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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 DNMT3B Anticorps (134) et DNMT3B Protéines (6) et beaucoup plus de produits pour cette protéine.
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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.
Developmental changes in expression of DNMT3B are indicative of a possible role in changes in methylation in cattle.
The expression levels of DNMT3a (Montrer DNMT3A Kits ELISA) and DNMT3b were associated with several beef quality traits.
Alternative splice variant of DNMT3B is associated with leukemia.
these results provided a plausible link between the observed reduction of miR-26a and MEG3 in HCCs. Together, the present study added miR-26a/DNMT3B/MEG3 axis to the complex mechanisms of HCC development.
Results show that DNMT1 (Montrer DNMT1 Kits ELISA) mRNA levels were significantly higher in alveolar rhabdomyosarcoma and embryonal rhabdomyosarcoma tumors compared to normal skeletal muscle. Thse data indicate that altered expression of DNMT3B plays a key role in embryonal rhabdomyosarcoma development since its silencing is able to reverse cell cancer phenotype by rescuing myogenic program.
The present study shows that DNMT3B rs2424913 promotor polymorphism represents a genetic risk factor that may play an important role in understanding the pathogenesis of chronic immune thrombocytopenia.
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 (Montrer DNMT1 Kits ELISA), DNMT3A (Montrer DNMT3A Kits ELISA), and DNMT3B 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
report the first crystal structure of the DNMT3B PWWP domain-H3K36me3 complex.
Results continue to establish ANG (Montrer ANG Kits ELISA) as an oncoprotein and further reveal that ANG (Montrer ANG Kits ELISA) contributes to oncogenesis by the activation of MMP2 (Montrer MMP2 Kits ELISA) through modulation of DNMT3b functions.
found association between DNMT3B rs2424913 in T allele carriers with Parkinson's disease
H19 (Montrer NCKAP1 Kits ELISA) might function as ceRNA (competing endogenous RNA) for miR (Montrer MLXIP Kits ELISA)-29b-3p and relieve the suppression for DNMT3B, which led to EMT (Montrer ITK Kits ELISA) and metastasis of bladder cancer (BC). Our findings highlight a novel mechanism of H19 (Montrer NCKAP1 Kits ELISA) in progression of BC and provide H19 (Montrer NCKAP1 Kits ELISA)/miR (Montrer MLXIP Kits ELISA)-29b-3p/DNMT3B axis as a promising therapeutic target for BC.
The epiblast expressed epithelial markers, MUC1 (Montrer MUC1 Kits ELISA) and E-CADHERIN (Montrer CDH1 Kits ELISA), and the pluripotency markers, DNMT3B and CRIPTO (Montrer TDGF1 Kits ELISA).
Altogether, the authors demonstrate that Dnmt3a (Montrer DNMT3A Kits ELISA) and Dnmt3b protect the epidermis from tumorigenesis and that squamous carcinomas are sensitive to inhibition of PPAR-gamma (Montrer PPARG Kits ELISA).
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 (Montrer CHEK2 Kits ELISA) expression through promoter methylation by Dnmt3b and also presented a novel role of Chk2 (Montrer CHEK2 Kits ELISA) 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, Dnmt3a, and Dnmt3b, have been identified. Dnmt3a and Dnmt3b are responsible for establishing DNA methylation patterns produced through their de novo-type DNA methylation activity in implantation stage embryos and during germ cell differentiation. Dnmt3-like (Dnmt3l), which is a member of the Dnmt3 family but does not possess DNA methylation
While lens epithelial cell survival requires DNMT1 (Montrer DNMT1 Kits ELISA), morphologically normal lenses develop in the absence of both DNMT3A (Montrer DNMT3A Kits ELISA) and DNMT3B.
Mechanical stimulation regulates osteoblastic genes expression via direct regulation of Dnmt3b.
a miR (Montrer MLXIP Kits ELISA)-125b-DNMT3b-p53 (Montrer TP53 Kits ELISA) 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 (Montrer MLXIP Kits ELISA)-196b promoter and increased miR (Montrer MLXIP Kits ELISA)-196b expression, which directly targets the mTORC2 component Rictor (Montrer RICTOR Kits ELISA).
dnmt7 specifically methylates no tail gene in the genome
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 3 beta
, DNA (cytosine-5)-methyltransferase 3B
, DNA methyltransferase HsaIIIB
, DNA (cytosine-5-)-methyltransferase 3 beta
, DNA MTase HsaIIIB
, DNA methyltransferase 3B
, DNA (cytosine-5)-methyltransferase 3B-like
, DNA MTase MmuIIIB
, DNA methyltransferase MmuIIIB
, DNA (cytosine-5-)-methyltransferase 3 beta, like
, DNA (cytosine-5-)-methyltransferase 7
, LOW QUALITY PROTEIN: DNA (cytosine-5)-methyltransferase 3B