Abstract: A method of enhancing the myelinating activity of oligodendrocytes or progenitors thereof is disclosed. The method comprises contacting the oligodendrocytes or the progenitors with an agent that binds to G Protein-Coupled Receptor 37 (GPR37) or a polynucleotide encoding same or an upstream activator of the GPR37 so as to up-regulate an amount and/or activity of Extracellular Signal-Regulated Kinase 1/2 (ERK1/2) in the oligodendrocytes or the progenitors.

Abstract: The invention provides polypeptides comprising isolated domains of Necl proteins, particularly of Necl4, that mediate axon-glia adhesion required for myelination. The invention further provides pharmaceutical compositions comprising as the active ingredient a polypeptide comprising an isolated Necl4 domain, or a polynucleotide encoding a polypeptide comprising an isolated Necl4 domain. Further provided are antibodies directed against isolated Necl domains, siRNA capable of down regulating Necl4 expression, and methods for treating neurological disorders which are associated with aberrant myelination.

Abstract: The present invention relates to pharmaceutical compositions comprising gliomedin and active fragments thereof, polynucleotides encoding gliomedin, host cells expressing gliomedin, antibodies to gliomedin and small interfering RNA (siRNA) molecules that down regulate the expression of gliomedin and methods of using same. The present invention also provides methods of treating and diagnosing neurological disorders using the pharmaceutical compositions and antibodies of the invention.

Abstract: The 190 kDa Contactin ASsociated PRotein (CASPR/p190) is identified and is implicated as the bridge between contactin and intracellular second messenger systems for the signal caused by the binding of the carboxy anhydrase domain of RPTP&bgr; to contactin and resulting in neurite growth, differentiation or survival. Mammalian CASPR/p190 cDNAs and proteins are described, including those from human and rat. In addition, particular domains of the proteins are characterized.

Abstract: The present invention relates to Alp polypeptides, nucleic acids encoding such polypeptides, cells, tissues and animals containing such nucleic acids, antibodies to such polypeptides, assays utilizing such polypeptides, and methods relating to all of the foregoing. Methods for treatment, diagnosis, and screening are provided for Alp related diseases or conditions characterized by an abnormal interaction between an Alp polypeptide and an Alp binding partner.

Abstract: The 190 kDa Contactin ASsociated PRotein (CASPR/p190) is identified and is implicated as the bridge between contactin and intracellular second messenger systems for the signal caused by the binding of the carboxy anhydrase domain of RPTP&bgr; to contactin and resulting in neurite growth, differentiation or survival. Mammalian CASPR/p190 cDNAs and proteins are described, including those from human and rat. In addition, particular domains of the proteins are characterized.

Abstract: The present invention relates to Alp polypeptides, nucleic acids encoding such polypeptides, cells, tissues and animals containing such nucleic acids, antibodies to such polypeptides, assays utilizing such polypeptides, and methods relating to all of the foregoing. Methods for treatment, diagnosis, and screening are provided for Alp related diseases or conditions characterized by an abnormal interaction between an Alp polypeptide and an Alp binding partner.

Abstract: The extracellular domain of RPTP.beta. is the ligand for contactin and its binding results in neurite growth and differentiation. The invention encompasses compounds that mimic, enhance, or suppress the effects of the ligand for contactin, assays for the identification of such compounds, and the use of such compounds to treat neurologic diseases including those characterized by insufficient, aberrant, or excessive neurite growth, differentiation or survival.