The Role of SliTrk5 in Central Nervous System

SLIT and NTRK-like protein-5 (SliTrk5) is one of the six members of SliTrk protein family, which is widely expressed in the central nervous system (CNS), regulating and participating in many essential steps of central nervous system development, including axon and dendritic growth, neuron differenti...

Full description

Saved in:
Bibliographic Details
Published inBioMed research international Vol. 2022; pp. 1 - 10
Main Authors Liu, Yan, Zhang, Linming, Mei, Rong, Ai, Mingda, Pang, Ruijing, Xia, Di, Chen, Ling, Zhong, Lianmei
Format Journal Article
LanguageEnglish
Published New York Hindawi 14.07.2022
John Wiley & Sons, Inc
Hindawi Limited
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:SLIT and NTRK-like protein-5 (SliTrk5) is one of the six members of SliTrk protein family, which is widely expressed in the central nervous system (CNS), regulating and participating in many essential steps of central nervous system development, including axon and dendritic growth, neuron differentiation, and synaptogenesis. SliTrk5, as a neuron transmembrane protein, contains two important conservative domains consisting of leucine repeats (LRRs) located at the amino terminal in the extracellular region and tyrosine residues (Tyr) located at the carboxyl terminal in the intracellular domains. These special structures make SliTrk5 play an important role in the pathological process of the CNS. A large number of studies have shown that SliTrk5 may be involved in the pathogenesis of CNS diseases, such as obsessive-compulsive-disorder (OCD), attention deficit/hyperactivity disorder (ADHD), glioma, autism spectrum disorders (ASDs), and Parkinson’s disease (PD). Targeting SliTrk5 is expected to become a new target for the treatment of CNS diseases, promoting the functional recovery of CNS. The purpose of this article is to review the current research progression of the role of SliTrk5 in CNS and its potential mechanisms in CNS diseases.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-3
content type line 23
ObjectType-Review-1
Academic Editor: Immacolata Castellano
ISSN:2314-6133
2314-6141
DOI:10.1155/2022/4678026