Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
1991-12-18
pubmed:abstractText
The expression of the protein products of the c-myc oncogene and retinoblastoma susceptibility gene (RB) was investigated during either goat anti-mouse immunoglobulin (GaMIg)- or phorbol ester (TPA)-induced growth arrest of the murine B-lymphoma cell line WEHI 231. Previously we have demonstrated that c-myc mRNA levels increase within 1-2 h of treatment, return to control levels by 4 h, and decline below these values by 24 h of treatment. Here we demonstrate that the level of c-myc protein synthesis and mRNA change in parallel. The predominant c-myc protein expressed during the time course is the one initiated at the AUG codon (P2). The myc protein synthesized following 1-2 h of anti-immunoglobulin or TPA treatment migrates more slowly in a polyacrylamide gel as a result of increased phosphorylation. This hyperphosphorylation was no longer detectable by 4-6 h of treatment. Furthermore, the hyperphosphorylated myc protein appears to be more readily extractable with salt than the hypophosphorylated form. The product of the RB gene is present in multiple phosphorylation states in exponentially growing WEHI 231 cells. By 8 h of GaMIg or TPA treatment, a hypophosphorylated form begins to be detectable and significant levels were seen by 15 h. Thus post-translational control of both c-myc and RB expression occurs during the growth arrest of WEHI 231 cells. These changes in phosphorylation may play a role in mediating the cessation of proliferation of these cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0950-9232
pubmed:author
pubmed:issnType
Print
pubmed:volume
6
pubmed:geneSymbol
c-myc
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1965-71
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Changes in phosphorylation of myc oncogene and RB antioncogene protein products during growth arrest of the murine lymphoma WEHI 231 cell line.
pubmed:affiliation
Department of Biochemistry, Boston University School of Medicine, Massachusetts 02118.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.