rdf:type |
|
lifeskim:mentions |
|
pubmed:issue |
1
|
pubmed:dateCreated |
1992-10-22
|
pubmed:databankReference |
|
pubmed:abstractText |
Hereditary tyrosinemia type I is caused by deficiency of the enzyme fumarylacetoacetate hydrolase (FAH) (EC 3.7.1.2), the final step in tyrosine degradation. We report here the cloning and sequencing of a full length cDNA coding for murine FAH. This cDNA is highly homologous to the previously cloned human and rat genes.
|
pubmed:grant |
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Aug
|
pubmed:issn |
0885-4505
|
pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:volume |
48
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
26-31
|
pubmed:dateRevised |
2007-11-14
|
pubmed:meshHeading |
|
pubmed:year |
1992
|
pubmed:articleTitle |
Nucleotide sequence of a cDNA encoding murine fumarylacetoacetate hydrolase.
|
pubmed:affiliation |
Department of Molecular and Medical Genetics, Oregon Health Sciences University, Portland 97201.
|
pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
|