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- Table of Contents
Facts about Neudesin.
Its neurotrophic activity is exerted via MAPK1/ERK2, MAPK3/ERK1 and AKT1/AKT pathways. Neurotrophic activity is enhanced by binding to heme.
Human | |
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Gene Name: | NENF |
Uniprot: | Q9UMX5 |
Entrez: | 29937 |
Belongs to: |
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cytochrome b5 family |
Cell immortalization-related protein 2; CIR2; CIR2cell growth-inhibiting protein 47; NENF; Neudesin; neuron derived neurotrophic factor; Neuron-derived neurotrophic factor; SCIRP10; SCIRP10-related protein; Secreted protein of unknown function; Spinal cord injury related protein 10; SPUF protein; SPUF; SPUFneudesin
Mass (kDA):
18.856 kDA
Human | |
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Location: | 1q32.3 |
Sequence: | 1; NC_000001.11 (212432920..212446379) |
Ubiquitously expressed with high expression in heart. Over-expressed in various tumors including carcinomas of the uterine cervix, lymphoma, colon, lung, skin and leukemia, as well as carcinoma of the breast.
Secreted, extracellular space. Mitochondrion. Endoplasmic reticulum. Localized to mitochondria and endoplasmic reticulum by PINK1 and PARK7.
NENF and BDNF are growth factors that regulate synaptic transmitting. This article will talk about the different uses for NENF/BDNF, and Boster's antibodies. In this article, we'll discuss a few of Boster's primary antibodies, which have been cited and validated in many scientific papers over the past 25 years.
BDNF is a growth hormone that is produced by neurons. It has many beneficial functions in the brain, including increasing the number, size, and complexity of dendritic spines. BDNF also promotes changes in spine morphology and is an important regulator of synaptic transmission and plasticity. To fully understand the mechanism, further research is required.
Neurons and immune cells produce BDNF in the CNS. They have a high affinity to brain cells. However, BDNF can also be produced outside the CNS by immune cell. This means that a new treatment which boosts the production may be necessary to treat Alzheimer’s disease or other neurodegenerative illnesses. These therapies would increase BDNF and improve memory.
BDNF is a neurotransmitter that acts on both the postsynaptic and pre-synaptic sides of the cell membrane. This receptor is necessary for BDNF to exert synaptic transmission effects. Therefore, inhibition of p75NTR will not affect BDNF signaling. It was shown that inhibition p75NTR does in fact inhibit BDNF activity on presynaptic function but does interfere with LTP at the hippocampal.
BDNF can be synthesized from a pre-pro-protein consisting of 270 amino acids. This prepro-protein contains the signal sequence (pro-domain), and the mature domain. Extracellular proteases, such as plasmin or pro-hormone converterase, cleave and remove the pro domain. The protein produced contains the BDNF genetic code.
Exercise is essential for BDNF production. However, exercise can also increase its activity. BDNF also increases activity of neuronal dierites. This activity is associated amplitude, decreased threshold, and synaptic and synaptic permeability. Exercise-induced plasticity is accompanied in part by an increase of BDNF, which suggests that it may act as a mediator. The increase in hippocampal volume could also be explained by increased vascularization.
Although the exact link between BNDF, AD, and AD remains elusive, some studies have shown that it is a key determinant in the development. The loss of dendritic spines and cell density are common characteristics of the disease, and this may affect BDNF levels in AD. Post-mortem research has shown that AD patients have higher levels of BDNF, TrkB, and this could be due compensatory mechanisms that affect b–amyloid levels. These differences could also be explained by other factors, such as genetics and the environment.
The BDNF exon III gene contains a regulatory element that is responsible for inducing luciferase. A mutation in this region can increase luciferase activity four- to five-fold. This reveals that BDNF regulates synaptic transmitting by stimulating the 5’ TCACGTCA-3’ element. Interestingly, the regulatory element that regulates BDNF transcription is the exonIII promoter.
Neurotrophins are proteins which promote the survival, differentiation and outgrowth neurons. Many of these proteins have a role in synaptic communication and influence the strength the connections between neuronal communities. Several neurotrophins, including NENF, regulate synaptic transmission. Interestingly, a decreased level of NENF within the brain is linked to psychiatric disorders.
Gap junctions are the key to synaptic transmission. These junctions allow for the formation of a continuous pathway in the cytoplasm between presynaptic cell and postsynaptic neuron. This direct ionic pathway creates minimal synaptic delay. After the presynaptic receptor cell releases a chemical transmitter to bind to the receptor site on its postsynaptic counterpart, the chemical diffuses through the cleft. The postsynaptic power is created by the resulting decrease in permeability.
BDNF is the most common NT among vertebrates. It is correlated to epilepsy and attention deficit disorder, depression, and autism. BDNF deregulation is also a major contributor to chronic pain. However, very few studies have been done on BDNF in flies. This is changing. Drosophila has been used by the research field as an excellent model for understanding gene networks, and also for studying disease mechanisms.
In vitro brain studies have shown that NENF is essential for controlling synaptic transmission. The expression of neudesin and MAP-2 was assessed using the loss-of-native-allelic assay. The Nenf/ genotype reduced neudesin levels in mice. This was a significant outcome, as it prevented neudesin synthesis.
Neudesin or neuron derived neurotrophic protein is a vital growth factor for the brain. The neurons can't form dendritic adria, and this causes impairment of dopaminergic activity at the ventral hippocampus. The neurons also have impaired dendritic Arborization and amBNST nucleus destruction.
Neudesin null mice have dendritic forests with significantly shorter length dendrites than their peers. The dendrites from the Nenf/ mice have significantly fewer intersections than their counterparts with imaginary globes. Neudesin/ mice also have fewer dendritic connections and dendritic arborization than their controls.
Interestingly, the same study also suggests that NENF plays a role in the taste perception of rats. While its involvement in the non-taste cells' synapses has not been confirmed by this study, it has provided important insights. These findings could have implications for the development therapies to improve taste perception. The next step will be to determine the best treatment. Neuroscientists should concentrate on identifying compounds that increase NENF concentrations in the brain.
PMID: 15605373 by Kimura I., et al. Neudesin, a novel secreted protein with a unique primary structure and neurotrophic activity.
PMID: 9771976 by Ma L., et al. Up-regulation of CIR1/CROC1 expression upon cell immortalization and in tumor-derived human cell lines.