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Validated All-in-One™ qPCR Primer for NTN1(NM_004822.2) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
Netrin is included in a family of laminin-related secreted proteins. The function of this gene has not yet been defined; however, netrin is thought to be involved in axon guidance and cell migration during development. Mutations and loss of expression of netrin suggest that variation in netrin may be involved in cancer development. [provided by RefSeq].
Gene References into function
- Netrin binds discrete subdomains of DCC and UNC5 and mediates interactions between DCC and heparin
- Data demonstrate that alpha6beta4 integrin mediates pancreatic epithelial cell adhesion to Netrin-1, whereas recruitment of alpha6beta4 and alpha3beta1 regulate the migration of putative pancreatic progenitors on Netrin-1.
- DCC/netrin-1 signaling may commit cells to the transition of endometrial gland architecture or function from a proliferating to a secretory phase.
- Binding of netrin-1 to its receptors inhibits tumour suppressor p53-dependent apoptosis (review)
- Netrin binds through multiple domains to both DCC and Unc5c.
- Raft localization of DCC is required for netrin-1-induced DCC-dependent ERK activation, and netrin-1-mediated axon outgrowth requires lipid raft integrity.
- Review suggests possible roles of netrin-1 in nervous system development, neovascularisation, adhesion and tumorigenesis.
- Ligand-mediated down-regulation of deleted in colorectal cancer might participate in loss of netrin-responsiveness in developing nervous system.
- Endothelial expression of netrin-1 may inhibit basal cell migration into tissues and its down-regulation with the onset of sepsis/inflammation may facilitate leukocyte recruitment.
- Both deleted in colorectal cancer (DCC) and neogenin become tyrosine phosphorylated in cortical neurons in response to netrin-1.
- Netrin-1 expression observed in a large fraction of human metastatic breast tumors confers a selective advantage for tumor cell survival.
- Although cAMP can alter response of axons to netrin-1, we conclude that netrin-1 does not alter cAMP levels in axons attracted by this cue and that soluble adenyl cyclase is not required for axon attraction to netrin-1.
- Data show that Netrin-1 expressing cells inhibited angiogenic sprouting of unc5b expressing blood vessels, but had no pro-angiogenic activity at any stage of development examined.
- PIKE-L acts as a downstream survival effector for netrin-1 through UNC5B in the nervous system
- Netrin 1, through its receptor DCC, inhibits RhoA in embryonic spinal commissural neurons.
- NF-kappaB activation that occurs in response to inflammation confers a selective advantage for tumor development through NF-kappaB-mediated netrin-1 up-regulation
- netrin-1 is not only an attractive cue for developing commissural axons but also promotes their survival
- the transcriptionally active TAp73alpha tumor suppressor is implicated in the apoptosis induced by netrin-1 in a p53-independent and DCC/ubiquitin-proteasome dependent manner.
- HIF-1alpha-dependent induction of netrin-1 attenuates hypoxia-elicited inflammation at mucosal surfaces
- High levels of netrin-1 found in 43 of the 92 NSCLC tumor samples. Interference with netrin-1 in human lung cancer cell lines was associated with UNC5H-mediated cell death in vitro and with tumor growth inhibition and/or regression in xenografted mice.
