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Human Polyclonal ALDH1A2 Primary Antibody for IHC, IHC (p) - ABIN4279209
Kostareli, Holzinger, Bogatyrova, Hielscher, Wichmann, Keck, Lahrmann, Grabe, Flechtenmacher, Schmidt, Seiwert, Dyckhoff, Dietz, Höfler, Pawlita, Benner, Bosch, Plinkert, Plass, Weichenhan, Hess: HPV-related methylation signature predicts survival in oropharyngeal squamous cell carcinomas. in The Journal of clinical investigation 2013
Show all 4 Pubmed References
The ALDH1A2 locus seems to increase the risk of hand osteoarthritis through decreased expression of ALDH1A2 in joint tissues, with the effect dependent on single-nucleotide polymorphism rs12915901.
The authors findings indicate that the SNP rs4238326 in ALDH1A2 gene may potentially modify individual susceptibility to knee OA in the Chinese population.
high transcription activities of ALDH1A2, ALDH1A3 and ALDH1L1 predicted worsen overall survival in gastric cancer patients
Data show that hRALDH2 is not inhibited by its oxidation product, all-trans-RA, suggesting the absence of a negative feedback regulatory loop. Expression of the Raldh2 gene is known to be regulated by RA itself, suggesting that the main regulation of the hRALDH2 activity level is transcriptional.
Study shows no evidence that genetic variants alter prostate cancer incidence, but show that SNPs in the ALDH1A2 gene affect prostate cancer mortality.
a critical role of ALDH1A2-RAR signaling in the pathogenesis of head and neck cancer.
High expression of ALDH1A2 and ALDH1B1 mRNA was found to be significantly correlated to worser survival in all NSCLC patients.
the distribution of RALDH1, RALDH2, and RALDH3 in the postnatal eye was determined.
ALDH1A2 is involved in the regulation of cancer stem cell properties in neuroblastoma.
Genetic association replicative and exploratory studies identify SNPs in ADA and MTR highly associated with isolated Neural tube defects (NTD)and SNP in ARID1A and ALDH1A2 associated with NTDs in whites and African Americans respectively.
At the transcript level, the cisplatin + DEAB-resistant cells showed upregulated mRNA expression levels for ALDH1A2, ALDH1A3 isozymes and CD44 indicating the involvement of these markers in conferring chemoresistance
DNA methylation at multiple CpG sites is associated with loss of control over alcohol drinking.
Severe osteoarthritis of the hand associates with common variants within the ALDH1A2 gene and with rare variants at 1p31.
These findings suggest that ALDH1A2 is the enzyme involved in retinoic acid biosynthesis in human germ cells.
all three proteins (RDH10, RALDH2, and CRABP2) appeared to be required for ATRA production induced by activation of PPARgamma
ALDH1A2 protein was effective in AraC resistance. ALDH1A2 knock-down induced sensitivity to AraC treatment in K562AC cells. ALDH1A2 overexpressed K562S cells acquired the AraC resistance. Ara-C-resistant patients had increased ALDH1A2.
In vivo reduction of vitamin A levels results in an increase in astrocyte RALDH2 expression in the hippocampus.
Aberrant methylation of ALDH1a2 gene is the main cause for gene transcriptional inactivation in human bladder cancer cell lines. 5-Aza-2'-deoxycitydine or trichostatin A treatment induces ALDH1a2 expression.
A human ALDH1A2 gene variant is associated with increased newborn kidney size and serum retinoic acid.
Individual variation in ALDH1A2/CRABP2 genes may account for subtle variations in retinoic acid-dependent human embryogenesis.
Zebrafish foxc1a plays a crucial role in early somitogenesis by restricting the expression of Raldh2 directly.
The novel aldh1a2 reporter line is driven by the complete set of regulatory sequences required for zebrafish development, reports novel sources of RA synthesis, and identifies the source of RA that promotes vertebral ossification.
aldh1a2 participate to a positive loop required for branchial arches development in zebrafish
Aldh1a2 is the primary aldehyde dehydrogenase acting during pancreas development and maternal Aldh1a2 activity persists in aldh1a2(um22) and aldh1a2(i26) mutant embryos.
Studies indicate that raldh2 expression is critical for the formation of wound epithelium and blastema.
Present in the mesoderm around the developing inner ear.
this study shows that PU.1 and IRF4 are transactivators of the Aldh1a2 gene in vitro and ex vivo
data do not support the hypothesis that retinal itself represses weight gain and adipogenesis independently of RA. Instead, the data indicate that Raldh1 functions as a retinal and atRA-independent promoter of adiposity during adolescence, and enhances adiposity through pre-adipocyte cell autonomous actions
these studies identify Notch signaling in dendritic cells as a crucial balancer of Th17/iTreg, which depends on the direct regulation of Aldh1a2 transcription in dendritic cells
ALDH2 mutation displays an inverse correlation of coronary collateral vessel formation in patients.
Data suggest that retinoic acid and GM-CSF-induced retinal dehydrogenase 2 (RALDH2) expression in dendritic cells requires cooperative binding of transcription factor Sp1 via the RA receptor/retinoid X receptor complex to the Aldh1a2 promoter.
Defects in interdigital programmed cell death and digit separation in Hoxa13 mutant mice may be caused in part by reduced levels of RA signaling stemming from a loss in the direct regulation of Aldh1a2
Raldh1 and Raldh3 influence enteric nervous system structure and function and heterozygosity for Raldh2 causes ENS defects
ALDH1A2 expression was highest in ALDH(very-br) cells, intermediate in ALDH(dim) cells, and lowest in ALDH(br) cells.
Upregulation of retinal dehydrogenase 2 in alternatively activated macrophages during retinoid-dependent type-2 immunity to helminth infection in mice.
rendered Fgfr2IIIb(-/-) embryos haploinsufficient for the Raldh2 and examined these embryos for the incidence and severity of duodenal atresia
Expression of ALDH1A2, BEX2, EGR2, CCL3 and PLAU are upregulated in Toxoplasma gondiisusceptible C57BL/6 mice.
RA via RALDH2 has separable functions in the developing spinal cord to (i) maintain high levels of FGF and Notch signaling and (ii) drive stem cell differentiation, thus restricting both the numbers and the pluripotent character of neural stem cells
In Fgfr2IIIb-/- mouse embryos, a reduction of Raldh2 expression is observed within the duodenal region that is forming the atresia.
regulation of fat depots through the concerted action of Aldh1 enzymes establishes retinoic acid-dependent tandem regulation of transcription factors ZFP423 and PPARgamma in a depot-specific manner
Analysis of Ret, Gata3 or Raldh2 mutant mice at birth reveals hydronephrosis and defective ureter maturation, abnormalities that our results suggest are caused, at least in part, by delayed insertion of the nephric duct.
Wt1 controls retinoic acid signalling in embryonic epicardium through transcriptional activation of Raldh2.
The heart phenotypes of Raldh2 mutants are very similar and are characterized by a prominent defect in ventricular compact zone growth.
These findings suggest that an increasing expression of Raldh3 deregulates the balanced mechanisms of insulin and glucagon secretion in the pancreatic islets and may induce beta-cell dysfunction leading to the development of type 2 diabetes.
Drastic down-regulation of Aldh1a2 observed at both E16 and E18; RT-PCR revealed post-natal reduction in expression (Aldh1a2, 1/13). Results suggest down-regulation of gene is important factor in normal odontogenesis in dental papillae.
This protein belongs to the aldehyde dehydrogenase family of proteins. The product of this gene is an enzyme that catalyzes the synthesis of retinoic acid (RA) from retinaldehyde. Retinoic acid, the active derivative of vitamin A (retinol), is a hormonal signaling molecule that functions in developing and adult tissues. The studies of a similar mouse gene suggest that this enzyme and the cytochrome CYP26A1, concurrently establish local embryonic retinoic acid levels which facilitate posterior organ development and prevent spina bifida. Four transcript variants encoding distinct isoforms have been identified for this gene.
, aldehyde dehydrogenase 1A2
, aldehyde dehydrogenase family 1 member A2
, aldehyde dehydrogenase family 1, subfamily A2
, retinal dehydrogenase 2
, retinal dehydrogenase, type II
, retinaldehyde-specific dehydrogenase type 2
, retinaldehyde dehydrogenase 2
, alcohol dehydrogenase family 1, subfamily A2
, alcohol dehydrogenase family 1, subfamily A7