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Results show an essential role of NumbL during Xenopus primary neurogenesis and provide evidence for a Notch (zeige NOTCH1 Proteine)-independent function of NumbL.
NumbL can act as an independent tumor suppressor inhibiting the Notch (zeige NOTCH1 Proteine) pathway and regulating the cancer stem cell pool
let-7c inhibits Notch (zeige NOTCH1 Proteine) and progression markers but up-regulates Numbl in pancreatic cancer treated with quercetin
investigations revealed that NUMB (zeige NUMB Proteine) and NUMBL interacted with small GTPase (zeige RACGAP1 Proteine) Rab7 (zeige RAB7B Proteine) to transition ERBB2 (zeige ERBB2 Proteine) from early to late endosome for degradation.
These findings highlight the importance of Numb (zeige NUMB Proteine) and Numbl in the control of myoepithelial cell fate determination, epithelial identity, and lactogenesis
Numb/Numbl control VEGF receptor (zeige FLT1 Proteine) 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 (zeige KLF4 Proteine) 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 (zeige TRAF5 Proteine)-induced activation of NF-KappaB (zeige NFKB1 Proteine)
NUMBL interacts with TRAF6 (zeige TRAF6 Proteine) and promotes the degradation of TRAF6 (zeige TRAF6 Proteine) in vivo, leading to the inhibition of NF-kappaB (zeige NFKB1 Proteine) signaling pathway.
Both gene sequence alterations and amplifications of LNX1 (zeige LNX1 Proteine) and Numbl are present in a subset of human gliomas.
investigations revealed that NUMB (zeige NUMB Proteine) and NUMBL interacted with small GTPase (zeige RACGAP1 Proteine) Rab7 (zeige RAB7A Proteine) to transition ERBB2 (zeige ERBB2 Proteine) from early to late endosome for degradation.
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 (zeige NUMB Proteine) and Numbl in different cardiac populations followed by lineage tracing, we determined that Numb (zeige NUMB Proteine) 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 (zeige NUMB Proteine) and Numblike in the developing heart leads to increased Notch2 (zeige NOTCH2 Proteine) activity along with hypertrabeculation, reduced compaction, and ventricular septum defects.
Numbl is a physiologically relevant target of miR (zeige MLXIP Proteine)-34a in neural progenitor cells, allowing for enhanced Notch (zeige NOTCH1 Proteine) signaling and inhibition of neuronal differentiation.
the data demonstrate that Numb (zeige NUMB Proteine) and Numblike have evolved to acquire at least partially distinct functions.
mouse numb (zeige NUMB Proteine) 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.
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