Linked Life Data

10050038

Source:http://linkedlifedata.com/resource/pubmed/id/10050038

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1999-6-25
pubmed:abstractText
Overproduction of microsomal cytochrome P450Alk1 (P450Alk1) of Candida maltosa in Saccharomyces cerevisiae resulted in an extensive proliferation of endoplasmic reticulum (ER) and induction of Kar2p and Pdi1p. The ire1 null mutation severely suppressed ER proliferation, reduced the level of functional P450Alk1, and showed no induction of these ER chaperones, suggesting that the function of Ire1p is required for ER proliferation upon the overproduction of P450Alk1. Cerulenin, a potent inhibitor of lipid biosynthesis, also induced these chaperones in an Ire1p-dependent manner and limited the production of functional P450Alk1. These results imply that Ire1p may function to restore the balance between membrane proteins and lipids of the ER when the ER is relatively overcrowded by membrane proteins.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0021-924X
pubmed:author
pubmed:issnType
Print
pubmed:volume
125
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
507-14
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Null mutation in IRE1 gene inhibits overproduction of microsomal cytochrome P450Alk1 (CYP 52A3) and proliferation of the endoplasmic reticulum in Saccharomyces cerevisiae.
pubmed:affiliation
Department of Biotechnology The University of Tokyo, Bunkyo-ku, Tokyo, 113-8657, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't