2015 Fiscal Year Annual 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 Institution | Tokai University |
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Principal Investigator |
チャンダ ビディシャ 東海大学, 医学部, 奨励研究員 (70725358)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Keywords | miR-195 / B cell development |
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| Outline of Annual Research Achievements |
The canonical notion of B cell fate determination implies that EBF1 is an indispensible factorfor B lymphopoiesis. However, in the present study, we showed that a single microRNA miR-195 rescued arrested 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 microenvironmental stimuli by miR-195,such as modulation of the expression of 3 miR-195 target genes belonging to the Tgfb family and their related pathway. By downregulating the TGFβ pathway, miR-195 might activate the NFκB pathway and rescue B cell development.
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