Molecular mechanisms of the suppression of axon regeneration by KLF transcription factors

被引:22
作者
Apara, Akintomide [1 ]
Goldberg, Jeffrey L. [2 ]
机构
[1] Univ Miami, Miller Sch Med, Miami, FL 33136 USA
[2] Univ Calif San Diego, Shiley Eye Ctr, La Jolla, CA 92093 USA
关键词
optic nerve; regeneration; axon growth; retina; retinal ganglion cells; spinal cord; transcription factors; SPINAL-CORD-INJURY; SULFATE PROTEOGLYCANS NEUROCAN; MYELIN-ASSOCIATED GLYCOPROTEIN; OPTIC-NERVE REGENERATION; CELL-DEATH; UP-REGULATION; WHITE-MATTER; ADULT CNS; IN-VIVO; GROWTH;
D O I
10.4103/1673-5374.139454
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Molecular mechanisms of the Kruppel-like family of transcription factors (KLFs) have been studied more in proliferating cells than in post-mitotic cells such as neurons. We recently found that KLFs regulate intrinsic axon growth ability in central nervous system (CNS) neurons including retinal ganglion cells, and hippocampal and cortical neurons. With at least 15 of 17 KLF family members expressed in neurons and at least 5 structurally unique subfamilies, it is important to determine how this complex family functions in neurons to regulate the intricate genetic programs of axon growth and regeneration. By characterizing the molecular mechanisms of the KLF family in the nervous system, including binding partners and gene targets, and comparing them to defined mechanisms defined outside the nervous system, we may better understand how KLFs regulate neurite growth and axon regeneration.
引用
收藏
页码:1418 / 1421
页数:4
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