Regulates clathrin-mediated receptor endocytosis (By similarity). Plays a role in the process of neurogenesis (PubMed:10841580, PubMed:12410312, PubMed:15273690, PubMed:17174898). Required throughout embryonic neurogenesis to maintain neural progenitor cells, also called radial glial cells (RGCs), by allowing their daughter cells to choose progenitor over neuronal cell fate (PubMed:15273690, PubMed:12410312). Not required for the proliferation of neural progenitor cells before the onset of neurogenesis (PubMed:15273690, PubMed:12410312). Also involved postnatally in the subventricular zone (SVZ) neurogenesis by regulating SVZ neuroblasts survival and ependymal wall integrity (PubMed:17174898). May also mediate local repair of brain ventricular wall damage (PubMed:17174898). Interacts with SIAH1 (By similarity). Interacts with LNX (PubMed:9535908). Interacts with CDH1 (PubMed:17174898). Interacts with TFAP2A and TFAP2B (By similarity). Interacts with RALBP1 in a complex also containing EPN1 and TFAP2A during interphase and mitosis (By similarity). Interacts with AAK1 (By similarity). May interact with DUOXA1 (By similarity). Localizes to perinuclear endosomes in an AAK1-dependent manner. Expressed in subventricular zone (SVZ) neuroprogenitors and ependymal cells. Expressed in neural progenitors and neuron cells throughout the developing nervous system. Expressed in somites and throughout the neural tube from 8.5 dpc, onward. Phosphorylated on Ser-276 and Ser-295 by CaMK1. Ubiquitinated; mediated by SIAH1 and leading to its subsequent proteasomal degradation (By similarity) Isoform 1 and isoform 2 are ubiquitinated by LNX leading to their subsequent proteasomal degradation. Mutant animals exhibit severe defects in cranial neuronal tube closure and die around 11.5 dpc, but neurogenesis abnormalities are limited. Mice lacking both Numb and Numbl genes die around 9.5 dpc, with severe defects in somite and vasculature formation, neuronal tube closure and axial turning. Conditional mutants, with expression abrogated in neural progenitor cells from 8.5 dpc are viable, fertile and exhibit no obvious phenotypes. Conditional double-knockout (cdKO) mutants (Numb and Numbl genes), with expression abrogated in neural progenitor cells from 8.5 dpc (just before the onset of neurogenesis), display a loss of neuronal progenitor cells formation and an overexpression of neurons as neurogenesis progresses; cdKO mutants become necrotic at 12.5 dpc and die around this stage. Conditional double-knockout (cdKO) mutants (Numb and Numbl genes), with expression abrogated in neural progenitor cells from 10.5 dpc (just after the onset of neurogenesis), display a premature depletion of neural progenitor cells in the dorsal forebrain ventrical zone of the neocortex and in the hippocampal CA fields as neurogenesis progresses; cdKO mutants are viable and fertile, but showed a reduction in the thickness of the neocortex and the hippocampus and a enlargement of the lateral ventricles. Tamoxifen-inducible double-knockout (cdKO) mutants (Numb and Numbl genes), with expression abrogated postnatally in the subventricular zone (SVZ) neuroprogenitors and in ependymal cells, display a loss of SVZ neuroblasts and show a disorganized ependyma lacking both interdigitation junction between neighboring cells and increasing number of separated cells.