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Epigenetic Control of Stem Cell Fate to Neurons and Glia
김현정,Michael G. Rosenfeld 대한약학회 2010 Archives of Pharmacal Research Vol.33 No.10
How a cell fate is determined and how tremendously diverse cells are generated during development are interesting and intriguing questions to be solved before using the stem cells for therapeutic purpose. Recently, it has been suggested that epigenetic control by the histone modifying enzymes and non-coding RNAs play important roles in guiding stem cells to differentiate into neurons or glia. In this review, we discuss the recent outcomes and advances in understanding the histone modifying enzymes and non-coding RNAs during neural cell-type specification of stem cells.
Ju, Bong-Gun,Solum, Derek,Song, Eun Joo,Lee, Kong-Joo,Rose, David W.,Glass, Christopher K.,Rosenfeld, Michael G. Elsevier 2004 Cell Vol.119 No.6
<P><B>Abstract</B></P><P>Switching specific patterns of gene repression and activation in response to precise temporal/spatial signals is critical for normal development. Here we report a pathway in which induction of CaMKIIδ triggers an unexpected switch in the function of the HES1 transcription factor from a TLE-dependent repressor to an activator required for neuronal differentiation. These events are based on activation of the poly(ADP-ribose) polymerase1 (PARP-1) sensor component of the groucho/TLE-corepressor complex mediating dismissal of the corepressor complex from HES1-regulated promoters. In parallel, CaMKIIδ mediates a required phosphorylation of HES1 to permit neurogenic gene activation, revealing the ability of a specific signaling pathway to modulate both the derepression and the subsequent coactivator recruitment events required for transcriptional activation of a neurogenic program. The identification of PARP-1 as a regulated promoter-specific exchange factor required for activation of specific neurogenic gene programs is likely to be prototypic of similar molecular mechanisms.</P>
Zhu, Ping,Baek, Sung Hee,Bourk, Eliot M.,Ohgi, Kenneth A.,Garcia-Bassets, Ivan,Sanjo, Hideki,Akira, Shizuo,Kotol, Paul F.,Glass, Christopher K.,Rosenfeld, Michael G.,Rose, David W. Elsevier 2006 Cell Vol.124 No.3
<P><B>Summary</B></P><P>Defining the precise molecular strategies that coordinate patterns of transcriptional responses to specific signals is central for understanding normal development and homeostasis as well as the pathogenesis of hormone-dependent cancers. Here we report specific prostate cancer cell/macrophage interactions that mediate a switch in function of selective androgen receptor antagonists/modulators (SARMs) from repression to activation in vivo. This is based on an evolutionarily conserved receptor N-terminal L/HX<SUB>7</SUB>LL motif, selectively present in sex steroid receptors, that causes recruitment of TAB2 as a component of an N-CoR corepressor complex. TAB2 acts as a sensor for inflammatory signals by serving as a molecular beacon for recruitment of MEKK1, which in turn mediates dismissal of the N-CoR/HDAC complex and permits derepression of androgen and estrogen receptor target genes. Surprisingly, this conserved sensor strategy may have arisen to mediate reversal of sex steroid-dependent repression of a limited cohort of target genes in response to inflammatory signals, linking inflammatory and nuclear receptor ligand responses to essential reproductive functions.</P>