The wee1 protein kinase is required for radiation-induced mitotic delay

Nature ◽  
1992 ◽  
Vol 356 (6367) ◽  
pp. 353-355 ◽  
Author(s):  
Roy Rowley ◽  
James Hudson ◽  
Paul G. Young
Keyword(s):  
Protein Kinase ◽  
Mitotic Delay ◽  
Radiation Induced

scholarly journals Radiation-Induced Mitotic Delay in L Cells

1967 ◽  
Vol 30 (1) ◽  
pp. 155 ◽  
Author(s):  
G. F. Whitmore ◽  
J. E. Till ◽  
S. Gulyas
Keyword(s):  
L Cells ◽  
Mitotic Delay ◽  
Radiation Induced

Granulocyte-Macrophage Colony-Stimulating Factor Rescues TF-1 Leukemia Cells From Ionizing Radiation-Induced Apoptosis Through a Pathway Mediated by Protein Kinase Cα

Blood ◽  
1998 ◽  
Vol 92 (2) ◽  
pp. 416-424 ◽  
Author(s):  
Mary L. Kelly ◽  
Yan Tang ◽  
Nitsa Rosensweig ◽  
Sanda Clejan ◽  
Barbara S. Beckman
Keyword(s):  
Protein Kinase ◽  
Ionizing Radiation ◽  
Colony Stimulating Factor ◽  
Gm Csf ◽  
Pkc Isoforms ◽  
Radiation Induced ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Induced Apoptosis ◽  
Stimulating Factor

Abstract Protein kinase C (PKC) activity has a recognized role in mediating apoptosis. However, the role of individual PKC isoforms in apoptosis is poorly defined. Therefore, we investigated the translocation of individual PKC isoforms during radiation-induced apoptosis with and without rescue from apoptosis by granulocyte-macrophage colony-stimulating factor (GM-CSF) in the human erythroleukemia cell line TF-1. PKCα was translocated from the particulate to cytosolic fraction of TF-1 cells within 5 minutes of treatment with apoptosis-inducing levels of ionizing radiation. However, this postirradiation translocation did not occur when cells were rescued from apoptosis by GM-CSF. Furthermore, treatment of cells with Gö6976, an inhibitor of classical PKC isoforms, abrogated the rescue effect of GM-CSF. The calcium-independent novel PKC isoform, PKCδ appeared to be degraded in both the particulate and cytosolic fractions of TF-1 cells after treatment with apoptosis-inducing levels of ionizing radiation in either the presence or absence of GM-CSF rescue. Levels of ceramide, a lipid mediator of apoptosis, were measured at 2, 4, 8, 10, and 60 minutes after treatment with ionizing radiation and were substantially reduced in TF-1 cells rescued from apoptosis by GM-CSF compared with apoptotic TF-1 cells. The largest decrease in ceramide production seen was at 4 minutes postirradiation, with a 46% reduction in ceramide levels in TF-1 cells rescued from apoptosis by GM-CSF compared with those in apoptotic TF-1 cells. Because ceramide has been shown to affect PKCα subcellular distribution, these data implicate a role for ceramide in mediating the rapid postirradiation translocation and inhibition of PKCα in TF-1 cells not rescued from apoptosis by GM-CSF. Expression of the antiapoptotic protein Bcl-2 doubled in TF-1 cells rescued from apoptosis by GM-CSF, but did not increase in unrescued cells. Our findings suggest that activated PKCα and increased expression of Bcl-2 after γ irradiation determine survival in TF-1 cells rescued from apoptosis with GM-CSF and that PKCδ plays a role in mediating signals involved in sensing cellular damage and/or regulation of cell damage repair.

Radiation-induced Surface IgG Modulation: Protein Kinase C Involvement

1991 ◽  
Vol 59 (1) ◽  
pp. 53-58 ◽  
Author(s):  
F. Ojeda ◽  
J. Andrade ◽  
C. Maldonado ◽  
M.I. Guarda ◽  
H. Folch
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Kinase C ◽  
Radiation Induced

scholarly journals p53 Is Phosphorylatedin Vitroandin Vivoby an Ultraviolet Radiation-induced Protein Kinase Characteristic of the c-Jun Kinase, JNK1

1995 ◽  
Vol 270 (10) ◽  
pp. 5511-5518 ◽  
Author(s):  
Diane M. Milne ◽  
Linda E. Campbell ◽  
David G. Campbell ◽  
David W. Meek
Keyword(s):  
Protein Kinase ◽  
Ultraviolet Radiation ◽  
Jun Kinase ◽  
Radiation Induced
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