1.14.11.51: DNA N6-methyladenine demethylase
This is an abbreviated version!
For detailed information about DNA N6-methyladenine demethylase, go to the full flat file.
Word Map on EC 1.14.11.51
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1.14.11.51
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dioxygenase
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demethylation
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histone
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2-oxoglutarate-dependent
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abasic
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alkbh7
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eraser
- 1.14.11.51
- dioxygenase
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demethylation
- histone
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2-oxoglutarate-dependent
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abasic
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alkbh7
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eraser
Reaction
Synonyms
6mA DNA demethylase, ALKBH1, DMAD, DNA 6mA demethylase, NMAD, NMAD-1
ECTree
1.14.11.51 DNA N6-methyladenine demethylaseAdvanced search results
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General Information on EC 1.14.11.51 - DNA N6-methyladenine demethylase
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GENERAL INFORMATION 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
malfunction
metabolism
N6-hydroxymethyladenine exists as an oxidized intermediate during N6-mA demethylation by ALKBH1
physiological function
malfunction
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enzyme deletion accelerates the progressive fertility defect of spr-5 mutant worms
malfunction
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enzyme-depleted mesenchymal stem cells exhibit a restricted capacity for bone formation in vivo
physiological function
the enzyme catalyses oxidative demethylation of DNA N6-methyladenine, a prevalent modification in LINE-1 transposons
physiological function
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the enzyme promotes differentiation of early germ cells in fly ovary
physiological function
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enzyme overexpression enhances osteoblastic differentiation of mesenchymal stem cells
physiological function
Alkbh1 expression in bone marrow mesenchymal stem cells declines during aging. Knockout of Alkbh1 promotes adipogenic differentiation of bone marrow mesenchymal stem cells while inhibits osteogenic differentiation. Bone marrow mesenchymal stem cells -specific Alkbh1 knockout mice exhibit reduced bone mass and increased marrow adiposity. Overexpression of Alkbh1 attenuates bone loss and marrow fat accumulation in aged mice
physiological function
ALKBH1 is critical for the myogenic differentiation of C2C12 cells. Overexpression of ALKBH1 reduces N6-mA levels, enhances proliferation and inhibits differentiation in C2C12 cells. ALKBH1 regulates a subset of genes and impairs multiple signaling required for muscle development
physiological function
ALKBH1 overexpression decreases hepatocellular carcinoma cell viability, induces apoptosis, and decreases migration and invasion
physiological function
knockdown of ALKBH1 inhibits adipogenic differentiation in both mesenchymal stem cells and 3T3-L1 preadipocytes, while overexpression of ALKBH1 leads to increased adipogenesis. Hypoxia-inducible factor HIF-1 signaling is a crucial downstream target of ALKBH1 activity. Depletion of ALKBH1 leads to hypermethylation of both HIF-1alpha and its downstream target GYS1
physiological function
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RNAi knockdown of 6mA methyltransferase METTL4 and 6mA demethylase NMAD induce cell cycle arrest at G1 phase and also result in defects of chromosome alignments at metaphase
physiological function
the 6-methyl adenine demethylase activity is very low. The demethylase activity is less than half that of the apurinic/apyrimidinic lyase activity when ALKBH1 samples are assayed using identical buffer conditions. The two enzymatic activities are located in distinct but partially overlapping active sites for the two reactions
