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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 (132) and DNMT3B Kits (11) 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.
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.
DNMT 3B was upregulated in invasive subclones and exerted on influence of E-cad gene methylation.
Transduction of miR (show MLXIP Proteins)-339 and miR (show MLXIP Proteins)-766 expressing viruses into colon cancer cell lines (SW480 and HCT116) decreased DNMT3B expression (1.5, 3-fold) and (3, 4-fold), respectively. In addition, DNA methylation (show HELLS Proteins) of some tumor suppressor genes decreased.
Immunodeficiency, centromere instability and facial anomalies syndrome specific DNMT3B dysfunction interferes with intragenic regulation of mRNA transcription and alternative splicing.
nickel exposure results in DNMT3b induction and MEG3 (show FAM129B Proteins) promoter hypermethylation and expression inhibition, further reduces its binding to c-Jun (show JUN Proteins) and in turn increasing c-Jun (show JUN Proteins) inhibition of PHLPP1 transcription, leading to the Akt (show AKT1 Proteins)/p70S6K (show RPS6KB1 Proteins)/S6 axis activation, and HIF-1alpha (show HIF1A Proteins) protein translation, as well as malignant transformation of human bronchial epithelial cells.
Overexpression of MAEL (show MAEL Proteins) in UCB cells substantially enhanced the enrichment of DNA methyltrans-ferase (DNMT (show DNMT1 Proteins))3B and histone deacetylase (HDAC)1 (show HDAC1 Proteins)/2 on the promoter of the MTSS1 (show MTSS1 Proteins), and thereby epigenetically suppressing the MTSS1 (show MTSS1 Proteins) transcription.
Data suggest that the overexpression of DNMT3B4 may play an important role in human kidney tumorigenesis through chromosomal instability and methylation of RASSF1A (show RASSF1 Proteins).
MUC1 (show MUC1 Proteins)-C is of functional importance to induction of DNMT1 (show DNMT1 Proteins) and DNMT3b and, in turn, changes in DNA methylation (show HELLS Proteins) patterns in cancer cells.
Dnmt3b plays a tumor suppressive role in MLL (show MLL Proteins)-AF9 (show MLLT3 Proteins) AML (show RUNX1 Proteins) progression
Studies indicate that DNA methylation (show HELLS Proteins) is mediated by three DNA (Cytosine-5-)-Methyltransferase (DNMTs): DNMT1 (show DNMT1 Proteins) is responsible for the maintenance of methylation patterns after DNA replication whereas DNMT3A (show DNMT3A Proteins) and DNMT3B carry out de novo methylation, and DNMT (show DNMT1 Proteins) inhibitors have showed promising results in clinical trials of prostate cancer.
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