Cold-induced protein RBM3 orchestrates neurogenesis via modulating Yap mRNA stability in cold stress
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چکیده
منابع مشابه
Cold stress protein RBM3 responds to temperature change in an ultra-sensitive manner in young neurons
Extremely mild hypothermia to 36.0 °C is not thought to appreciably differ clinically from 37.0 °C. However, it is possible that 36.0 °C stimulates highly sensitive hypothermic signaling mechanism(s) and alters biochemistry. To the best of our knowledge, no such ultra-sensitive pathway/mechanisms have been described. Here we show that cold stress protein RNA binding motif 3 (RBM3) increases in ...
متن کاملCold stress-induced protein Rbm3 binds 60S ribosomal subunits, alters microRNA levels, and enhances global protein synthesis.
The expression of Rbm3, a glycine-rich RNA-binding protein, is enhanced under conditions of mild hypothermia, and Rbm3 has been postulated to facilitate protein synthesis at colder temperatures. To investigate this possibility, Rbm3 was overexpressed as a c-Myc fusion protein in mouse neuroblastoma N2a cells. Cells expressing this fusion protein showed a 3-fold increase in protein synthesis at ...
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Cooling and hypothermia are profoundly neuroprotective, mediated, at least in part, by the cold shock protein, RBM3. However, the neuroprotective effector proteins induced by RBM3 and the mechanisms by which mRNAs encoding cold shock proteins escape cooling-induced translational repression are unknown. Here, we show that cooling induces reprogramming of the translatome, including the upregulati...
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Cold-inducible RNA-binding protein (RBM3) is suggested to be involved in the regulation of skeletal muscle mass. Cell death pathways are implicated in the loss of muscle mass and therefore the role of RBM3 in muscle apoptosis in C(2)C(12) myoblasts was investigated in this study. RBM3 overexpression was induced by either cold shock (32°C exposure for 6 h) or transient transfection with a myc-ta...
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ژورنال
عنوان ژورنال: Journal of Cell Biology
سال: 2018
ISSN: 0021-9525,1540-8140
DOI: 10.1083/jcb.201801143