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Results show an essential role of NumbL during Xenopus primary neurogenesis and provide evidence for a Notch-independent function of NumbL.
NumbL can act as an independent tumor suppressor inhibiting the Notch pathway and regulating the cancer stem cell pool
let-7c inhibits Notch and progression markers but up-regulates Numbl in pancreatic cancer treated with quercetin
investigations revealed that NUMB and NUMBL interacted with small GTPase Rab7 to transition ERBB2 from early to late endosome for degradation.
These findings highlight the importance of Numb and Numbl in the control of myoepithelial cell fate determination, epithelial identity, and lactogenesis
Numb/Numbl control VEGF receptor endocytosis, signaling, and recycling in endothelial cells, which promotes the angiogenic growth of blood vessels.
Numbl might be involved in the inhibition of growth, proliferation, and invasion of 95-D lung cancer cells.
Numbl-Klf4 signaling is critical to maintain multiple nodes of metastatic progression, including persistence of cancer-initiating cells.
data suggest that Numbl regulates glioma cell migration and invasion by abrogating TRAF5-induced activation of NF-KappaB
NUMBL interacts with TRAF6 and promotes the degradation of TRAF6 in vivo, leading to the inhibition of NF-kappaB signaling pathway.
Both gene sequence alterations and amplifications of LNX1 and Numbl are present in a subset of human gliomas.
our data suggest that NUMBL and TAK1 are reciprocally regulated and that NUMBL acts as an endogenous regulator of NF-kappaB signaling and osteoclastogenesis by targeting the TAK1-TRAF6-NEMO axis.
findings demonstrate that Nb and Nbl are intrinsic factors crucial for the renewal of CPCs in the PA2 and that the PA2 serves as a microenvironment for their expansion
By ablating Numb and Numbl in different cardiac populations followed by lineage tracing, we determined that Numb and Numbl in the second heart field are required for outflow tract (OFT) and atrioventricular septation and OFT alignment.
Concomitant but not separate ablation of Numb and Numblike in the developing heart leads to increased Notch2 activity along with hypertrabeculation, reduced compaction, and ventricular septum defects.
Numbl is a physiologically relevant target of miR-34a in neural progenitor cells, allowing for enhanced Notch signaling and inhibition of neuronal differentiation.
the data demonstrate that Numb and Numblike have evolved to acquire at least partially distinct functions.
mouse numb and numblike play redundant but critical roles in maintaining neural progenitor cells during embryogenesis, by allowing their progenies to choose progenitor over neuronal fates
Numblike plays an essential role in the control of cortical morphogenesis, a process requiring precise regulation of neural progenitor cell proliferation, differentiation, and apoptosis.
evidence for previously unidentified functions of Numb and Numblike in sensory axon arborization by regulating Notch1 via the endocytic-lysosomal pathways
Removal of Numb/Numblike from postnatal SVZ progenitors and ependymal cells resulted in severe damage to brain lateral ventricle integrity and identified roles for Numb/Numblike in regulating ependymal wall integrity and SVZ neuroblast survival.
Both numb and numblike are dispensable for hemopoesis and lymphopoiesis in the adult mouse, despite their proposed role in neuronal stem cell development.
Numbl is required for the tissue architecture of neurogenic niches and the cerebral cortex
Plays a role in the process of neurogenesis. 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. Not required for the proliferation of neural progenitor cells before the onset of embryonic neurogenesis. Also required postnatally in the subventricular zone (SVZ) neurogenesis by regulating SVZ neuroblasts survival and ependymal wall integrity. Negative regulator of NF-kappa-B signaling pathway. The inhibition of NF- kappa-B activation is mediated at least in part, by preventing MAP3K7IP2 to interact with polyubiquitin chains of TRAF6 and RIPK1 and by stimulating the 'Lys-48'-linked polyubiquitination and degradation of TRAF6 in cortical neurons.
, numb-like protein
, numb-related protein