Linked Life Data

16484322

Source:http://linkedlifedata.com/resource/pubmed/id/16484322

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2006-4-17
pubmed:abstractText
ACTH regulates the steroidogenic capacity, size, and structural integrity of the adrenal cortex through a series of actions involving changes in gene expression; however, only a limited number of ACTH-regulated genes have been identified, and these only partly account for the global effects of ACTH on the adrenal cortex. In this study, a National Institute on Aging 15K mouse cDNA microarray was used to identify genome-wide changes in gene expression after treatment of Y1 mouse adrenocortical cells with ACTH. ACTH affected the levels of 1275 annotated transcripts, of which 46% were up-regulated. The up-regulated transcripts were enriched for functions associated with steroid biosynthesis and metabolism; the down- regulated transcripts were enriched for functions associated with cell proliferation, nuclear transport and RNA processing, including alternative splicing. A total of 133 different transcripts, i.e. only 10% of the ACTH-affected transcripts, were represented in the categories above; most of these had not been described as ACTH-regulated previously. The contributions of protein kinase A and protein kinase C to these genome-wide effects of ACTH were evaluated in microarray experiments after treatment of Y1 cells and derivative protein kinase A-defective mutants with pharmacological probes of each pathway. Protein kinase A-dependent signaling accounted for 56% of the ACTH effect; protein kinase C-dependent signaling accounted for an additional 6%. These results indicate that ACTH affects the expression profile of Y1 adrenal cells principally through cAMP- and protein kinase A- dependent signaling. The large number of transcripts affected by ACTH anticipates a broader range of actions than previously appreciated.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0013-7227
pubmed:author
pubmed:issnType
Print
pubmed:volume
147
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2357-67
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:16484322-Adrenal Cortex, pubmed-meshheading:16484322-Adrenocorticotropic Hormone, pubmed-meshheading:16484322-Alternative Splicing, pubmed-meshheading:16484322-Animals, pubmed-meshheading:16484322-Cell Line, pubmed-meshheading:16484322-Cyclic AMP, pubmed-meshheading:16484322-Cyclic AMP-Dependent Protein Kinases, pubmed-meshheading:16484322-DNA, Complementary, pubmed-meshheading:16484322-DNA Primers, pubmed-meshheading:16484322-Down-Regulation, pubmed-meshheading:16484322-Gene Expression, pubmed-meshheading:16484322-Gene Expression Regulation, pubmed-meshheading:16484322-Genome, pubmed-meshheading:16484322-Mice, pubmed-meshheading:16484322-Models, Biological, pubmed-meshheading:16484322-Mutation, pubmed-meshheading:16484322-Oligonucleotide Array Sequence Analysis, pubmed-meshheading:16484322-Protein Kinase C, pubmed-meshheading:16484322-RNA, Messenger, pubmed-meshheading:16484322-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:16484322-Signal Transduction, pubmed-meshheading:16484322-Steroids, pubmed-meshheading:16484322-Up-Regulation
pubmed:year
2006
pubmed:articleTitle
Global profiles of gene expression induced by adrenocorticotropin in Y1 mouse adrenal cells.
pubmed:affiliation
Banting and Best Department of Medical Research, University of Toronto, Ontario, Canada. bernard.schimmer@utoronto.ca
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't