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FDXR encodes a mitochondrial flavoprotein that initiates electron transport for cytochromes P450 receiving electrons from NADPH. De plus, nous expédions Ferredoxin Reductase Protéines (11) et Ferredoxin Reductase Kits (7) et beaucoup plus de produits pour cette protéine.
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We constructed cDNA including genes of the bovine cholesterol hydroxylase/lyase (CHL (Montrer CHRDL1 Anticorps)) system proteins-cytochrome P450scc (CYP11A1 (Montrer CYP11A1 Anticorps)), adrenodoxin (Adx (Montrer FDX1 Anticorps)) and adrenodoxin reductase (AdR), that are fused into a single ORF using FMDV 2A nucleotide sequences.
S. pombe is either very robust to mitochondrial reactive oxygen species (ROS (Montrer ROS1 Anticorps)) production or does not undergo apoptotic cell death in response to mitochondrial ROS (Montrer ROS1 Anticorps) at all.
FDXR and p53 (Montrer TP53 Anticorps) are mutually regulated and that the FDXR-p53 (Montrer TP53 Anticorps) loop is critical for tumor suppression via iron homeostasis.
we identified a novel disease-causing gene FDXR associated with mitochondrial diseases. The biallelic FDXR mutations cause optic atrophy and neuropathy. we found that FDXR levels are significantly lower in the patient fibroblast cells with the homozygous mutations R392W. Fourteen missense or nonsense FDXR mutations were identified in this study and eight of them (I143F, V158M, T211A, I213F, K280*, R315*, C359Y, D374N) clu (Montrer CLU Anticorps)
Using surface plasmon resonance, physiologically relevant concentrations of isatin (25-100 muM) were found to increase affinity of interactions between human recombinant ferrochelatase (FECH (Montrer FECH Anticorps)) and NADPH (Montrer NQO1 Anticorps)-dependent adrenodoxin reductase (ADR).
Mutation in FDXR gene is associated with Sensorial Neuropathies.
NOS-3 (Montrer NANOS3 Anticorps) overexpression resulted in an increased sensitivity to anti-Fas (Montrer FAS Anticorps) induced cell death, independently of AR expression and CatD (Montrer CTSD Anticorps) activity.
These results indicated that abundant FDXR expression in these steroidogenic cells was maintained through SF-1 (Montrer NR5A1 Anticorps) binding to the intronic enhancer of the FDXR gene
results suggest that both FDX1 (Montrer FDX1 Anticorps) and FDX2 and their likely reductase partner, FDXR, contribute to iron-sulfur cluster biogenesis
comparison of catalytic properties between conditions of limiting and saturating adrenodoxin reductase [cytochrome P450scc (Montrer CYP11A1 Anticorps)]
The ferredoxin reductase gene is regulated by the p53 (Montrer TP53 Anticorps) family and sensitizes cells to oxidative stress-induced (Montrer SQSTM1 Anticorps) apoptosis
ADXR rate of hydroxylation was linear with incubation time.
This gene encodes a mitochondrial flavoprotein that initiates electron transport for cytochromes P450 receiving electrons from NADPH. Multiple alternatively spliced transcript variants have been found for this gene.
NADPH:adrenodoxin oxidoreductase, mitochondrial
, adrenodoxin reductase
, ferredoxin--NADP(+) reductase
, ferredoxin reductase
, ferredoxin--NADP reductase
, adrenodoxin-NADP(+) reductase
, ferredoxin reductase L homeolog