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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 DNMT3B Antibodies (135) and DNMT3B Kits (13) and many more products for this protein.
Showing 6 out of 6 products:
Human DNMT3B Protein expressed in HEK-293 Cells - ABIN2719618
Cree, Fredericks, Miller, Pearce, Filichev, Fee, Kennedy: DNA G-quadruplexes show strong interaction with DNA methyltransferases in vitro. in FEBS letters 2016
dnmt7 specifically methylates no tail gene in the genome
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 (show HELLS Proteins) content are rather a function of time, and not a genetic component.
LMP1-mediated NF-kappaB can up-regulate DNMT3b transcription, thereby leading to relatively higher methylation intensity at PTEN CpG islands, and ultimately silencing major tumor suppressor PTEN
DNMT1 (show DNMT1 Proteins), DNMT3A (show DNMT3A Proteins), and DNMT3B were overexpressed in 36.9, 26, and 23 % of the OSCC patients, respectively. DNMT1 (show DNMT1 Proteins) overexpression was significantly associated with the overall survival, p = 0.029, and relapse-free survival of OSCC patients, p = 0.003. Patients with DNMT1 (show DNMT1 Proteins) overexpression, as an independent prognostic factor, had a 2.385 times higher risk to relapse than those with lower expression. The DNMT1 (show DNMT1 Proteins) A201G gene polymorphi
report the first crystal structure of the DNMT3B PWWP domain-H3K36me3 complex.
Results continue to establish ANG (show ANG Proteins) as an oncoprotein and further reveal that ANG (show ANG Proteins) contributes to oncogenesis by the activation of MMP2 (show MMP2 Proteins) through modulation of DNMT3b functions.
found association between DNMT3B rs2424913 in T allele carriers with Parkinson's disease
H19 (show NCKAP1 Proteins) might function as ceRNA (competing endogenous RNA) for miR (show MLXIP Proteins)-29b-3p and relieve the suppression for DNMT3B, which led to EMT (show ITK Proteins) and metastasis of bladder cancer (BC). Our findings highlight a novel mechanism of H19 (show NCKAP1 Proteins) in progression of BC and provide H19 (show NCKAP1 Proteins)/miR (show MLXIP Proteins)-29b-3p/DNMT3B axis as a promising therapeutic target for BC.
DNMT1 (show DNMT1 Proteins) up-regulation induced by IL-6 (show IL6 Proteins)/STAT3 (show STAT3 Proteins) signaling was indispensable for IL-6 (show IL6 Proteins)-mediated hepaCAM (show HEPACAM Proteins) loss in renal cell carcinoma (show MOK Proteins) (RCC (show XRCC1 Proteins)) cell lines ACHN (show LARP6 Proteins) and 769-P, while DNMT3b up-regulation was crucial for hepaCAM (show HEPACAM Proteins) loss in A498.
A Methylated DNA Quantification Kit was used to quantify global DNA methylation (show HELLS Proteins), and single nucleotide polymorphisms (SNPs) in DNMT3A (show DNMT3A Proteins) (rs36012910, rs1550117, and R882) and DNMT3B (rs1569686, rs2424909, and rs2424913) were identified using the restriction fragment length polymorphism method
A novel homozygous missense mutation, Ala585Thr, was found in DNMT3B.
Definitive diagnosis should be done using metaphase analysis to identify centromeric instability and/or ICF disease gene mutations analysis. Bilateral VUR may occur in ICF patients with homozygous DNMT3B mutations in early childhood. Renal ultrasonography should be included in ICF1 patients for the screening of congenital anomalies.
The epiblast expressed epithelial markers, MUC1 (show MUC1 Proteins) and E-CADHERIN (show CDH1 Proteins), and the pluripotency markers, DNMT3B and CRIPTO (show TDGF1 Proteins).
Developmental changes in expression of DNMT3B are indicative of a possible role in changes in methylation in cattle.
The expression levels of DNMT3a (show DNMT3A Proteins) and DNMT3b were associated with several beef quality traits.
a new paradigm of transcriptional regulation critical for cardiac development and maturation that is controlled by the interaction of REST, DNMT3B and non-CpG methylation.
Together, this study described the regulation of Chk2 (show CHEK2 Proteins) expression through promoter methylation by Dnmt3b and also presented a novel role of Chk2 (show CHEK2 Proteins) during neuronal differentiation, which is independent of its previously known function in DNA damage response.
in mouse embryonic stem cells, Dnmt3b-dependent intragenic DNA methylation protects the gene body from spurious RNA polymerase II entry and cryptic transcription initiation
three DNA methyltransferases, Dnmt1 (show DNMT1 Proteins), Dnmt3a (show DNMT3A Proteins), and Dnmt3b, have been identified. Dnmt3a (show DNMT3A Proteins) and Dnmt3b are responsible for establishing DNA methylation (show HELLS Proteins) patterns produced through their de novo-type DNA methylation (show HELLS Proteins) activity in implantation stage embryos and during germ cell differentiation. Dnmt3-like (Dnmt3l (show TRDMT1 Proteins)), which is a member of the Dnmt3 family but does not possess DNA methylation (show HELLS Proteins)
While lens epithelial cell survival requires DNMT1 (show DNMT1 Proteins), morphologically normal lenses develop in the absence of both DNMT3A (show DNMT3A Proteins) and DNMT3B.
Mechanical stimulation regulates osteoblastic genes expression via direct regulation of Dnmt3b.
a miR (show MLXIP Proteins)-125b-DNMT3b-p53 (show TP53 Proteins) signal pathway may exist in the vascular smooth muscle cells proliferation induced by homocysteine.
miR-29a mimic transfection lowered collagen 1alpha1, DNMT1, DNMT3b and SET1A expression in hepatic stellate cells.
Loss of DNMT3B results in hypomethylation of the miR-196b promoter and increased miR-196b expression, which directly targets the mTORC2 component Rictor.
The findings define PRMT7 (show PRMT7 Proteins) as a regulator of the DNMT3b/p21 axis required to maintain muscle stem cell regenerative capacity.
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 which is thought to function in de novo methylation, rather than maintenance methylation. The protein localizes primarily to the nucleus and its expression is developmentally regulated. Mutations in this gene cause the immunodeficiency-centromeric instability-facial anomalies (ICF) syndrome. Eight alternatively spliced transcript variants have been described. The full length sequences of variants 4 and 5 have not been determined.
DNA (cytosine-5)-methyltransferase 3B
, DNA (cytosine-5-)-methyltransferase 3 beta
, DNA cytosine-5 methyltransferase 3 beta
, DNA (cytosine-5)-methyltransferase 3B-like
, DNA methyl transferase beta
, DNA methyltransferase 3B
, DNA MTase HsaIIIB
, DNA methyltransferase HsaIIIB
, DNA (cytosine-5-)-methyltransferase 3 beta, like
, DNA (cytosine-5-)-methyltransferase 7
, DNA MTase MmuIIIB
, DNA methyltransferase MmuIIIB