2015 Fiscal Year Final Research Report
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
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Keywords | miR-195 / B cell development |
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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Free Research Field |
血液内科学
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