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anti-Human Neurotrophin 3 Antikörper:
anti-Mouse (Murine) Neurotrophin 3 Antikörper:
anti-Rat (Rattus) Neurotrophin 3 Antikörper:
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Cow (Bovine) Polyclonal Neurotrophin 3 Primary Antibody für ELISA - ABIN451691
Walz, Andreazza, Frey, Cacilhas, Ceresér, Cunha, Weyne, Stertz, Santin, Gonçalves, Kapczinski: Serum neurotrophin-3 is increased during manic and depressive episodes in bipolar disorder. in Neuroscience letters 2007
Human Polyclonal Neurotrophin 3 Primary Antibody für IF (p), IHC (p) - ABIN725645
Guo, Cui, Peng, Fang, Zuo, Deng, Wang, Wu, Chen, Deng: Dietary NiCl₂ causes G₂/M cell cycle arrest in the broiler's kidney. in Oncotarget 2015
Human Monoclonal Neurotrophin 3 Primary Antibody für IHC, WB - ABIN2727202
Louie, Chen, Coomes, Ji, Tsirka, Chen: Neurotrophin-3 modulates breast cancer cells and the microenvironment to promote the growth of breast cancer brain metastasis. in Oncogene 2013
Human Polyclonal Neurotrophin 3 Primary Antibody für IHC (p), WB - ABIN3043024
Guo, Zeng, Li, Huang, Liu, Li, Ding, Wu, Cai: Cotransplant of neural stem cells and NT-3 gene modified Schwann cells promote the recovery of transected spinal cord injury. in Spinal cord 2007
In patients with schizophrenia, serum levels of neurotrophin-3 are increased only if depressive symptoms are also present.
NTF3 is a novel target gene of POU3F2 and that the POU3F2/NTF3 pathway plays a role in the process of neuronal differentiation.
brain-derived neurotrophic factor (BDNF) and neurotrophin 3 (NT3) levels in post-mortem brain tissue from patients with depression compared to healthy individuals - a proof of concept study
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 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 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-Akt-cyclin D1 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 and NGF 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 (NT-3, BDNF, NGF) concentrations determined.
There were no differences in neurotrophin levels between patients with schizophrenia and controls. We found lower BDNF 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-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.
NT-3 expression was found in axons of olfactory bulb.
genetic variation in the NTF3 gene is related to susceptibility to emotional side effects in response to methylphenidate treatment in Korean children with ADHD.
NT-3 appears to promote growth of metastatic breast cancer cells in the brain
Patients with mastocytosis featured elevated serum levels of NGF, NT-3, and NT-4. TrkA, TrkB, and TrkC expression was also elevated.
NT-3 promoted motility, migration, invasion, soft-agar colony growth and cytoskeleton restructuring in TrkC-expressing U2OS cells
There was no association between the presence of rs11063714 and curve progression in adolescent idiopathic scoliosis in a 2117-person Japanese cohort.
Results suggested that an NT-3 polymorphism, rs6332, may significantly influence executive function, reflecting interference performances among patients with mild-stage AD.
By immunohistochemistry, the localization of Neurotrophinss has been observed mainly in Purkinje cells; TrkA and TrkB-receptors in cells and fibers of granular and molecular layers. TrkC was faintly detected
Deletion of a kinesin I motor unmasks a mechanism of homeostatic axon-branching control by neurotrophin-3.
NT-3 modulates both synaptic transmission and plasticity in the striatum; nonetheless, synaptic plasticity was modified by 3-nitropropionic acid treatment, where instead of producing striatal long-term depression (LTD), long-term potentiation (LTP) was obtained. Moreover, the administration of NT-3 in the recording bath restored the plasticity observed under control conditions (LTD) in this model of striatal degeneration.
studies for the first time have shown that NT-3 increases muscle fiber diameter in the neurogenic muscle through direct activation of mTOR pathway and that the fiber size increase is more prominent for fast twitch glycolytic fibers
that the NT3-TrkA complex uses Ras/MAPK and/or PI3K-AKT signaling to induce axon growth and inhibit axon branching along intermediate targets
Here the authors demonstrate a novel function for p75(NTR) 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), 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, expression by postnatal supporting cells regulates cochlear function.
Study shows that dissociated cochlear nucleus neurons can be stimulated by neurotrophic factors BDNF, NT-3, and FGF2
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 plays an important role in subcellular locality (axonal vs. somato-dendritic) of enhanced BDNF 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(NTR)) in photoreceptor degeneration
NT3 is involved in the laminar formation of the developing cerebral cortex through the intercellular MEK/ERK pathway.
This study demonistrated that NT-3(-/-) mutants had 65% fewer TG neurons than found in age-matched wild-type (WT) mice.
Although microstructural analysis did not reveal a decrease in the rate of decay of eating in smooth muscle-specific-NT-3(KO) mice, they ate continuously during the 30-min meal, whereas controls terminated feeding
Data indicate that BDNF, NT3 and NT4 trophic factors were detected in the conditioned medium of both wild-type and Friedreich's ataxia YG8 stem cells.
Data indicate that calcineurin regulates levels of STAT3 and neurotrophin dependence.
This study indicates that excessive NT-3 from astrocytes contributes to the abnormal neuronal dendritic development and that astrocytes could be a potential therapeutic target for Fragile X syndrome .
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)