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Knockout of the cytochrome P450 reductase by CRISPR/Cas9 technology (POR(-/-)) in HEK293 cells overexpressing Nox4 or Nox5 did not interfere with ROS production in intact cells. However, POR(-/-) abolished the signal in NADPH-stimulated assays using membrane fractions from the very same cells. Moreover, membranes of rat smooth muscle cells treated with angiotensin II showed an increased NADPH-dependent signal with lucigen
we observed that miR (show MLXIP Proteins)-378 modulates the oscillation amplitudes of Cdkn1a (show CDKN1A Proteins) in the control of cell cycle and Por in the regulation of oxidation reduction by forming partnership with different circadian transcription factors
Highest level of Rac1 activation was achieved on the smallest nanofibers, a trend that was lost in POR1 knockdown. This supports the hypothesis that on small nanofibers, POR1 binds to highly curved cell membranes, allowing Rac1 to dissociate and activate.
Results are the first to show that some forms of opioid-mediated stress-induced analgesia require brain neuronal P450 activity.
Immunological and metabolic changes resulting from a genetic deficiency in CPR (show GRID2 Proteins) expression in the intestine in mice.
An apparent link exists between the cytochrome p450 reductase and FGF signaling pathways.
These data collectively indicate a novel role of the Cpr (show GRID2 Proteins) gene in fear conditioning and memory.
this study provides novel insights into the regulation of gap junction function by CYPOR and suggests that Cx43 (show GJA1 Proteins) may play an important role(s) in CYPOR-mediated bone defects seen in patients.
inactivation of the hepatic cytochrome P450 system by conditional deletion of this enzyme
Changes in hepatic mRNA expression using microarray analysis and real-time PCR in POR null mice are reported.
NADPH-P450 reductase (NPR) was purified from hepatic microsomes of Xenopus laevis.
Suggest that hepatic POR and P450s are coregulated, and that POR plays a complex role in P450 (show CYP2B6 Proteins)-mediated metabolism.
A homodimer model can resolve the conundrum as to how cytochrome P450 oxidoreductase (show TXNRD1 Proteins) and cytochrome b5 (show CYB5A Proteins) compete for the same binding site on cytochrome P450c17 (show CYP17A1 Proteins). (Review)
Compound heterozygosity of a paternal submicroscopic deletion and a maternal missense mutation in POR gene: Antley-bixler syndrome phenotype in three sibling fetuses
To promote intracellular iron flux, an iron chaperone appears to be essential for receiving iron from heme catabolism. Data suggest that PCBP2 (show PCBP2 Proteins) competes with CPR for binding HO1 (show HMOX1 Proteins); PCBP2 (show PCBP2 Proteins) K homology 3 domain is important for HO1 (show HMOX1 Proteins)/PCBP2 (show PCBP2 Proteins) interaction; heme prompts HO1 (show HMOX1 Proteins)/CPR multimer and decreases HO1 (show HMOX1 Proteins)/PCBP2 (show PCBP2 Proteins) multimer. [PCBP2 (show PCBP2 Proteins) = poly(rC) binding protein 2 (show PCBP2 Proteins); CPR = cytochrome P450 reductase; HO1 (show HMOX1 Proteins) = heme oxidase 1]
analysis of mutations and polymorphisms in POR linked to metabolism of steroids and xenobiotics and pathology of P450 (show CYP2B6 Proteins) oxidoreductase (show TXNRD1 Proteins) deficiency (PORD)
No significant differences in the distribution of haplotypes between cases and controls were detected. In conclusion, this study reveals that four SNPs in the POR gene (rs3823884, rs3898649, rs239953 and rs17685) may affect the susceptibility of smoking cessation in a Chinese Han population.
analysis of the role of the active site loop in coenzyme binding and flavin reduction in cytochrome P450 reductase
Current studies demonstrate that, unlike previously described mutations, A287P causes POR deficiency disorder due to conformational instability leading to proteolytic susceptibility in vivo, rather than through an inherent flavin-binding defect.
population pharmacokinetic analysis identified that the combined genotype of CYP3A5 (show CYP3A5 Proteins)-POR was the only covariant for the apparent clearance of tacrolimus
Case Report: delayed diagnosis of 46, XY disorder of sex development due to P450 (show CYP2B6 Proteins) oxidoreductase (show TXNRD1 Proteins) (POR) deficiency.
Data indicate not only that binding of b5 and P450 reductase on the proximal surface of P450 2B4 (show CD244 Proteins) results in electron transfer but also that each redox partner transmits unique structural information to the active site proton delivery network.
This gene encodes an endoplasmic reticulum membrane oxidoreductase with an FAD-binding domain and a flavodoxin-like domain. The protein binds two cofactors, FAD and FMN, which allow it to donate electrons directly from NADPH to all microsomal P450 enzymes. Mutations in this gene have been associated with various diseases, including apparent combined P450C17 and P450C21 deficiency, amenorrhea and disordered steroidogenesis, congenital adrenal hyperplasia and Antley-Bixler syndrome.
, NADPH-cytochrome P450 oxidoreductase
, P450 reductase
, cytochrome P450 reductase
, cytochrome c reductase (NADPH)
, P450 (cytochrome) oxidoreductase
, NADPH--cytochrome P450 reductase-like
, ADP-ribosylation factor-interacting protein 2
, Arfaptin 2
, partner of RAC1
, ADP-ribosylation factor interacting protein 2 (arfaptin 2)
, partner of Rac1
, NADPH--cytochrome P450 reductase
, NADPH-P450 reductase
, NADPH-dependent cytochrome P450 reductase
, NADPH-cytochrome P450 reductase
, NADPH-cytochrome P-450 oxidoreductase
, NADH cytochrome P450 oxydoreductase