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Literature summary for 2.3.1.37 extracted from
- Hypoxia induces erythroid-specific 5-aminolevulinate synthase expression in human erythroid cells through transforming growth factor-beta signaling (2009), FEBS J., 276, 1370-1382.
Application
| Application | Comment | Organism |
|---|---|---|
| medicine | hypoxia induces the expression of TGF-beta1 and mitoferrin mRNAs through separate mechanisms in erythroid cells. TGF-beta1 subsequently induces erythroidspecific 5-aminolevulinate synthase ALAS2 expression | Homo sapiens |
Organism
| Organism | UniProt | Comment | Textmining |
|---|---|---|---|
| Homo sapiens | - |
- |
- |
Source Tissue
| Source Tissue | Comment | Organism | Textmining |
|---|---|---|---|
| YN-1 cell | - |
Homo sapiens | - |
Expression
| Organism | Comment | Expression |
|---|---|---|
| Homo sapiens | increased expression of erythroid specific 5-aminolevulinate synthase ALAS2 and gamma-globin mRNAs after 48 h of hypoxia. Exogenous TGF-beta1 induces hemoglobinization and the expression of ALAS2 mRNA in YN-1-0-A cells, but not of c-globin and mitoferrin mRNAs. A specific inhibitor of intracellular TGF-b signaling markedly reduces the degree of the hypoxia-mediated increase in the expression of ALAS2 mRNA in YN-1-0-A cells | up |
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