PMID- 1719463
OWN - NLM
STAT- MEDLINE
DCOM- 19911218
LR  - 20131121
IS  - 0950-9232 (Print)
IS  - 0950-9232 (Linking)
VI  - 6
IP  - 11
DP  - 1991 Nov
TI  - Changes in phosphorylation of myc oncogene and RB antioncogene protein products 
      during growth arrest of the murine lymphoma WEHI 231 cell line.
PG  - 1965-71
AB  - 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.
FAU - Maheswaran, S
AU  - Maheswaran S
AD  - Department of Biochemistry, Boston University School of Medicine, Massachusetts 
      02118.
FAU - McCormack, J E
AU  - McCormack JE
FAU - Sonenshein, G E
AU  - Sonenshein GE
LA  - eng
GR  - CA 36355/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - Oncogene
JT  - Oncogene
JID - 8711562
RN  - 0 (Proto-Oncogene Proteins c-myc)
RN  - 0 (Retinoblastoma Protein)
RN  - 63231-63-0 (RNA)
RN  - NI40JAQ945 (Tetradecanoylphorbol Acetate)
SB  - IM
GS  - c-myc
MH  - Animals
MH  - Blotting, Northern
MH  - Blotting, Western
MH  - Cell Division
MH  - Cell Line
MH  - Electrophoresis, Polyacrylamide Gel
MH  - *Gene Expression Regulation, Neoplastic/drug effects
MH  - *Genes, myc
MH  - Lymphoma/*genetics
MH  - Mice
MH  - Phosphorylation
MH  - Protein Biosynthesis
MH  - Proto-Oncogene Proteins c-myc/drug effects/*physiology
MH  - RNA/analysis
MH  - Retinoblastoma Protein/drug effects/*physiology
MH  - Tetradecanoylphorbol Acetate/pharmacology
MH  - Tumor Cells, Cultured
EDAT- 1991/11/01 00:00
MHDA- 1991/11/01 00:01
CRDT- 1991/11/01 00:00
PHST- 1991/11/01 00:00 [pubmed]
PHST- 1991/11/01 00:01 [medline]
PHST- 1991/11/01 00:00 [entrez]
PST - ppublish
SO  - Oncogene. 1991 Nov;6(11):1965-71.