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CpG methylation is an epigenetic modification that is important for embryonic development, imprinting, and X-chromosome inactivation. De plus, nous expédions DNMT3A Anticorps (262) et DNMT3A Protéines (6) et beaucoup plus de produits pour cette protéine.
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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).
the immunohistochemical expressions of Klotho (Montrer KL Kits ELISA) and DNMT3a in tissues obtained from oral dysplasia and oral squamous cell carcinoma, is reported.
this epigenetic antagonism precedes malignant transformation and can be observed in preleukemic LSK (Montrer LCK Kits ELISA) cells from Idh2 (Montrer IDH2 Kits ELISA)(R140Q) or Dnmt3a(R882H) single-mutant and Idh2 (Montrer IDH2 Kits ELISA)(R140Q)/Dnmt3a(R882H) double-mutant mice. IDH (Montrer IDH1 Kits ELISA)/DNMT3A double-mutant acute myeloid leukemia (Montrer BCL11A Kits ELISA) (AML (Montrer RUNX1 Kits ELISA))manifested upregulation of a RAS signaling signature and displayed unique sensitivity to MEK (Montrer MAP2K1 Kits ELISA) inhibition ex vivo as compared with AMLs with either single mutation.
The current findings confirmed that downregulation of DNMT3A protein expression and the ensuing disturbance of the maintenance DNA methylation may serve an important role in the pathogenesis of early embryo growth arrest.
Our results provided novel insight into the role of the DNMT3A R882H mutation in AML (Montrer RUNX1 Kits ELISA) pathogenesis and suggested that targeting the cellular GSH synthetic pathway could enhance the current therapy for AML (Montrer RUNX1 Kits ELISA) patients with the DNMT3A R882H mutation.
data confirm MLL-PTD (Montrer BCS1L Kits ELISA) and, to a lesser extent, FLT3 (Montrer FLT3 Kits ELISA)-ITD as common events in +11 AML (Montrer RUNX1 Kits ELISA).6, 7, 8 However, the high mutation frequencies of U2AF1 and genes involved in methylation (DNMT3A, IDH2 (Montrer IDH2 Kits ELISA)) have hitherto not been reported in +11 AML (Montrer RUNX1 Kits ELISA)
Silencing DNMT3A inhibits proliferation and invasion in ESCC cells by inducing demethylation of DOK7 (Montrer DOK7 Kits ELISA).
Data show that DNA methyltransferase 3A (DNMT3A) mutation was significantly associated with adverse outcome in addition to conventional risk stratification.
DNMT3A polymorphisms may be potential predictive markers for acute myelogenous leukemia patients' outcomes in China
this study shows that DNMT3A mutations are present in a significant proportion of SF3B1mut patients with RARS (Montrer RARS Kits ELISA) and its presence has a clearly negative impact on outcomes, determining a higher RBC (Montrer CACNA1C Kits ELISA) transfusion dependency, higher risk of progression to AML (Montrer RUNX1 Kits ELISA), and lower OS.
DNMT1 (Montrer DNMT1 Kits ELISA), DNMT3A, and DNMT3B (Montrer DNMT3B Kits ELISA) were overexpressed in 36.9, 26, and 23 % of the OSCC patients, respectively. DNMT1 (Montrer DNMT1 Kits ELISA) overexpression was significantly associated with the overall survival, p = 0.029, and relapse-free survival of OSCC patients, p = 0.003. Patients with DNMT1 (Montrer DNMT1 Kits ELISA) overexpression, as an independent prognostic factor, had a 2.385 times higher risk to relapse than those with lower expression. The DNMT1 (Montrer DNMT1 Kits ELISA) A201G gene polymorphi
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 (Montrer TP53 Kits ELISA) expression on the development of cloned embryos, and its interaction with HDAC1 (Montrer HDAC1 Kits ELISA) and DNMT3A are reported.
The expression levels of DNMT3a and DNMT3b (Montrer DNMT3B Kits ELISA) were associated with several beef quality traits.
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 (Montrer FRAP1 Kits ELISA) 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 (Montrer DPEP1 Kits ELISA)-mediated epigenetic silencing of the MOR (Montrer OPRM1 Kits ELISA) and KOR (Montrer OPRK1 Kits ELISA) 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 (Montrer DNMT3B Kits ELISA) protect the epidermis from tumorigenesis and that squamous carcinomas are sensitive to inhibition of PPAR-gamma (Montrer PPARG Kits ELISA).
Upon lysolecithin injection in the spinal cord of transgenic mice, study detected defective oligodendrocyte progenitor cells differentiation and inefficient remyelination in the DNA methyltransferase 3a null and DNA methyltransferase 1/DNA methyltransferase (Montrer DNMT1 Kits ELISA) 3a null mice.
This is attributed in part to ineffective repression of Tcf1 (Montrer HNF1A Kits ELISA) expression in knockout T cells, as DNMT3a localizes to the Tcf7 (Montrer TCF7 Kits ELISA) promoter and catalyzes its de novo methylation in early effector WT CD8 (Montrer CD8A Kits ELISA)(+) T cells. These data identify DNMT3a as a crucial regulator of CD8 (Montrer CD8A Kits ELISA)(+) early effector cell differentiation and effector versus memory fate decisions.
Compared the activity of individual DNMT3A isoforms in embryonic stem and neuronal progenitor cells and report that these isoforms differ in their genomic binding and DNA methylation activity at regulatory sites. We identify that the longer isoform DNMT3A1 preferentially localizes to the methylated shores of bivalent CpG island promoters in a tissue-specific manner.
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