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Validated All-in-One™ qPCR Primer for KEAP1(NM_012289.3) Search again
Product ID:
HQP023233
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
INrf2, KLHL19
Gene Description:
kelch like ECH associated protein 1
Target Gene Accession:
NM_012289.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
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].
Gene References into function
- In epithelial cells derived from retina and inner ear, Keap1 is a component of focal adhesions and zipper junctions.
- Keap1 dimerization causes Nrf2 sequestration
- phosphorylation of serine 40 is necessary for nuclear factor((erythroid-derived 2)like 2(Nrf2) release from Inhibitor of Nrf2(INrf2)
- Data show that Keap1 associates with the N-terminal region of Cullin 3 through the IVR domain and promotes the ubiquitination of Nrf2 in cooperation with the Cullin 3-Roc1 complex.
- hKeap1 regulates fetal Alz-50 reactive clone 1 in addition to its known role in control of Nrf2
- structure of the Kelch domain of Keap1 protein represents a high quality model for the superfamily of eukaryotic kelch repeat proteins
- KEAP1 is a redox-regulated substrate adaptor protein for a Cul3-dependent ubiquitin ligase complex.
- crystallographic analysis of the Kelch domain from human Keap1
- Keap1 negatively regulates Nrf2 function in part by targeting Nrf2 for ubiquitination by the CUL3-ROC1 ligase and subsequent degradation by the proteasome
- A downstream product of COX-2, 15-deoxy-Delta(12,14)-prostaglandin J2 (15d-PGJ2), activated the Nrf2 regulatory pathway in HAECs through binding to the cysteines of Keap1
- Keap1 is a BTB-Kelch substrate adaptor protein for Cul3, which targets it for degradation by a proteasome-independent pathway
- stabilization of Nrf2 in cells under stress represents the central regulatory response mediated by mechanisms that interfere with its interaction with Keap1, leading to the induction of antioxidant enzymes important to maintain cellular redox homeostasis
- Modifying specific cysteines of the electrophile-sensing human Keap1 protein is insufficient to disrupt binding to the Nrf2 domain Neh2.
- These findings suggest a role for FAC1 in apoptosis following release of Nrf2 from Keap1 in response to oxidative stress.
- x-ray crystallographic analysis of solvent and side-chain interactions in the Kelch domain of Keap1
- Somatic mutation and a gene variation in human lung cancer cells change glycine to cysteine in the KEAP1 DGR domain, introducing local conformational changes that reduce Keap1's affinity for Nrf2.
- A recombinant protein containing both the Kelch/DGR domain and the C-terminal region of mouse Keap1 was expressed in Escherichia coli, purified to near-homogeneity and crystallized by the sitting-drop vapour-diffusion method.
- Loss of KEAP1 function leading to constitutive activation of NRF2-mediated gene expression in cancer suggests that tumor cells manipulate the NRF2 pathway for their survival against chemotherapeutic agents
- The N terminus of the PGAM5 protein contains a conserved NXESGE motif that binds to the substrate binding pocket in the Kelch domain of Keap1.
- review will discuss recent progress in the field of the Nrf2-Keap1 signaling pathway, with emphasis on the mechanistic studies of Nrf2 regulation by Keap1--{REVIEW}
- Nrf2-Keap1-dependent UGT1A1 induction by prooxidants might represent a key adaptive response to cellular oxidative stress
- In 84 Japanese type 2 diabetes subjects, 18 genetic variations were detected in the KEAP1 gene, including 13 novel ones.
- KEAP1 controls postinduction repression of the NRF2-mediated antioxidant response by escorting nuclear export of NRF2.
- Importantly, our findings suggest that a paradox exists whereby Nrf2 activity is beneficial in non-malignant cells but in cancer cells it may provide a selective advantage for clonal expansion.
- endogenous Keap1 remains mostly in the cytoplasm, and electrophiles promote nuclear accumulation of Nrf2 without altering the subcellular localization of Keap1
- Nrf2 regulates INrf2 by controlling its transcription, and INrf2 controls Nrf2 by degrading it.
- C151 is the most important site of alkylation on Keap1 by chemoprevention agents that function by activating the antioxidant response element through Nrf2.
- in response to CSNO Keap1 accumulates in the nucleus with a time course similar to that of Nrf2.
- ProTalpha and Nrf2 compete for interaction with Keap1, therefore ProTalpha is able to liberate Nrf2 from complex with Keap1 and hence contribute to Nrf2-dependent transcription.
- Cys151 adduction confers a critical alkylation sensor function upon Keap1
- Keap1 prevents activation of Nrf2 and lung cancer cell growth
- ap1-dependent signaling pathway for the induction of the constitutive GST A1 expression during epithelial cell differentiati in Caco-2 cells.
- Keap1 expression is regulated by an epigenetic mechanism in lung cancer.
- Aberrant Nrf2 activation provoked by Keap1 alteration is one of the molecular mechanisms for chemotherapeutic resistance in gallbladder cancer
- provides in vivo validation of the two-site substrate recognition model for Nrf2 activation by the Keap1-Cul3-based E3 ligase
- Targeting Nrf2 activity in lung cancers, particularly those with Keap1 mutations, could be a promising strategy to inhibit tumor growth and circumvent chemoresistance.