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anti-Human CYP26A1 Anticorps:
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Human Polyclonal CYP26A1 Primary Antibody pour ELISA, WB - ABIN543563
Heise, Mey, Neis, Marquardt, Joussen, Ott, Wiederholt, Kurschat, Megahed, Bickers, Merk, Baron: Skin retinoid concentrations are modulated by CYP26AI expression restricted to basal keratinocytes in normal human skin and differentiated 3D skin models. dans The Journal of investigative dermatology 2006
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Human Monoclonal CYP26A1 Primary Antibody pour IHC (p), ELISA - ABIN533614
Sakai, Luo, McCaffery, Hamada, Dräger: CYP26A1 and CYP26C1 cooperate in degrading retinoic acid within the equatorial retina during later eye development. dans Developmental biology 2004
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We applied whole-genome sequencing (WGS) on 9 trios where the probands are sporadically affected with the most severe form of the disorder and harbor no coding sequence variants affecting the function of known Hirschsprung disease (HSCR) genes. We found de novo protein-altering variants in three intolerant to change genes-CCT2, VASH1, and CYP26A1-for which a plausible link with the enteric nervous system (ENS) exists
Accumulating evidence suggest that cytochrome P450 (CYP26), the primary retinoid-inactivating enzyme, plays a critical role in the integration of two neoplastic molecular programs: the retinoid metabolism and Hedgehog pathways. (Review)
CYP26A1 polymorphisms were associated with increased risk of malignant oral disorders in betel quid chewers.
CYP26A1-mediated oncogenic characteristics may be partially responsible for the elevated expression of fascin.
Molecular recognition of CYP26A1 binding pockets and structure-activity relationship studies for design of potent and selective retinoic acid metabolism blocking agents has been described.
data suggested that CYP26A1 overexpression might contribute to the development and progression of cervical malignancies and squamous neoplasia of the head and neck
HNF4alpha coordinates with retinoic acid receptors in a retinoic acid-dependent manner to strongly induce CYP26A1 gene expression in the liver, which may explain the high level of response to retinoic acid observed in vivo.
In liver microsomes, CYP26A1 plays a role in clearing bioactive retinoids.
CYP26 is able to inactivate retinoids in serum, preventing retinoic acid signaling and thus bone-marrow hematopoietic stem cell differentiation.
The promoter region of CYP26A1 is significantly hypermethylated in allergic asthmatic subjects.
Our observation suggests an involvement of enhanced CYP26A1 expression causing a functional vitamin A deficieny state in skin that can potentially lead to neoplastic transformation of keratinocytes in an early phase during skin carcinogenesis
CYP26A1 and CYP26B1 are qualitatively similar retinoic acid hydroxylases with overlapping expression profiles; CYP26A1 has higher catalytic activity than CYP26B1.
CYP26A1 and CYP26C1 play a pivotal role in the pathogenesis of nonsyndromic bilateral and unilateral optic nerve aplasia.
Primary metabolites of all-trans-retinoic acid formed by CYP26A1 are identified and the ligand selectivity and ligand interactions of CYP26A1 are characterized.
the functioning of multiple RAREs may account for the strong inducibility of CYP26A1 in liver, which, in turn, may be important physiologically for restoring retinoid homeostasis when the concentration of RA rises.
CYP26A1 is expressed in human liver microsomes; its expression correlates with retinoic acid hydroxylation.
increased CYP26-mediated catabolism of retinoic by CRABP-I transfection might decrease the amount of retinoic acid that is accessible to the nuclear receptors
The identification of a functional retinoic acid response element located 2.0 kb upstream of the Cyp26A1 transcriptional start site is reported.
induction and regulation of CYP26A1 expression in human intestinal (Caco-2), liver (HepG2), endothelial (HUVEC), and APL (NB4) cell lines
Variants in CYP26A1 are unlikely to be a major risk factor for caudal regression syndrome; further study with a larger number of genotyped subjects is required.
These findings provide a new line of evidence correlating the deleterious effects of blocking CYP26A1 in pregnancy with the aberrant regulation of NK cells in the uterus.
Cyp26a1, which encodes a key enzyme for catabolic inactivation of retinoic acid (RA) required for tight control of local RA concentrations, is significantly downregulated in embryos of diabetic mice. Embryonic tissues expressing Cyp26a1 show reduced efficiency of RA clearance.
The results of this study suggest that CYP2R1 and CYP26A1 are important in the differentiation of oval cells into hepatoblast-like cells in the injured liver
These results suggest that CYP2R1 and CYP26A1 may play a major role in hepatoblast cell differentiation during the development of the liver.
deletion of both Cyp26a1 and Cyp26b1 in either sertoli or germ cells resulted in increased vacuolization within the seminiferous tubules, delayed spermatid release, and an increase in the number of STRA8-positive spermatogonia
Analysis of retinoic-responsive genes, such as Cyp26a1 in embryos suggests that beta-carotene cleavage results in the production of retinoic acid which then can be used by the embryo during severe vitamin A deficiency.
The cytochrome P450 enzyme Cyp26a1, which metabolizes all-trans-retinoic acid (RA) and thereby reduces RA levels, plays a crucial role in specifying motor neuron columnar subtypes.
Liver Cyp26a1 activity is increased during pregnancy.
These data demonstrate that uterine cyp26a1 activity is important for the maintenance of pregnancy, especially during the process of blastocyst implantation.
Differential expression of the retinoic acid-metabolizing enzymes CYP26A1 and CYP26B1 during murine organogenesis.
Cyp26a1(-/-) mouse fetuses have lethal morphogenetic phenotypes mimicking those generated by excess retinoic acid administration.
Ablation of the gene for RARgamma (Rarg) rescues Cyp26a1-null mutant animals from caudal regression and embryonic lethality.
Cyp26a1 degrades retinoic acid within the equatorial retina during later eye development.
in RAC65 cells, RARbeta 2 is transcriptionally repressed as well as Cyp26a1; Cyp26a1-regulated retinoic acid metabolism likely represents critical differentiation swtich in embryocarcinoma cells
Expression of CYP26A1 in endometrial epithelial cells is regulated by progesterone and not significantly influenced by co-administration of estrogen.
Activity of CYP26A1 and CYP26C1 is required for correct A-P patterning and production of migratory cranial neural crest cells in the developing mammalian brain.
LRAT acts together with Cyp26A1, one of the enzymes that catalyze the degradation of retinoic acid, and possibly with STRA6, the recently identified cell surface receptor for retinol-RBP
Fluconazole exposure was associated with an up-regulation of CYP26a1 in mouse embryos.
Retinoic acid is regulated by CYP26 in vertebrate lens regeneration.
Results suggest that xCOUP-TF and xCyp26 are both regulated by Wnt signaling, and cooperatively function in retinoic acid (RA) signaling to affect anterior-posterior (A-P) neural patterning.
Data support a model in which retinoic acid (RA) on the dorsal side of the embryo induces anterior kidney fates while posterior kidney progenitors are protected ventrally by the RA-catabolizing enzyme Cyp26a1.
Cyp26a1 expression can shape a retinoic acid gradient.
Retinoic acid (RA)-responsive genes are differentially sensitive to alterations in the RA pathway and, in particular, cyp26a1 and raraa are under a high pressure to maintain signaling integrity.
In zebrafish, two Cyp26 enzymes, Cyp26a1 and Cyp26c1, are expressed in the anterior lateral plate mesoderm (ALPM) and predominantly overlap with vascular progenitors (VPs).
Zebrafish cyp26a1 promoter contains a novel retinoic acid response element that plays crucial roles in regulating its expression during early development.
cyp26 has an important role in linking the Fgf, Wnt and RA signals to regulate AP patterning of the neural ectoderm in the late blastula to gastrula embryo in zebrafish
The metabolites of all-trans RA produced by Cyp26D1 were the same as that produced by Cyp26A1, which are mainly 4-hydroxy-all-trans-RA and 4-oxo-all-trans-RA.
Expression of Cyp26a1 is under complex feedback and feedforward control by retinoic acid and fibroblast growth factor signaling.
2.5 k fragment underlies the regulation of the zebrafish cyp26a1 gene by retinoic acid
Cyp26 enzymes function in endoderm to regulate pancreatic field size
This gene encodes a member of the cytochrome P450 superfamily of enzymes. The cytochrome P450 proteins are monooxygenases which catalyze many reactions involved in drug metabolism and synthesis of cholesterol, steroids and other lipids. This endoplasmic reticulum protein acts on retinoids, including all-trans-retinoic acid (RA), with both 4-hydroxylation and 18-hydroxylation activities. This enzyme regulates the cellular level of retinoic acid which is involved in regulation of gene expression in both embryonic and adult tissues. Two alternatively spliced transcript variants of this gene, which encode the distinct isoforms, have been reported.
P450, retinoic acid-inactivating, 1
, cytochrome P450 26A1
, cytochrome P450 retinoic acid-inactivating 1
, cytochrome P450, subfamily XXVIA, polypeptide 1
, cytochrome P450RAI
, retinoic acid 4-hydroxylase
, retinoic acid-metabolizing cytochrome
, cytochrome P450, 26, retinoic acid A1
, retinoic acid hydrolase
, retinoic acid-converting enzyme
, retinoic acid-degrading enzyme CYP26
, cytochrome P450, 26, retinoic acid
, retinoic acid hydroxylase
, retinoic acid converting enzyme
, cytochrome P450 retinoic acid hydroxylase
, cytochrome P450 26