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anti-Human Neurotrophin 4 Antikörper:
anti-Rat (Rattus) Neurotrophin 4 Antikörper:
anti-Mouse (Murine) Neurotrophin 4 Antikörper:
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Human Polyclonal Neurotrophin 4 Primary Antibody für ELISA, WB - ABIN449725
Ghinelli, Johansson, Ríos, Chen, Zoukhri, Hodges, Dartt: Presence and localization of neurotrophins and neurotrophin receptors in rat lacrimal gland. in Investigative ophthalmology & visual science 2003
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Polyclonal Neurotrophin 4 Primary Antibody für ELISA, WB - ABIN539804
Nalbandian, Pang, Rennert, Chan, Ravindranath, Djakiew: A novel function of differentiation revealed by cDNA microarray profiling of p75NTR-regulated gene expression. in Differentiation; research in biological diversity 2005
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Cow (Bovine) Polyclonal Neurotrophin 4 Primary Antibody für WB - ABIN2774156
Mercader, Saus, Agüera, Bayés, Boni, Carreras, Cellini, de Cid, Dierssen, Escaramís, Fernández-Aranda, Forcano, Gallego, González, Gorwood, Hebebrand, Hinney, Nacmias, Puig, Ribasés, Ricca, Romo, Sorbi, Versini, Gratacòs, Estivill: Association of NTRK3 and its interaction with NGF suggest an altered cross-regulation of the neurotrophin signaling pathway in eating disorders. in Human molecular genetics 2008
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.
Elevated intra-amniotic levels of docosahexaenoic acid and arachidonic acid in the mid-trimester are correlated with increased NT4 concentrations.
No differences in plasma BDNF, NGF, NT3, NT4 and GDNF were found between autism spectrum disorders and control.
Patients with mastocytosis featured elevated serum levels of NGF, NT-3, and NT-4. TrkA, TrkB, and TrkC expression was also elevated.
The NTF4 variants p.Gly157Ala and p.Ala182Val have been shown to be functional mutations, occurring in 2 of a total of 720 Chinese primary open-angle glaucoma patients.
Studies indicate neurotrophin family comprises nerve growth factor, brain-derived neurotrophic factor, neurotrophin-3 and neurotrophin-4 , and Zn(2+) and Cu(2+) interactions with them and modulate their activities through conformational changes.
NT-4/5 expression is associated with atrophy of the brain-parenchymal fraction measured by magnetic resonance imaging methods in patients with relapsing-remitting multiple sclerosis.
Suggest that a dysregulated TrkB/NT4/5 axis may contribute to several of the pathological lesions associated with pulmonary fibrosis, including type 2 alveolar cell hyperplasia and the proliferation of fibroblasts.
neurotrophin 4 contributes to breast cancer cell survival and can serve as prospective target to inhibit tumor growth
In vitro follicular assembly is significantly increased in fetal ovaries cultured with NT-4.
Identification of a single mutation in our study suggests that NTF4 mutations are a rare cause of primary open-angle glaucoma (0.6%, 95%CI 0.02%-3.16%) in Chinese people.
present data indicate a lack of involvement of variations in NTF4, VAV2, and VAV3 with glaucoma pathogenesis in an Indian population.
Expression of human NTF4 was unchanged during gestation in the developping ovary.
No evidence of association of heterozygous NTF4 mutations in patients with primary open-angle glaucoma.
The gene expression of this protein was studied in the developing human tooth.
Data suggest that activation of bronchial eosinophils by neurotrophins (nerve growth factor, brain-derived neurotrophic factor, neurotrophins-3 and -4) might play a role in the regulation of eosinophilic inflammation in allergic asthma.
A mechanism to understand the defect associated with variant BDNF and provide a framework two ligands for BDNF and NT-4.
Re-expression of the p75NTR appears to partially reverse de-differentiation of prostate cancer cells by up-regulating the expression of CRABPI for localized sequestration of retinoids.
Results revealed the expression of NT-4/5 mainly in oocytes and, in a minority of samples, also in the granulosa cells (GCs).
These novel data demonstrate that neurotrophins influence ASM [Ca(2+)](i) and force regulation and suggest a potential role for neurotrophins in airway diseases
This study provided evidence that NT-4 protein was presented in the mature bull spermatozoa and can influence the mitochondrial activity of bovine spermatozoa through TrkB tyrosine kinase-dependent pathways.
Neurotrophin 4 may have a role in regulating the function of bovine oviducts by interacting with gonadotrophins.
mast cell degranulation and NT4 release serve as upstream events that ultimately trigger long-lasting changes in airway smooth muscle innervation and function following early life insults. These findings suggest that blockade of mast cell degranulation may be a preventative strategy for young children at high risk of asthma.
BDNF and NT4 play interchangeable roles in gustatory development.
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.
during early embryonic development, NT-4 produced in the ganglion and along the projection pathway inhibits cell death through an activated caspase-3 independent mechanism
The results of the present study demonstrate the post-transcriptional up-regulation of the Cav3.2 T-current through TrkB activation and identify NT-4 as a target-derived factor that regulates the mechanosensitive function of D-hair neurons.
the enhancing effects of treadmill training on axon regeneration include NT-4 5 in the proximal stump.
Findings indicate that NT4 functions at early embryonic stages and is derived from different sources than Bdnf.
Data show that gustatory neurons are equally dependent on BDNF and NT-4 expression for survival, regardless of what peripheral target they innervate, but taste buds are more sensitive to BDNF than NT-4 removal.
NT-4, alone or when co-expressed with brain-derived neurotrophic factor, is processed within and secreted by the constitutive secretory pathway
results suggest that the NT-4 gene knock-in, probably involving increased intestinal intraganglionic laminar ending innervation, altered short-term feeding, in particular by enhancing satiation and sensitivity to CCK.
NT-4 is not implicated in the development of Meissner corpuscles in murine glabrous skin.
Requirement for NT-4/5 from within the pathway used by regenerating axons for the successful growth of those axons in peripheral nerves.
Nt-4/5 gene depletion causes a delay in formation and maturation of the periodontal Ruffini endings by inhibiting the growth of the periodontal nerves at an early stage.
Epithelial overexpression of NT4 produces distinct gustatory axon morphologies that disrupt initial targeting.
Moreover, on high-fat access days the alternating NT-4 mutants significantly increased caloric intake by 9% compared to alternating wild types.
These results suggest that post-traumatic increases in endogenous NT-4/5 may be part of an adaptive neuroprotective response in the injured brain, and that administration of this neurotrophic factor may be useful as a therapeutic strategy following TBI.
NT4-OE mice had increased innervation to the skin but no increase in sensory neuron number. NT4 overexpression also enhanced hair follicle innervation and the size and density of innervation to Meissner corpuscles.
Findings indicate that the nt-4/5-depletion causes a delay in the regeneration of the periodontal Ruffini endings, but the delay is shortened by an exogenous administration of NT-4/5.
These results support the hypothesis that NT-4KO mice have deficits in macronutrient feedback from the gastrointestinal tract.
This gene is a member of a family of neurotrophic factors, neurotrophins, that control survival and differentiation of mammalian neurons. The expression of this gene is ubiquitous and less influenced by environmental signals. While knock-outs of other neurotrophins including nerve growth factor, brain-derived neurotrophic factor, and neurotrophin 3 prove lethal during early postnatal development, NTF5-deficient mice only show minor cellular deficits and develop normally to adulthood.
neurotrophin 5 (neurotrophin 4/5)
, neurotrophic factor 4
, neurotrophic factor 5
, neutrophic factor 4
, Neurotrophin 5 (neurotrophin 4/5)
, neurotrophin 4