSTP1 ELISA Kits). This positive feedback regulatory loop represents a novel mechanism by which GSTP (show GSTP1 ELISA Kits) elicits antioxidant protection in the brain.
EMT (show ITK ELISA Kits) signalling and the KEAP1/NFE2L2 (show NFE2L2 ELISA Kits)-axis are likely to be involved in metastatic spread of malignant melanoma and also appear to have potential interactions.
the expression of NRF2 (show GABPA ELISA Kits), KEAP1, NQO-1 (show NQO1 ELISA Kits) and HO-1 (show HMOX1 ELISA Kits) are increased significantly in advanced laryngeal squamous cell carcinoma, compared with the adjacent normal mucosa. Remarkable relevance exists between high expression of KEAP1, NQO-1 (show NQO1 ELISA Kits), HO-1 (show HMOX1 ELISA Kits) and nuclear NRF2 (show GABPA ELISA Kits). their expression levels were independent of age, tumor stage (clinical stage III and IV), tumor size and lymph node metastasis.
miR (show MLXIP ELISA Kits)-200a was found to interact with the 3'-untranslated region of Keap1, the native regulator of Nrf2 (show GABPA ELISA Kits).
We present the case that chemoprevention through the Keap1/Nrf2 (show GABPA ELISA Kits) system may be context dependent and that the Nrf2 (show GABPA ELISA Kits) "dose-response curve" for electrophilic and redox balance may not be monotonic.
Immunohistochemical assays were used to measure the expression of Keap1 protein in breast cancer tissue and adjacent normal tissue, and its clinical significance was explored. We observed that 24.6% breast cancer tissue samples were positive for Keap1, a significantly lower proportion than that seen with adjacent normal tissue specimens
c-myc (show MYC ELISA Kits) plays a key role in MBD1 (show DPEP1 ELISA Kits) mediated epigenetic silencing of KEAP1.
Results show up-regulation of TrkB (show NTRK2 ELISA Kits) and down-regulation of Runx3 (show RUNX3 ELISA Kits) and Keap1 in breast cancer cells and suggest that TrkB (show NTRK2 ELISA Kits) plays a key role in tumorigenicity and metastasis of breast cancer cells through suppression of Runx3 (show RUNX3 ELISA Kits) or Keap1.
the potency of 15d-PGJ2 as a signalling molecule (show GDF5 ELISA Kits) 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 study found that under oxidative stress induced (show SQSTM1 ELISA Kits) by experimental periodontitis, the Nrf2 (show NFE2L2 ELISA Kits)/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 (show NFE2L2 ELISA Kits) activation by decreasing the expression of its inhibitor protein Keap1 and blocking the binding of Nrf2 (show NFE2L2 ELISA Kits) with Keap1.
Hepatocyte-specific deletion of Keap1 triggering constitutive Nrf2 (show NFE2L2 ELISA Kits) 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 (show CTTN ELISA Kits) independently of its role in oxidant stress responses.
chronic hyperglycemic conditions, Keap1 inhibition increased Nrf2 (show NFE2L2 ELISA Kits) nuclear translocation, increased antioxidant gene expression, and reduced ROS (show ROS1 ELISA Kits) production to normoglycemic levels.
conclusion, increased Keap1/Nrf2 (show NFE2L2 ELISA Kits) signaling in the liver is accompanied by repressed gluconeogenesis and lipogenesis that can, at least partially, explain the ameliorated diabetic phenotype in the Keap1-hypo mice.
Keap1 utilizes multiple cysteine residues specifically and/or collaboratively as sensors for the detection of a wide range of environmental stresses.
iron deficiency induced the nuclear translocation of Nrf2 (show NFE2L2 ELISA Kits) via Keap1 degradation by autophagy and subsequently upregulated expression of HO-1 (show HMOX1 ELISA Kits).
These results strongly suggest that p62 plays a crucial role in preventing fenofibrate-induced cell death.
Keap1 knockdown caused severe disruption in both the redox cycle and the cell cycle of replicating hepatocytes.
mutation of either residual cysteine residue in Keap1a and Keap1b disrupted the ability of Keap1 to repress Nrf2 (show NFE2L2 ELISA Kits), indicating that the presence of either Cys (show DNAJC5 ELISA Kits)-273 or Cys (show DNAJC5 ELISA Kits)-288 is sufficient for fish Keap1 molecules to fully function
study reports that the Keap1-Nrf2 (show NFE2L2 ELISA Kits) system comprises discrete sensor sites, including the Keap1 cysteines Cys (show DNAJC5 ELISA Kits)-151 and Cys (show DNAJC5 ELISA Kits)-273, for a variety of Nrf2 (show NFE2L2 ELISA Kits)-activating compounds
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.
kelch-like ECH-associated protein 1
, cytosolic inhibitor of Nrf2
, kelch-like family member 19
, kelch-like protein 19
, NRF2 cytosolic inhibitor
, ring canal protein