Biochemical analysis of tumor rejection antigen and its role of oncogenesis.
| Project/Area Number |
08670252
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Experimental pathology
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| Research Institution | Okayama University |
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Principal Investigator |
UENAKA Akiko Okayama University Medical School, Assistant Professor, 医学部, 助手 (50273967)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1997: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1996: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | murine leukemia / tumor rejection antigen / peptide recognized by CTL / proto-oncogene akt / over expression / プロト癌遺伝子akt / 拒絶抗原 / CTL認識ペプチド / 原癌遺伝子akt |
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| Research Abstract |
The antigen peptides recognized by RL*1 specific CTL were determined by direct sequencing of the fraction separated by reversed-phase high performance liquid chromatography. Molecular analysis revealed the antigen peptide were derived from the 5'-untransrated region of proto-oncogene c-akt by insertion of a murine leukemia virus LTR together with six nucleotides of unknown origin. In this study, we investigated this altered Akt molecule and its role of oncogenesis in RL*1.
1. Western blot analysis using plyclonal rabbit anti c-Akt synthetic polypeptide antibodies revealed a protein 59 KD in addition to 56 KD normal c-Akt protein in RL*1 cells. 2. The 59 KD altered Akt molecule (RL-Akt) was expressed at about ten times level to normal c-Akt and was detected in the membrane fraction and in the cytosolic fraction, although the c-Akt was detected only in the cytosolic fraction. 3. RL-akt transgeneic NIH 3T3 cells grew well, forming colonies in soft apr. 4. RL-Akt deletion mutant and RL-Akt weakly expressed mutant were established. 5. To assess the effect of RL-Akt in the growth rate in vivo, these mutants and parental RL*1 cells transplanted in BALB/c mice, respectively, parental RL*1 cells grow rapidlly, but weakly expressed mutant grow slowly, and deletion mutant did more slowly.
These observations suggests that the over expression and localization in the membrane of RL-Akt resulted in effective signal transduction of growth factor-PI3 pathway and these participates in malignancy in RL*1 leukemia. The study of the effects of RL-Akt to the host immune system are going now.
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Report
(3 results)
Research Products
(19 results)
