GO curators for mouse genes have assigned the following annotations to the gene product of Alad. (This text reflects annotations as of Wednesday, January 23, 2013.) MGI curation of this mouse gene is considered complete, including annotations derived from the biomedical literature as of March 13, 2009. If you know of any additional information regarding this mouse gene please let us know. Please supply mouse gene symbol and a PubMed ID.Summary from NCBI RefSeq
[Summary is not available for the mouse gene. This summary is for the human ortholog.] The ALAD enzyme is composed of 8 identical subunits and catalyzes the condensation of 2 molecules of delta-aminolevulinate to form porphobilinogen (a precursor of heme, cytochromes and other hemoproteins). ALAD catalyzes the second step in the porphyrin and heme biosynthetic pathway; zinc is essential for enzymatic activity. ALAD enzymatic activity is inhibited by lead and a defect in the ALAD structural gene can cause increased sensitivity to lead poisoning and acute hepatic porphyria. [provided by RefSeq, Jul 2008]Summary text based on GO annotations supported by experimental evidence in mouse
Researchers have inferred from direct assay, that the gene product of Alad
participates in the following biological processes:
Chu CC et al. (1998) Expressed genes in interleukin-4 treated B cells identified by cDNA representational difference analysis. Mol Immunol, 35:487-502. (PubMed:9798653)
Coleman DL. (1966) Purification and properties of delta-aminolevulinate dehydratase from tissues of two strains of mice. J Biol Chem, 241:5511-7. (PubMed:4959158)
Doyle D et al. (1969) The genetic and developmental regulation of hepatic delta-aminolevulinate dehydratase in mice. J Biol Chem, 244:5449-59. (PubMed:4981581)
Russell RL et al. (1963) Genetic control of hepatic delta-aminolevulinate dehydratase in mice Genetics, 48:1033-39. (PubMed:14050799)
Suzuki H et al. (2001) Protein-protein interaction panel using mouse full-length cDNAs. Genome Res, 11:1758-65. (PubMed:11591653)