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activating Nrf2 antioxidant pathway suppresses Epithelial mesenchymal transition during pulmonary fibrosis via inhibiting the abnormal expression of Numb.
The combination of the protein microarray screening with computer-aided prediction produced the most expansive interactome for Numb to date.
The depalmitoylating enzyme acyl-protein thioesterase 1 (APT1) directs the asymmetric localization of Numb and beta-catenin in MDA-MB-231 triple receptor-negative breast cancer cells.
NUMB overexpression inhibited cell proliferation, migration and invasion in colorectal cancer cells.
Study found that NUMB protein was significantly upregulated in esophageal squamous cell carcinoma (ESCC) tissues as compared with paired non-tumor samples. This rise in NUMB protein expression was an independent indicator of a poor prognosis in ESCC patients.
Phosphorylated form of Numb by Plk1 is associated with drug-resistant Osteosarcoma.
The Numb-Mdm2 interaction represents a fuzzy complex mediated by a short Numb sequence encompassing its alternatively spliced exon 3 (Ex3), which is necessary and sufficient to inhibit Mdm2 and prevent p53 degradation.
High NUMB expression is associated with endometriosis.
The results provide new evidence of Numb and Gli1 on the clinical characteristics of Malignant pleural mesothelioma, which may be helpful in clinical diagnosis and targeted therapy. Further research with larger sample size is needed
Numb is associated with modulation of Notch-driven epithelial-mesenchymal transition.
Numb(-/low) prostate cancer cells were smaller and quiescent, preferentially expressed Notch and Hedgehog downstream and stem-cell-associated genes, and associated with a greater resistance to androgen-deprivation therapy
MAP17 overexpression activates Notch pathway by sequestering NUMB. High levels of MAP17 correlated with tumorsphere formation and Notch and Stem gene transcription. Its direct modification causes direct alteration of tumorsphere number and Notch and Stem pathway transcription
NUMB has a role in negatively regulating the epithelial-mesenchymal transition of triple-negative breast cancer by antagonizing Notch signaling
In the present study, we identified that the adaptor protein Numb, which is demonstrated to be a novel binding partner of NEDD4-1, plays important roles in controlling PTEN ubiquitination through regulating NEDD4-1 activity and the association between PTEN and NEDD4-1.
Numb expression is not associated with favorable prognosis in small cell lung cancer.
Data suggest that over-expression of NUMB has anti-cancer effects to prostatic cancer cells; these studies included experiments both in vitro and in vivo (xenograft experiments in nude mice).
Using patient-derived xenografts, the study shows that expansion of the cancer stem cells pool, due to altered self-renewing divisions, is also a feature of Numb-deficient human breast cancers .
Numb binds to another docking regulator, Mon1b, and is required for the recruitment of cytosolic Mon1b to the early endosomes membrane.
this study identified a novel molecular determinant of breast cancer progression, uncovering a potential oncogenic role for the NUMB6 protein in cancer cell migration and invasion, coupled to the maintenance of mesenchymal-like cells.
Low NUMB expression is associated with pancreatic cancer.
beta1-integrin is a key mediator of the Numb pathway in cardiac progenitor cell maintenance.
Given the apparent absence of major NUMB dysfunction in LNX null animals
Data suggest that Numb acts as a Notch antagonist by controlling intracellular destination and stability of the Notch ligand Delta-like 4 (DLL4) through a post-endocytic sorting process; Numb negatively controls DLL4 plasma membrane recycling through well-documented recycling regulator protein AP1.
NUMB is necessary for establishing polarity in coelomic epithelium cells.
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
RBM4 depletion reduced the expression of the proneural gene Mash1, and such reduction was reversed by an RBM4-induced Numb isoform containing exon 3 but lacking exon 9. RBM4 was also essential for neurite outgrowth from cortical neurons in vitro. Neurite outgrowth defects of RBM4-depleted neurons were rescued by RBM4-induced exon 9-lacking Numb isoforms. RBM4 modulates exon selection of Numb.
role in the mediation of TCR degradation
miR-34a directly suppresses Numb in early-stage colon cancer stem cells (CCSCs), forming an incoherent feedforward loop (IFFL) targeting Notch to separate stem and non-stem cell fates robustly.
Novel Role of Numb as A Regulator of Pro-inflammatory Cytokine Production in Macrophages in Response to Toll-like Receptor 4.
Loss of Numb induces a p53-dependent senescence following skeletal muscle injury.
Numb is a regulator for constitutive expression and dynamic transport of mGlu1.
we observed a glial reaction and an activity-dependent modification of Shh, Noggin, and Numb proteins. we found that Shh and Noggin could affect motor performance and that these proteins could be associated with both TDP-43 and Numb
Numb ensures the asymmetric outcome of self-renewing divisions by partitioning into the progeny that retains the stem cell identity, where it sustains high p53 activity.
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
Numb/Numbl control VEGF receptor endocytosis, signaling, and recycling in endothelial cells, which promotes the angiogenic growth of blood vessels.
Nuclear localization of Numb in early thymocyte precursors favors p53 nuclear stabilization, whereas pre-T-cell receptor-dependent Numb nuclear exclusion promotes the p53 downmodulation essential for further differentiation.
Numb promotes the trafficking of Cnga1 in rod photoreceptor cilia.
Numb and Numblike are involved in zebrafish erythroid differentiation during primitive hematopoiesis
The numb isoform is localized in the cell membrane in dividing neuroepithelial cells during neurulation.
The protein encoded by this gene plays a role in the determination of cell fates during development. The encoded protein, whose degradation is induced in a proteasome-dependent manner by MDM2, is a membrane-bound protein that has been shown to associate with EPS15, LNX1, and NOTCH1. Four transcript variants encoding different isoforms have been found for this gene.
, protein numb homolog
, numb gene homolog
, numb homolog