Literature summary for 1.14.11.53 extracted from

Zhang, C.; Samanta, D.; Lu, H.; Bullen, J.W.; Zhang, H.; Chen, I.; He, X.; Semenza, G.L.
Hypoxia induces the breast cancer stem cell phenotype by HIF-dependent and ALKBH5-mediated m6A-demethylation of NANOG mRNA (2016), Proc. Natl. Acad. Sci. USA, 113, E2047-E2056.

Search for more literature for 1.14.11.53

Natural Substrates/ Products (Substrates)

Natural Substrates	Organism	Comment (Nat. Sub.)	Natural Products	Comment (Nat. Pro.)	Rev.	Reac.
N6-methyladenine in NANOG mRNA + 2-oxoglutarate + O2	Homo sapiens	-	adenine in NANOG mRNA + formaldehyde + succinate + CO2	-	?

Organism

Organism	UniProt	Comment	Textmining
Homo sapiens	-	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
breast cancer cell	-	Homo sapiens	-
MCF-7 cell	-	Homo sapiens	-
MDA-MB-231 cell	-	Homo sapiens	-
MDA-MB-435 cell	-	Homo sapiens	-
SUM-159PT cell	-	Homo sapiens	-

Substrates and Products (Substrate)

Substrates	Comment Substrates	Organism	Products	Comment (Products)	Rev.	Reac.
N6-methyladenine in NANOG mRNA + 2-oxoglutarate + O2	-	Homo sapiens	adenine in NANOG mRNA + formaldehyde + succinate + CO2	-	?

Synonyms

Synonyms	Comment	Organism
AlkB homolog 5	-	Homo sapiens
ALKBH5	-	Homo sapiens

Expression

Organism	Comment	Expression
Homo sapiens	ALKBH5 mRNA levels are significantly increased under hypoxic conditions by greater than 1.6fold in SUM-159 and MDA-MB-435 cells and greater than 2fold in MDA-MB-231 and MCF-7 cells	up

General Information

General Information	Comment	Organism
malfunction	enzyme knockdown in MDAMB-231 human breast cancer cells significantly reduces their capacity for tumor initiation as a result of reduced numbers of breast cancer stem cells	Homo sapiens
metabolism	the enzyme enhances NANOG mRNA stability by catalyzing m6A demethylation	Homo sapiens
physiological function	enzyme expression promotes m6A RNA demethylation in hypoxic breast cancer cells	Homo sapiens

Use of this online version of BRENDA is free under the CC BY 4.0 license. See terms of use for full details.

Release 2023.1 (January 2023)