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Literature summary for 2.1.1.244 extracted from

  • Bonsignore, L.A.; Butler, J.S.; Klinge, C.M.; Schaner Tooley, C.E.
    Loss of the N-terminal methyltransferase NRMT1 increases sensitivity to DNA damage and promotes mammary oncogenesis (2015), Oncotarget, 6, 12248-12263.
    View publication on PubMedView publication on EuropePMC
Search for more literature for 2.1.1.244

Organism

Organism UniProt Comment Textmining
Homo sapiens
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Source Tissue

Source Tissue Comment Organism Textmining
breast adenocarcinoma cell
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 Homo sapiens
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breast cancer cell
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 Homo sapiens
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MCF-7 cell
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 Homo sapiens
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MCF-7/LCC9 cell
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 Homo sapiens
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MDA-MB-231 cell low enzyme expression level Homo sapiens
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SKBR-3 cell low enzyme expression level Homo sapiens
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Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
3 S-adenosyl-L-methionine + N-terminal-peptide-[BAP1 protein] i.e. BRCA1 associated protein 1, a DNA repair protein Homo sapiens 3 S-adenosyl-L-homocysteine + N-terminal-trimethyl-peptide-[BAP1 protein]
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 ?
3 S-adenosyl-L-methionine + N-terminal-peptide-[DDB2 protein] DDB2 is a DNA repair protein Homo sapiens 3 S-adenosyl-L-homocysteine + N-terminal-trimethyl-peptide-[DDB2 protein]
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 ?
3 S-adenosyl-L-methionine + N-terminal-peptide-[PARP3 protein] i.e. poly-ADP-ribosylase 3, a DNA repair protein Homo sapiens 3 S-adenosyl-L-homocysteine + N-terminal-trimethyl-peptide-[PARP3 protein]
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 ?

Synonyms

Synonyms Comment Organism
N-terminal methyltransferase
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 Homo sapiens
NRMT1
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 Homo sapiens

General Information

General Information Comment Organism
malfunction loss of the N-terminal methyltransferase NRMT1 increases sensitivity to DNA damage and promotes mammary oncogenesis. Enzyme NRMT1 knockdown significantly enhances the sensitivity of breast cancer cell lines to both etoposide treatment and gamma-irradiation, as well as, increases proliferation rate, invasive potential, anchorage-independent growth, xenograft tumor size, and tamoxifen sensitivity, e.g. in MCF-7 cells. NRMT1 knockdown promotes growth of excision repair positive breast cancer cell lines, but has no effect on the normally low NRMT1-expressing SKBR-3 and MDA-MB-231 cells. Phenotype, overview Homo sapiens
physiological function enzyme NRMT1 acts as a tumor suppressor protein involved in multiple DNA repair pathways, role of N-terminal methylation in DNA repair. N-terminal methylation of DDB2 by NRMT1 is necessary for its recruitment to UV-induced DNA damage and proper execution of nucleotide excision repai. Additional NRMT1 targets, BRCA1 associated protein 1 (BAP1) and poly-ADP-ribosylase 3 (PARP3), are involved in DNA double strand break repair. BAP1 is a deubiquitinating enzyme recruited to DNA and required for appropriate assembly of homologous recombination factors during DSB. PARP3 poly-ADP-ribosylates proteins at DSBs and promotes NHEJ Homo sapiens