Mir-195 rescue B cell development independently of transcription factor in EBF KO hematopoietic progenitor cells
Project/Area Number |
26860739
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Hematology
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Research Institution | Tokai University |
Principal Investigator |
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Project Period (FY) |
2014-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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Keywords | miR-195 / B cell development / microRNA / Leukemia / Lymphoma |
Outline of Final Research Achievements |
The canonical notion of B cell fate determination implies that EBF1 is an indispensible factor for B lymphopoiesis. However, in the present study, we showed that a single microRNA miR-195 rescued pro-B cell differentiation induced by EBF1 deficiency. Thus, miR-195 acted more than a fine tuner at least with regard to B cell lineage commitment. One of the mechanisms can be explained by the modulation of micro environmental stimuli by miR-195, such as modulation of the expression of three miR-195 target genes belonging to the TGF beta family and their related pathway. By down regulating the TGF beta pathway, miR-195 might activate the NF khappa B pathway and rescue B cell development.
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Report
(3 results)
Research Products
(3 results)
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[Presentation] A single micro-RNA can completely rescue B-cell differentiation arrest due to EBF1 deficiency-Can micro-RNA control cell fate as a potential alternative of transcriptional factor?2015
Author(s)
B Chanda, T Ikawa, K Okuyama, K Hozumi, K Ando, A Tojo, H Kawamoto,A Kotani
Organizer
Haematopoiesis (B6),Keystone Symposium,
Place of Presentation
Keystone, Colorado, USA
Year and Date
2015-02-22 – 2015-02-27
Related Report
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