Functions to regulate alternative splicing in neurons by binding pre-mRNA in a sequence-specific manner to activate exon inclusion or exclusion. It binds specifically to the sequences 5'-YCAY-3' and regulates splicing in only a subset of regulated exons (PubMed:14615540). Binding to an exonic 5'-YCAY-3' cluster changes the protein complexes assembled on pre-mRNA, blocking U1 snRNP binding and exon inclusion, whereas binding to an intronic 5'-YCAY-3' cluster enhances spliceosome assembly and exon inclusion (PubMed:16041372). With NOVA1, they perform unique biological functions in different brain areas and cell types. Uniquely regulates alternative splicing events of a series of axon guidance related genes during cortical development, being essential for central nervous system development by regulating neural networks wiring (PubMed:27223325, PubMed:16041372). Regulates differentially alternative splicing on the same transcripts expressed in different neurons. This includes functional differences in transcripts expressed in cortical and cerebellar excitatory versus inhibitory neurons where is required for, respectively, development of laminar structure and motor coordination and synapse formation. Also the regulation the regulation of intron retention can sequester the trans-acting splicing factor PTBP2, acting as a variable cis-acting scaffolding platform for PTBP2 across various natural conditions (PubMed:30638744). Interacts with PTBP2; the interaction is direct. Expressed in brain cortex (PubMed:27223325). Expression is enriched in excitatory neuronal-linage (PubMed:30638744). Expression level is progressively up-regulated during neural differentiation from neural progenitor cells at 12.5 dpc to 18.5 dpc. The third KH domain (KH3) recognizes specifically 5'-YCAY-3'. Knockouts are born indistinguishable from littermates but failed to thrive, demonstrating progressive motor dysfunction and overt motor weakness, and they die an average of 14-18 days after birth. They have agenesis of the corpus callosum, and axonal outgrowth defects specific to ventral motoneuron axons and efferent innervation of the cochlea (PubMed:27223325). Conditional knockouts in excitatory neurons die between three and four weeks old and show disorganized cortical and hippocampal CA1 and CA3 laminar structure. Conditional knockouts in inhibitory neurons show no neuronal migration or position abnormality. They display reduced thickness of CA1 stratum lacunosum-moleculare (SLM) and dentate gyrus molecular layer (PubMed:30638744). Conditional knockouts in Purkinje cells have progressive motor discoordination and cerebellar atrophy. They show a marked defect in dendritic morphology, Purkinje cells degeneration, loss of synaptic layer thickness accompanied by neuritic swelling and reduced spine density (PubMed:30638744).