Dysregulation of clathrin-dependent traffic causes hematopoietic neoplasm
Project/Area Number |
23770137
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Multi-year Fund |
Research Field |
Functional biochemistry
|
Research Institution | Tohoku University |
Principal Investigator |
SHUNSUKE Kon 東北大学, 加齢医学研究科, 助教 (70506641)
|
Project Period (FY) |
2011 – 2012
|
Project Status |
Completed (Fiscal Year 2012)
|
Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2011: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
|
Keywords | 細胞内小胞輸送 / SMAP1 / 骨髄異形成症候群 / 白血病 / 国際情報交流 アメリカ合衆国 |
Research Abstract |
Approximately 50% of aged SMAP1(-/-) mice developed anemia associated with morphologically dysplastic cells of erythroid-myeloid lineage, which are hematological abnormalities reminiscent of those seen in myelodysplastic syndrome (MDS) in humans. Furthermore, some SMAP1(-/-) mice developed acute myeloid leukemia (AML) of various subtypes. The transport analysis showed that transferrin endocytosis was enhanced in erythroblasts of SMAP1(-/-) mice. In mast cells cultured in stem cell factor, SMAP1 deficiency did not affect the internalization of c-Kit but impaired the sorting of internalized c-Kit from multivesicular bodies to lysosomes, which caused the intracellular accumulation of undegraded c-Kit accompanied by a significant increase in ERK phosphorylation and cell growth activity. Collectively, these results provide the first evidence in a mouse model that the deregulation of clathrin-dependent membrane trafficking involving the transferrin receptor and c-Kit may be involved inthe development of MDS and subsequent AML.
|
Report
(3 results)
Research Products
(9 results)
-
-
-
-
-
-
-
[Book] 細胞工学2013
Author(s)
昆 俊亮
Total Pages
2
Publisher
学研メディカル秀潤社
Related Report
-
-