Induction of cyclin B and H1 kinase activity in apoptotic PC12 cells.
The present study examines whether cyclin B may be involved in apoptosis of neuronally differentiated PC12 cells following withdrawal of NGF. Cyclin B mRNA increased approximately 10-fold 4 days after NGF withdrawal, as indicated by competitive RT/PCR. Sequencing of the PCR product confirmed that it was derived from cyclin B mRNA. Cyclin B protein increased in parallel with cyclin B mRNA, as shown by immunoblotting. Immunoprecipitation with anti-cyclin B antibody demonstrated that cyclin B was associated with H1K activity, which reached a maximum 5 days after NGF withdrawal. When proteins immunoprecipitated with anti-cyclin B antibody were immunoblotted with anti-PSTAIR antibody, a protein with apparent molecular weight of 34 kDa was detected. This protein was identified as p34cdc2 on the basis of immunoreactivity with antibody against the C-terminal portion of mouse p34cdc2. Since cyclin B/p34cdc2 complexes are known to catalyze chromosomal condensation and nuclear envelope breakdown during mitosis, these results suggest that cyclin B/p34cdc2 may play some role in the nuclear changes accompanying apoptosis of PC12 cells.
Gao
C Y
CY
Laboratory of Molecular and Developmental Biology, National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
Zelenka
P S
PS
D000818:Animals; D017209:Apoptosis; D001483:Base Sequence; D002461:Cell Line, Transformed; D016213:Cyclins / Q000096:biosynthesis*; D016200:Maturation-Promoting Factor / Q000096:biosynthesis*; D008969:Molecular Sequence Data; D016716:PC12 Cells; D011494:Protein Kinases / Q000096:biosynthesis*; D051381:Rats
D016213:Cyclins; D011494:Protein Kinases; D016200:Maturation-Promoting Factor