Pathway: CHL1 interactions
Reactions in pathway: CHL1 interactions :
CHL1 interactions
Close homolog of L1 (CHL1) is a member of the L1 family of cell adhesion molecules expressed by subpopulations of neurons and glia in the central and peripheral nervous system. CHL1 like L1 promotes neuron survival and neurite outgrowth. CHL1 shares the basic structural arrangement of L1 family members yet in contrast to all the members it is not capable of forming homophilic adhesion. The second Ig-like domain of CHL1 contains the integrin interaction motif RGD rather than with in the sixth Ig-like domain as in L1, however the sixth Ig-like domain of CHL1 has another potential integrin binding motif DGEA. CHL1 binds NP-1 via the Ig1 sequence FASNRL to mdediate repulsive axon guidance to Sema3A. CHL1 is the only L1 family member with an altered sequence (FIGAY) in the ankyrin-binding domain, and it lacks the sorting/endocytosis RSLE motif, which is characteristic of other L1 family members.
Neurogenesis is the process by which neural stem cells give rise to neurons, and occurs both during embryonic and perinatal development as well as in specific brain lineages during adult life (reviewed in Gotz and Huttner, 2005; Yao et al, 2016; Kriegstein and Alvarez-Buylla, 2009).
As early steps towards capturing the array of processes by which a fertilized egg gives rise to the diverse tissues of the body, examples of several processes have been annotated. Aspects of processes involved in most developmental processes, transcriptional regulation of pluripotent stem cells, gastrulation, and activation of HOX genes during differentiation are annotated. More specialized processes include nervous system development , aspects of the roles of cell adhesion molecules in axonal guidance and myogenesis, transcriptional regulation in pancreatic beta cell, cardiogenesis, transcriptional regulation of granulopoeisis, transcriptional regulation of testis differentiation, transcriptional regulation of white adipocyte differentiation, and molecular events of "nodal" signaling, LGI-ADAM interactions, and keratinization.