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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 DNA (Cytosine-5-)-Methyltransferase 3 Like Antibodies (162) and DNA (Cytosine-5-)-Methyltransferase 3 Like Kits (1) and many more products for this protein.
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Dnmt3l-KO donor cells may offer a more permissive epigenetic state that is beneficial for Nuclear transfer reprogramming
By interacting with TRIM28 (show TRIM28 Proteins), DNMT3L can attract various enzymes to form a DNMT3L-induced repressive complex to remove active marks and add repressive marks to histone proteins.
Hypomethylation of highly methylated CpG islands was caused by the downregulation of Dnmt3L and Dnmt3a (show DNMT3A Proteins) due to hepatitis B X-protein bound to their promoters.
DNMT3L is required to delicately balance the cycling and quiescence of spermatogonial progenitor cells
Study demonstrates that Dnmt3L interacts with the Polycomb (show CBX2 Proteins) PRC2 complex in competition with the DNA methyltransferases Dnmt3a (show DNMT3A Proteins) and Dnmt3b (show DNMT3B Proteins) to maintain low methylation levels at the Histone 3 H3K27me3 regions.
Data indicate that expression of Dnmt3a (show DNMT3A Proteins), Dnmt3b (show DNMT3B Proteins), Dnmt3L as well as maintenance Dnmt1o (show DNMT1 Proteins) in oocytes and zygotes was not disrupted.
Reduced expression of DNMT3L in male germ cells, associated with haploinsufficiency of the paternal-effect gene Dnmt3L, results in abnormal hypomethylation of prenatal germline progenitor cells.
The maternal store of Dnmt3L is not involved in embryonic de novo methylation.
Dnmt3l is one of the key players in de novo DNA methylation (show HELLS Proteins) of imprinting control elements and retrotransposons, which occurs after genome-wide epigenetic erasure during germ cell development. (Review)
We observe evidence for a context-dependent contribution of Dnmt3l to set and maintain CpG and non-CpG methylation at distinct classes of repetitive elements and selected single copy genes
the present study has demonstrated that variations in the DNMT3L gene do not contribute to stage I-II endometriosis-associated infertility.
DNMT3L rs2070565 (genotype P = 0.007, allele P = 0.0026) confers an increased risk of developing schizophrenia at an early age in individuals with family history.
crystal structures of DNMT3A (show DNMT3A Proteins)-DNMT3L (autoinhibitory form) and DNMT3A (show DNMT3A Proteins)-DNMT3L-H3 (active form) complexes at 3.82 and 2.90 A resolution, respectively
DNMT3L can address DNMT3A (show DNMT3A Proteins)/B to specific sites by directly interacting with TFs that do not directly interact with DNMT3A (show DNMT3A Proteins)/B
CpG island encompassing the promoter and first exon of human DNMT3L gene is a PcG/TrX (show VAC14 Proteins) response element
DNMT3L is one of the key players in de novo DNA methylation (show HELLS Proteins) of imprinting control elements and retrotransposons, which occurs after genome-wide epigenetic erasure during germ cell development. (Review)
SNP rs2070565, as well as haplotypes AAA (show APP Proteins) and GAA (show GAA Proteins), may be associated with male infertility; DNMT3L may contribute to azoospermia susceptibility in humans
Genetic polymorphisms of DNMT3L involved in hypermethylation of chromosomal ends are associated with greater risk of developing ovarian endometriosis.
mutation analysis of SYCP3 (show SYCP3 Proteins), DNMT3L and MSH4 (show MSH4 Proteins) in patients with maturation arrest of spermatogenesis and couples with recurrent miscarriages.
This study offers insights into the manner by which DNA methylation (show HELLS Proteins) patterns are deposited and reveals a new level of interplay between members of the de novo DNMT (show DNMT1 Proteins) family.
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 nuclear protein with similarity to DNA methyltransferases, but is not thought to function as a DNA methyltransferase as it does not contain the amino acid residues necessary for methyltransferase activity. However, it does stimulate de novo methylation by DNA cytosine methyltransferase 3 alpha and is thought to be required for the establishment of maternal genomic imprints. This protein also mediates transcriptional repression through interaction with histone deacetylase 1. Alternatively spliced transcript variants encoding different isoforms have been found for this gene.
DNA (cytosine-5-)-methyltransferase 3-like
, cytosine-5-methyltransferase 3-like protein
, DNA (cytosine-5)-methyltransferase 3-like
, human cytosine-5-methyltransferase 3-like protein