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CpG methylation is an epigenetic modification that is important for embryonic development, imprinting, and X-chromosome inactivation. Additionally we are shipping DNMT3A Antibodies (282) and DNMT3A Proteins (6) and many more products for this protein.
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Data show that the expression levels of the 5 epigenetic modifying genes Dnmt1, Dnmt3a, Hdac1, Kdm3a and Uhrf1 were higher in group pig in highland (TH) than in group Yorkshire in highland (YH).
we found that DNMT3A was responsible for the down-regulation of miR (show MLXIP ELISA Kits)-105 in gastric cancer cells
Taken together, these data demonstrate that adipose Dnmt3a is a novel epigenetic mediator of insulin (show INS ELISA Kits) resistance in vitro and in vivo.
Low frequency of DNMT3A mutations in pediatric T-ALL is in striking contrast to adult T-ALL and renders the necessity for the search of other candidate prognostic markers. Combined Sanger sequencing-HRM approach offers a cost-effective option for genotyping DNMT3A coding sequence, with potential clinical application in other hematological malignancies.
2.65-angstrom crystal structure of the DNMT3A-DNMT3L-DNA complex in which two DNMT3A monomers simultaneously attack two cytosine-phosphate-guanine (CpG) dinucleotides, with the target sites separated by 14 base pairs within the same DNA duplex; mechanistic basis for DNMT3A-mediated DNA methylation and establishment of its aetiological link to human disease
based on the investigation of previously reported variants in patients with Tatton-Brown-Rahman syndrome , we found overlap in the spectrum of DNMT3A variants observed in this disorder and somatic variants in hematological malignancies
The emodininduced downregulation of UHRF1 led to an increase in the level of DNA methyltransferase 3A.
Data suggest that miR (show MLXIP ELISA Kits)-200b-3p may exhibit targeting and suppressive effects on DNA methyltransferase 3A (DNMT3A).
Prostaglandin E2 promotes the acquisition of DNMT3A-dependent tolerogenic functions in human myeloid-derived suppressor cells.
human mammary epithelial cells reprogramming is dependent on gene silencing by the DNA methyltransferase (show DNMT1 ELISA Kits) DNMT3A and loss of histone transcriptional marks following downregulation of the methyltransferase DOT1L (show DOT1L ELISA Kits).
the immunohistochemical expressions of Klotho (show KL ELISA Kits) and DNMT3a in tissues obtained from oral dysplasia and oral squamous cell carcinoma, is reported.
Among 18 genotypes analyzed, we were unable to record any significant differences in 5-methyl-2'-deoxycytidine levels, which suggested that age-related changes in global DNA methylation content are rather a function of time, and not a genetic component.
The effect of p53 (show TP53 ELISA Kits) expression on the development of cloned embryos, and its interaction with HDAC1 (show HDAC1 ELISA Kits) and DNMT3A are reported.
The expression levels of DNMT3a and DNMT3b (show DNMT3B ELISA Kits) were associated with several beef quality traits.
individual pain vulnerability may be inherent mostly in the emotional/affective component of chronic pain and remain consistent in different aspects of negative emotion, in which adaptive changes in the function of DNA methyltransferase 3a for DNA methylation in central amygdala may play an important role.
The aim of the present study is to investigate spatial and temporal expression levels and subcellular localizations of the DNMT1 (show DNMT1 ELISA Kits), DNMT3A, and DNMT3B (show DNMT3B ELISA Kits) proteins in the mouse germinal vesicle (GV) and metaphase II (MII) oocytes, and early embryos from 1-cell to blastocyst stages.
our Dnmt3a R878H mice have shown that leukemic cells have altered gene expression and epigenetic regulatory patterns contributing to the growth/survival advantage over WT mice.The present study found that the DNMT3A mutation contributed to hypomethylation in the gene body region of mTOR (show FRAP1 ELISA Kits) in Dnmt3aR878H/WT mice.
Knockdown of DNMT3A or DNMT1 protected neurons against mutant Htt-induced toxicity, together demonstrating a requirement for DNMTs in mutant Htt-triggered neuronal death and suggesting a neurodegenerative mechanism based on DNA methylation-mediated transcriptional repression.
Data demonstrate that DNMT3A and DNA methylation are key modulators of mast cell responsiveness to acute and chronic stimulation.
These data suggest that DNMT3a is required for nerve injury-induced and MBD1 (show DPEP1 ELISA Kits)-mediated epigenetic silencing of the MOR (show OPRM1 ELISA Kits) and KOR (show OPRK1 ELISA Kits) in the injured DRG. DNMT3a inhibition may serve as a promising adjuvant therapy for opioid use in neuropathic pain management.
Data show that conditional deletion of Dnmt3a and simultaneous "knock in" of Flt3ITD/+, cooperate to drive leukemia development at a faster rate than Dnmt3a loss alone.
Deletion of DNMT3a in postnatal forebrain neurons does no alter affective behavior.
Altogether, the authors demonstrate that Dnmt3a and Dnmt3b (show DNMT3B ELISA Kits) protect the epidermis from tumorigenesis and that squamous carcinomas are sensitive to inhibition of PPAR-gamma (show PPARG ELISA Kits).
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.
DNA (cytosine-5-)-methyltransferase 3 alpha
, DNA cytosine methyltransferase 3 alpha
, DNA (cytosine-5)-methyltransferase 3A
, DNA methyl transferase alpha
, DNA methyltransferase 3A
, DNA MTase HsaIIIA
, DNA cytosine methyltransferase 3A2
, DNA-methyltransferase 3a
, DNA MTase MmuIIIA
, DNA methyltransferase MmuIIIA