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Validated All-in-One™ qPCR Primer for DNMT3A(NM_175629.2) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
CpG methylation is an epigenetic modification that is important for embryonic development, imprinting, and X-chromosome inactivation. Studies in mice have demonstrated that DNA methylation is required for mammalian development. This gene encodes a DNA methyltransferase that is thought to function in de novo methylation, rather than maintenance methylation. The protein localizes to the cytoplasm and nucleus and its expression is developmentally regulated. Alternative splicing results in multiple transcript variants encoding different isoforms. [provided by RefSeq].
Gene References into function
- recruited to the RARbeta2 promoter by the PML-RAR fusion protein
- These findings suggest that Dnmt3a and Dnmt3a2 may have distinct DNA targets and different functions in development.
- the human de novo enzymes hDNMT3a and hDNMT3b form complexes with the major maintenance enzyme hDNMT1.
- cloned and characterized the 5'-end of the mRNA and promoter regions
- DNMT3L stimulates de novo methylation by Dnmt3a.
- Over-expressed in squamous cell carcinoma of the mouth.
- Findings are consistent with a model in which Dnmt3a initiates methylation on one of the DNA strands of duplex DNA, and these hemimethylated sites then stimulate Dnmt1 activity for further methylation.
- DNMT3A was shown to have a very pronounced flanking sequence preference for human DNA methylation.
- cDNA microarray analysis identified several genes involved in DNA methylation, such as DNMT2 and DNMT3a that were more highly expressed in LNCaP-r (an androgen sensitive prostate cancer cell line).
- histone methyltransferase SETDB1 and the DNA methyltransferase DNMT3A interact directly and localize to promoters silenced in cancer cells
- In human cells maintenance of XIST methylation is controlled differently than global genomic methylation and in the absence of both DNMT1 and DNMT3B.
- LANA associated with repressed cellular promoters, recruited Dnmt3a to DNA, and facilitated de novo promoter methylation of a down-regulated gene, cadherin 13 (H-cadherin).
- Sex-specific time windows for concomitant upregulation of DNMT3A are associated with prenatal remethylation of the human male and female germ line.
- The genes DNMT1, DNMT3A, and DNMT3B were over-expressed in the ectopic endometrium as compared with normal control subjects or the eutopic endometrium of women with endometriosis
- Progressive up-regulation of the gene encoding DNMT3A was found in the colorectal adenoma-carcinoma sequence.
- Up-regulation of DNMT3A expression is associated with hypomethylation of intron25 in testicular germ cell tumors.
- We found clinically relevant levels of Hcy (0-500 microM) induced elevation of SAH, declination of SAM and SAM/SAH ratio and reduced expression of SAHH and MBD2, but increased activity of DNMT3a and DNMT3b affecting DNA methylation
- Expression of microRNA is inversely correlated with DNMT3A in non-small cell lung cancer.
- the autocrine hGH-stimulated increases in DNMT3A and DNMT3B expression mediate repression of plakoglobin gene transcription by direct hypermethylation of its promoter and consequent phenotypic conversion of mammary carcinoma cells
- DNMT3a was over expressed in gastric neoplasms.
- a negative association of DNMT3a and 3b expression with MDS disease risk
- Epigenetic modification induced by hepatitis B virus X protein via interaction with de novo DNA methyltransferase DNMT3A.
- This functional characterization of SALL3 sheds light on regulatory mechanisms for DNMT3A and provides new strategies to inhibit aberrant methylation in cancer.
- Loss of the H4 arginine 3 methylation mark through short hairpin RNA-mediated knockdown of PRMT5 leads to reduced DNMT3A binding, loss of DNA methylation and gene activation.
