Anti-DNMT1 Antibody

Methylates CpG residues. Preferentially methylates hemimethylated DNA. Associates with DNA replication sites in S phase maintaining the methylation pattern in the newly synthesized strand, that is essential for epigenetic inheritance. Associates with chromatin during G2 and M phases to maintain DNA methylation independently of replication. It is responsible for maintaining methylation patterns established in development. DNA methylation is coordinated with methylation of histones. Mediates transcriptional repression by direct binding to HDAC2. In association with DNMT3B and via the recruitment of CTCFL/BORIS, involved in activation of BAG1 gene expression by modulating dimethylation of promoter histone H3 at H3K4 and H3K9. Probably forms a corepressor complex required for activated KRAS-mediated promoter hypermethylation and transcriptional silencing of tumor suppressor genes (TSGs) or other tumor-related genes in colorectal cancer (CRC) cells (PubMed:24623306). Also required to maintain a transcriptionally repressive state of genes in undifferentiated embryonic stem cells (ESCs) (PubMed:24623306). Associates at promoter regions of tumor suppressor genes (TSGs) leading to their gene silencing (PubMed:24623306). Promotes tumor growth (PubMed:24623306). {PubMed:16357870, PubMed:18413740, PubMed:18754681, PubMed:24623306}.

ELISA Immunoblotting: use at 2ug/ml. A band of ~190kDa is detected. <br><br>These are recommended concentrations. End user should determine optimal concentrations for their applications. <br><br>Positive controls: ES and H1299 cell lysates.

Methylation of DNA at cytosine residues is important in regulation of gene expression and genomic imprinting. Hyper- methylation of CpG islands in tumor suppressor genes or hypomethylation of bulk genomic DNA may be linked to development of cancer. Thus far three families of mammalian DNA methyl- transferase genes have been identified: DNMT1, DNMT2, and DNMT3. DNMT1 is constitutively expressed in proliferating cells, and inactivation of this gene causes global demethylation of genomic DNA and embryonic lethality. DNMT1 co-purifies with the retinoblastoma (Rb) tumor suppressor gene product E2F1 and with HDAC1. DNMT1 cooperates with Rb to repress transcription from promoters containing E2F-binding sites which suggests a link between DNA methylation, histone deacetylase and sequence- specific DNA binding activity as well as a growth-regulatory pathway that is disrupted in cancer cells.