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NT-3 has been shown to be both an osteogenic and angiogenic factor, and can also enhance expression of the key osteogenic factor, BMP-2, as well as the major angiogenic factor, VEGF, to promote bone formation, vascularization, and bone healing
High expression of NT-3 is associated with glioblastoma.
Meta-analysis found the levels of both NT-3 and NT-4/5 (show NTF4 Proteins) were significantly increased in bipolar disorder patients. Through subgroup analysis, this increase persisted only in patients in depressed state, but not in manic or euthymic state. In addition, we found the differences in NT-3 and NT-4/5 (show NTF4 Proteins) were significantly associated with the duration of illness, but not by the mean age or female proportion.
NT3 upregulates cellular proliferation, extracellular matrix protein production, and collagen deposition in human aortic valve interstitial cells through the Trk (show NTRK1 Proteins)-Akt (show AKT1 Proteins)-cyclin D1 (show CCND1 Proteins) cascade.
The analysis of covariance (ANCOVA) indicated that the mean serum GDNF and NTF3 levels of ADHD patients were significantly higher than that of controls. However, serum BDNF (show BDNF Proteins) and NGF (show NGFB Proteins) levels did not show any significant differences between groups. These results suggest that elevated serum GDNF and NTF3 levels may be related to ADHD in children.
All patients had serum neurotrophin (show BDNF Proteins) (NT-3, BDNF (show BDNF Proteins), NGF (show NGFB Proteins)) concentrations determined.
There were no differences in neurotrophin (show BDNF Proteins) levels between patients with schizophrenia and controls. We found lower BDNF (show BDNF Proteins) and higher NT-3 serum levels in depressed patients with schizophrenia.
The results suggest a gene dose-association between the A allele of rs6332 and the onset of AD in varepsilon4 non-carriers and the NTF-3 rs6489630 polymorphism being a relevant risk factor for AD in patients lacking the ApoE (show APOE Proteins)-varepsilon4 allele in this Chinese sample.
Survival, differentiation, and neuroprotective mechanisms of human stem cells complexed with neurotrophin-3-releasing pharmacologically active microcarriers in an ex vivo model of Parkinson's disease.
No differences in plasma BDNF, NGF, NT3, NT4 and GDNF were found between autism spectrum disorders and control.
By immunohistochemistry, the localization of Neurotrophinss has been observed mainly in Purkinje cells; TrkA (show NTRK1 Proteins) and TrkB (show NTRK2 Proteins)-receptors in cells and fibers of granular and molecular layers. TrkC (show NTRK3 Proteins) was faintly detected
Deletion of a kinesin I motor unmasks a mechanism of homeostatic axon-branching control by neurotrophin-3.
Here the authors demonstrate a novel function for p75(NTR (show NGFR Proteins)) in regulating proper cell cycle exit of neuronal progenitors in the developing rat and mouse external granule layer, which is stimulated by proneurotrophin-3. In the absence of p75(NTR (show NGFR Proteins)), cerebellar granule cell progenitors continue to proliferate beyond their normal period, resulting in a larger cerebellum that persists into adulthood, with consequent motor defici
NT-3-transduced bone marrow- derived neural stem cells differentiated into a greater number of cholinergic neurons.
Ntf3, but not Bdnf (show BDNF Proteins), expression by postnatal supporting cells regulates cochlear function.
Study shows that dissociated cochlear nucleus neurons can be stimulated by neurotrophic factors BDNF (show BDNF Proteins), NT-3, and FGF2 (show FGF2 Proteins)
Data show that acteoside can up-regulate the expression of brain neurotrophin-3 (NT-3) in D-galactose combined with aluminum trichloride treated mice.
CAPS2 (show CADPS2 Proteins) plays an important role in subcellular locality (axonal vs. somato (show SSTR5 Proteins)-dendritic) of enhanced BDNF (show BDNF Proteins) and NT-3 release, which is indispensable for proper development of postnatal cerebellum.
Uptake of NT-3 from irrigating vasculature and cerebrospinal fluid induces the rapid phosphorylation of endothelial nitric oxide
Loss of Ntf3, by contrast, causes an increase in layer VI neurons but does not rescue the Sip1 mutant phenotype, implying that other parallel pathways also control the timing of progenitor cell fate switch.
it was PDGF, NT-3 and IGF-2 in combination that conducted the transdifferentiation
This study aimed to examine the roles of mature neurotrophin-3 (NT3), pro-NT3 and p75 neurotrophin receptor (P75 (show NGFR Proteins)(NTR (show NGFR Proteins))) in photoreceptor degeneration
The protein encoded by this gene is a member of the neurotrophin family, that controls survival and differentiation of mammalian neurons. This protein is closely related to both nerve growth factor and brain-derived neurotrophic factor. It may be involved in the maintenance of the adult nervous system, and may affect development of neurons in the embryo when it is expressed in human placenta. NTF3-deficient mice generated by gene targeting display severe movement defects of the limbs. The mature peptide of this protein is identical in all mammals examined including human, pig, rat and mouse.
, nerve growth factor 2
, neurotrophic factor
, neurotrophin 3 - pending
, neurotrophin 3
, neurotrophin-3 (HDNF/NT-3)