Dnmt1 Antibody

Rabbit Ig

Store at 4˚ C for three months and -20˚ C, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.

Methylation of DNA at cytosine residues plays an important role in regulation of gene expression, genomic imprinting and is essential for mammalian development. Hypermethylation of CpG islands in tumor suppressor genes or hypomethylation of bulk genomic DNA may be linked with development of cancer. To date, 3 families of mammalian DNA methyltransferase genes have been identified which include 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. Dnmt2 is expressed at low levels in adult tissues and its inactivation does not affect DNA methylation or maintenance of methylation. The Dnmt3 family members, Dnmt3a and Dnmt3b, are strongly expressed in ES cells but their expression is down regulated in differentiating ES cells and is low in adult somatic tissue. Dnmt1 co-purifies with the retinoblastoma (Rb) tumour suppressor gene product, E2F1, and HDAC1. Dnmt1 also cooperates with Rb to repress transcription from promoters containing E2Fbinding sites suggesting a link between DNA methylation, histone deacetylase and sequence-specific DNA binding activity, as well as a growth-regulatory pathway that is disrupted in nearly all cancer cells.

None

This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis

Supplied in PBS with 0.09% (W/V) sodium azide.

This Dnmt1 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 1588-1616 amino acids from the C-terminal region of human Dnmt1.

DNA (cytosine-5)-methyltransferase 1

Optimal dilutions/concentrations should be determined by the end user. The information provided is a guideline for product use. This product is for research use only.