2000 Fiscal Year Final Research Report Summary
Research for unknown targets of cyclin-dependent kinases
| Project/Area Number |
10480203
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| Research Category |
Grant-in-Aid for Scientific Research (B).
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Cell biology
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| Research Institution | NATIONAL CANCER CENTER RESEARCH INSTITUTE |
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Principal Investigator |
TAYA Yoichi National Cancer Center Research Institute, Radiobiology Division, Chief, 放射線研究部, 部長 (60133641)
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| Project Period (FY) |
1998 – 2000
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| Keywords | p16^<INK4a> / Cdk4 / Cdk6 / cyclin D / p34^<SEI-1> / RB protein / Cdk2 |
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| Research Abstract |
The p16INK4a tumor suppressor inhibits cyclin-dependent kinases (CDK4 and CDK6). Here we report the isolation of a novel gene, SEI-1, whose product (p34^<SEI-1>) appears to antagonize the function of p16^<INK4a>. Addition of p34^<SEI-1> to cyclin D1-CDK4 renders the complex resistant to inhibition by p16^<INK4a>. Expression of SEI-1 is rapidly induced onaddition of serum to quiescent fibroblasts, and ectopic expression of p34^<SEI-1> enables fibroblasts to proliferate even in low serum concentrations. p34^<SEI-1> seems to act as a growth factor sensor and may facilitate the formation and activation of cyclin D-CDK complexes in the face of inhibitory levels of INK4 proteins.
The p16INK4a tumor suppressor inhibits cyclin-dependent kinases (CDK4 and CDK6). Here we report the isolation of a novel gene, SEI-1, whose product (p34^<SEI-1>) appears to antagonize the function of p16^<INK4a>. Addition of p34^<SEI-1> to cyclin D1-CDK4 renders the complex resistant to inhibition by p16^<INK4a> a. Expression of SEI-1 is rapidly induced on addition of serum to quiescent fibroblasts, and ectopic expression of p34^<SEI-1> enables fibroblasts to proliferate even in low serum concentrations. p34^<SEI-1> seems to act as a growth factor sensor and may facilitate the formation and activation of cyclin D-CDK complexes in the face of inhibitory levels of INK4 proteins.
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