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Retinoic acid homeostasis regulates meiotic entry in developing anuran gonads and in Bidder's organ through Raldh2 (show ALDH1A2 ELISA Kits) and Cyp26b1 proteins.
we provide the third family affected by the disorder and the first affected individual to survive beyond infancy. This woman homozygous for c.1303G>A; p.(Gly435Ser) in CYP26B1, which was associated with multisutural synostosis, radiohumeral synostosis, normal bone mineral density, and apparent intellectual disability, a phenotype with significant similarities to Antley-Bixler and Pfeiffer syndromes.
Study investigated the distribution of Cyp26a1 (show CYP26A1 ELISA Kits) and Cyp26b1 transcripts in the rat and human brain, identifying several novel regions of expression, including the cerebral cortex for both enzymes and striatum for Cyp26b1.
Holo-CRABPs had higher affinity for CYP26B1 than free atRA, but both apo (show C9orf3 ELISA Kits)-CRABPs(CRABP-I (show CRABP1 ELISA Kits) and CRABP-II (show CRABP2 ELISA Kits) ) inhibited the formation of 4-OH-RA by CYP26B1.
There was increased expression of mRNA CYP26B1 in oral cancer tissue compared to adjacent noncancerous tissues.
SNPs in three genes CYP26B1 rs2241057, CISD1 rs2251039, rs2590370, and TBX1 rs4819522 were involved in six potential pathways to influence serum prostate-specific antigen levels.
Our results suggested that the CYP26B1 splice variant is associated with the occurrence of BQ-related oral cancer.
homozygous carriers of the major (T) allele, relative to homozygous carriers of the minor (C) allele, of the CYP26B1 polymorphism rs2241057 may have an increased risk for the development of Crohn's disease.
We report a 2p13.2 microdeletion in 2 subjects encompasing 2 genes, EXOC6B (show EXOC6B ELISA Kits) and CYP26B12 with clinical effects on cognitive function, and craniofacial and skeletal development.
Single nucleotide polymorphisms in CYP26B1, NANOS1 and STRA8 genes support involvement of meiotic program initiation genes in modifying the risk of azoospermia and oligozoospermia in a Han-Chinese population
CYP26B1 capacity is genetically regulated and suggest that local CYP26B1 activity may influence atherosclerosis.
elimination of CYP26B1 activity within both germ and Sertoli cells resulted in severe male subfertility, with a loss of advanced germ cells from the seminiferous epithelium.
The results of this study concluded that stimulus-dependent neuronal activity can control the expression of the RA catabolic enzyme Cyp26B1 and downstream genes such as BACE1 (show BACE ELISA Kits).
The study showed that a stimulus-dependent gradient of a retinoic acid-inactivating enzyme Cyp26B1 modifies the composition, localization
Cyp26b1 in the growth plate regulates the proliferation rates of chondrocytes and is responsible for the normal function of the growth plate and growing bones
results show that T cell-specific expression of Cyp26b1 is required for the development of T cell-mediated colitis and may be applicable to the development of therapeutics that target Cyp26b1 for the treatment of inflammatory bowel disease
CYP26B1 suppresses two distinct genetic programs induced by retinoic acid: a Stra8-dependent meiotic pathway, and a Stra8-independent mitotic pathway.
CYP26B1 has a role in regulating retinoid levels and is important for lymphatic vascular development in the mouse embryo
Data demonstrated that CYP26B1 is essential during palatogenesis. The regulation of endogenous retinoic acid level through CYP26B1 is required for elevation of palatal shelves.
Absence of Cyp26b1, a retinoic-acid-degrading enzyme, results in aberrant epidermal differentiation and filaggrin (show FLG ELISA Kits) expression, defective cornified envelopes and skin barrier formation, in conjunction with peridermal retention.
Cyp26b1 regulates retinoic acid signaling in spinal cord progenitor cell populations.
The data demonstrate that RA-induced osteoblast-preosteocyte transitioning has multiple effects on developing bone in Cyp26b1 mutants, ranging from gain to loss of bone, depending on the allelic strength, the developmental stage and the cellular context.
cyp26b1 is involved in limiting the activity of retinoic acid. Zygotic cyp26b1 was localized to presumptive rhombomere 3 and rhombomere 4 at early two-somite (2S) stage. Expression expands anteriorly to include rhombomere 2 at the 10S stage.
effects of the inhibitor rather than excess retinoic acid most closely phenocopied the jaw defects seen with the Cyp26B1 morpholino
Cyp26b1 is expressed within osteoblast cells, demonstrating that retinoic acid levels within these cells need to be tightly controlled
cyp26b1 mutants may serve as a model to study the etiology of human vertebral disorders such as Klippel-Feil anomaly
This gene encodes a member of the cytochrome P450 superfamily. The cytochrome P450 proteins are monooxygenases which catalyze many reactions involved in drug metabolism and synthesis of cholesterol, steroids and other lipids. The encoded protein is localized to the endoplasmic reticulum, and functions as a critical regulator of all-trans retinoic acid levels by the specific inactivation of all-trans retinoic acid to hydroxylated forms. Mutations in this gene are associated with radiohumeral fusions and other skeletal and craniofacial anomalies, and increased levels of the encoded protein are associated with atherosclerotic lesions. Alternative splicing results in multiple transcript variants.
cytochrome P450 26B1
, cytochrome P450, family 26, subfamily B, polypeptide 1
, cytochrome P450 retinoic acid-inactivating 2
, cytochrome P450 retinoid metabolizing protein
, cytochrome P450, subfamily XXVIB, polypeptide 1
, retinoic acid-metabolizing cytochrome
, cytochrome P450, 26, retinoic acid B1
, cytochrome P450RAI-2
, retinoic acid B1
, retinoic acid hydroxylase