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methyl-CpG-binding domain protein 4; methyl-CpG-binding protein MBD4; methyl-CpG-binding endonuclease 1; Mismatch-specific DNA N-glycosylase (MBD4, MED1)

Function: 1) mismatch-specific DNA N-glycosylase 2) DNA mismatch repair 3) thymine glycosylase activity 4) specific for G:T mismatches within methylated & unmethylated CpG sites 5) can remove uracil or 5-fluorouracil in G:U mismatches 6) no lyase activity 7) interacts with MLH1 Structure: contains 1 MBD domain (methyl-CpG-binding) Compartment: nucleus Alternative splicing: named isoforms=3 Pathology: - germline defects may predispose to early onset AML [4]

Related

DNA methylation (promoter methylation)

General

DNA glycosylase methyl-CpG-binding protein (MECP, Me-CpG-BP)

Properties

SIZE: MW = 66 kD entity length = 580 aa COMPARTMENT: cell nucleus MOTIF: MBD {76-148} HHH-GPD {461-524} aspartate residue {D560}

Database Correlations

OMIM 603574 UniProt O95243 PFAM correlations Entrez Gene 8930 Kegg hsa:8930

References

  1. OMIM :accession 603574
  2. UniProt :accession O95243
  3. NIEHS-SNPs http://egp.gs.washington.edu/data/mbd4/
  4. O'Neil A DNA Repair Mutations Lead to AML Predisposition. In early research, germline mutations shut down a mechanism that guards against harmful mutations that increase leukemia risk. MedPage Today, ASCO Reading Room. Feb 21, 2018 https://www.medpagetoday.com/reading-room/asco/hematologic-malignancies/71284 - Sanders MA, Chew E, Flensburg C et al Germline loss of MBD4 predisposes to leukaemia due to a mutagenic cascade driven by 5mC. bioRxiv preprint first posted online Nov. 1, 2017 https://www.biorxiv.org/content/biorxiv/early/2017/11/01/180588.full.pdf