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The protein encoded by PSPN is a neurotrophic factor, belonging to the GDNF family. De plus, nous expédions Persephin Anticorps (47) et Persephin Protéines (18) et beaucoup plus de produits pour cette protéine.
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Results suggested that PSPN is a possible key regulator of oral squamous cell carcinoma (OSCC) progression via PSPN-RET (Montrer RET Kits ELISA)-mitogen-activated protein kinase (Montrer MAPK1 Kits ELISA) activation and that PSPN overexpression may have diagnostic potential for OSCC.
Results identify persephin, a GDNF (Montrer GDNF Kits ELISA) family member, as a novel ligand for GFRalpha1 (Montrer GFRA1 Kits ELISA)/RET (Montrer RET Kits ELISA) receptor complex.
Persephin/GFRalpha4 is unable to recruit RET (Montrer RET Kits ELISA) protein into lipid rafts.
The results obtained suggest the involvement of NTN (Montrer NRTN Kits ELISA), PSP (Montrer MSMB Kits ELISA), and ART in processes subserving both the organization of this cortical region during development and the functional activity and maintenance of the mature human hippocampal neurons.
Mice lacking Pspn by homologous recombination show normal development and behavior, but are hypersensitive to cerebral ischemia.
TGF-beta (Montrer TGFB1 Kits ELISA) with neurturin (Montrer NRTN Kits ELISA) and persephin are required for the induction of dopaminergic neurons, whereas GDNF (Montrer GDNF Kits ELISA) is required for regulating and/or maintaining a differentiated neuronal phenotype
The protein encoded by this gene is a neurotrophic factor, belonging to the GDNF family. Neurotrophic factors are important for the proper development and maintenance of the nervous system. These factors promote neuronal survival and can prevent the neuronal degeneration associated with injury, toxin exposure, or neurodegenerative disease. The encoded protein has amino acid similarity to its other family members, glial cell line-derived neurotrophic factor and neurturin. This gene product promotes the survival of ventral midbrain dopaminergic neurons in culture and prevents their degeneration after 6-hydroxydopamine treatment in vivo.