Chromodomain helicase DNA binding protein 4 in cell fate decisions

被引:2
作者
Laureano, Alejandra [1 ]
Kim, Jihyun [2 ,3 ,4 ]
Martinez, Edward [2 ,3 ,4 ]
Kwan, Kelvin Y. [2 ,3 ,4 ]
机构
[1] Harvard Med Sch, Dept Neurobiol, Boston, MA 02115 USA
[2] Rutgers State Univ, Dept Cell Biol & Neurosci, Nelson Labs D250 604 Allison Rd, Piscataway, NJ 08854 USA
[3] Rutgers State Univ, Stem Cell Res Ctr, Piscataway, NJ 08854 USA
[4] Rutgers State Univ, Keck Ctr Collaborat Neurosci, Piscataway, NJ 08854 USA
关键词
Epigenetics; Chromatin remodeling; Chromodomain helicase dna binding protein; CHD4; Inner ear regeneration; HAIR-CELLS; INNER-EAR; SPIRAL GANGLION; HISTONE DEACETYLASE; SENSORY EPITHELIA; PROGENITOR CELLS; SUPER-ENHANCERS; NURD COMPLEX; STEM-CELLS; CHROMATIN;
D O I
10.1016/j.heares.2023.108813
中图分类号
R36 [病理学]; R76 [耳鼻咽喉科学];
学科分类号
100104 ; 100213 ;
摘要
Loss of spiral ganglion neurons (SGNs) in the cochlea causes hearing loss. Understanding the mechanisms of cell fate transition accelerates efforts that employ directed differentiation and lineage conversion to repopulate lost SGNs. Proposed strategies to regenerate SGNs rely on altering cell fate by activating transcriptional regulatory networks, but repressing networks for alternative cell lineages is also essential. Epigenomic changes during cell fate transitions suggest that CHD4 represses gene expression by altering the chromatin status. Despite limited direct investigations, human genetic studies implicate CHD4 function in the inner ear. The possibility of CHD4 in suppressing alternative cell fates to promote inner ear regeneration is discussed. Published by Elsevier B.V.
引用
收藏
页数:10
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