Breast cancer regulation by traffic and degradation of ErbB family
| Project/Area Number |
22791265
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
General surgery
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| Research Institution | Miyagi Cancer Center Research Institute |
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Principal Investigator |
SAKURAI Yu 地方独立行政法人宮城県立病院機構宮城県立がんセンター(研究所), がん先進治療開発研究部, 共同研究員 (80451574)
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| Project Period (FY) |
2010 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2011: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2010: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 乳腺外科 / がん / 乳がん / ErbB3 / ユビキチン / 分解 / ErbB2 / プロテアソーム / ユビキチン化酵素 |
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| Research Abstract |
ErbB2/ErbB3 heterodimer is expressed on many breast cancers, and the signals derived from the dimer plays significant roles on malignant phenotypes. In the present study, I analyzed how the heterodimer is degraded. Whereas ErbB2 was relatively stable, ErbB3 was continuously degraded by the proteasome and lysosomes. NRG1βstimulation induced proteasome-dependent degradation. Among several E3s tested, I identified Nrdp1 and two additional E3s that ubiquitinated ErbB3.Further, intracellular portion of ErbB3 comprizing of 100 aminoacids was required for the degradation, suggesting the possible ubiquitination target of ErbB3.
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Report
(3 results)
Research Products
(2 results)
