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- Table of Contents
Facts about High affinity nerve growth factor receptor.
However, NTF3 only supports axonal extension through NTRK1 but has no effect on neuron survival (By similarity). Upon dimeric NGF ligand-binding, undergoes homodimerization, autophosphorylation and activation (PubMed:1281417).
Human | |
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Gene Name: | NTRK1 |
Uniprot: | P04629 |
Entrez: | 4914 |
Belongs to: |
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protein kinase superfamily |
DKFZp781I14186; EC 2.7.10; EC 2.7.10.1; MTChigh affinity nerve growth factor receptor; Neurotrophic tyrosine kinase receptor type 1; neurotrophic tyrosine kinase, receptor, type 1; NTRK1; NTRK-1; p140-TrkA; TRK1-transforming tyrosine kinase protein; TrkA; Trk-A; TRKAOncogene TRK; TRKTRK1; tyrosine kinase receptor A
Mass (kDA):
87.497 kDA
Human | |
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Location: | 1q23.1 |
Sequence: | 1; NC_000001.11 (156815750..156881850) |
Isoform TrkA-I is found in most non-neuronal tissues. Isoform TrkA-II is primarily expressed in neuronal cells. TrkA-III is specifically expressed by pluripotent neural stem and neural crest progenitors.
Cell membrane; Single-pass type I membrane protein. Early endosome membrane; Single-pass type I membrane protein. Late endosome membrane; Single-pass type I membrane protein. Recycling endosome membrane; Single-pass type I membrane protein. Rapidly internalized after NGF binding (PubMed:1281417). Internalized to endosomes upon binding of NGF or NTF3 and further transported to the cell body via a retrograde axonal transport. Localized at cell membrane and early endosomes before nerve growth factor (NGF) stimulation. Recruited to late endosomes after NGF stimulation. Colocalized with RAPGEF2 at
Learn more about the Boster Bio and the best uses for it by calling Sanbio. They also offer custom services, as well as BeNeLux delivery. The best way to get started with the Boster Bio is to learn about it. It is also possible to read to learn more about the best uses of the NTRK1 marker. You may also be interested in creating DsRNAs that target specific protein or gene, if you have a particular gene.
A strategy targeting SEC-16 allows you to produce dsRNAs for human TFG-1, a transcription element required for the normal assembly complexes. Although TFG-1 and SEC-16 co-vary in animals, their functions are different. TFG-1 functions to facilitate the assembly of complexes with COPII proteins. Thus, removing TFG-1 cells prevents the formation of SEC-16.
In cells, the release of cargoes from the ER occurs at designated locations that contain the scaffolding protein SEC-16. Depletion of TFG-1 in the ER results in an increase in the amount of SEC-16, indicating that it controls the export of cargoes. Studies on hydrodynamics revealed that TFG-1 is a Hexamer. Studies of hydrodynamics have demonstrated that TFG-1 can form hexamers if combined with SEC-16.
The dsRNA was spray-painted on leaf tissues, and its fluorescent signal was detected inside fungal germtubesand conidia, and mycelium. These results suggest that dsRNAs can be processed by fungi by translocation of the system. This mechanism could be used to target fungal CYP51 gene. These findings have implications for the development of disease-control strategies that depend on dsRNA.
We utilized primer sets to create dsRNAs that target TFG-1. These primer sets were designed specifically for TFG-1 and GW182. The siRNA sequence is highlighted in red. The blue nucleotides are the presumed star sequence for the dpp2 siRNA. To ensure that the stem-loop stem-loop is maintained in the pre-m structure two mismatched bases must be present in the sequence of dsRNA.
TFG functions as a proto-oncogene that results in the activation of multiple effectors including ERKs, and promotes cell transformation. TFG-NTRK1 fusion protein TFG -NTRK1 activate the ERK2 signaling pathway and directs ERK2 to the ER exit sites, thus helping to promote cell transformation. This feed-forward mechanism could play a major role in oncogenesis.
We made use of a PCR-generated DNA Template that has primers that recognize T7 to produce dsRNAs in response to TFG1. We can produce up to 2 mg of dsRNA from a single template. This method is cost-effective and efficient, but it's not as efficient on large scales. A clean and sterile working environment is essential for high-throughput production. Workers should wear gloves while dsRNA production to avoid contamination.
RNAi is a process by which small amounts of RNA or DNA are introduced into a cell and then shut down its expression. To ensure that they were in line with the target, the dsRNAs created by this process were tested. The Silencer(tm), siRNA Labeling Kit was used to label dsRNAs using Cy3 and then introduced into Drosophila L2 cell. Fluorescent microscopy was used to view RNAi in action.
Golgi complexes are three-dimensional structures. Furthermore, ER exit sites are linked to Golgi complexes. To locate ER exit sites, gonads dissected from the body had to be stained with antibodies against TFG-1 and SEC-16. Using Cy3-labeled a-TFG-1 antibody and SEC-16 antibodies, it was possible to observe the pattern of fluorescence intensity across TFG-1-depleted and control animals. The intensity of these proteins was measured in low-, mediumhigh threshold animals. We also measured the number of exit sites from the ER in each animal's area.
Since dsRNAs are sequence-specific which means they're not as harmful to other plants. Furthermore, since dsRNA is present in the human diet, the population could have a higher tolerance to it than other methods of protecting plants. This means that dsRNAs could be utilized to treat a variety of plant diseases. This means that this method could be an alternative to conventional pesticides.
Using novel expression vectors, researchers can now create siRNAs with distinct targets. In plant cells, the siRNAs dpp1 and dpp2-siRNAs are created. They originate from a distinct gene within the plant. The siRNA dpp1 targets two distinct regions of the mRNA dpp. Through northern blot tests, the target genes are further verified.
To generate dsRNA that is a part of the firefly Luciferase the 450 ng GFP code sequence was transfected into cells S2. The Luc DsRNA, which contained 500-bps of the firefly Luciferase code region, was transcribed using MEGAscript T7 (Ambion).
To assess the effectiveness of each dsRNA in fighting TFG-1 we used the transgenic shmiR–dpp-dsRNA line. The two dsRNAs are expressed in the wings imaginal disks of male and female Drosophila embryos. The dpp -dsRNA expression mechanism is able to produce the dpp knockdown effect in both genders. Similar results were also observed with the UAS-dpp-dsRNA transgenic strain 48A.1.
To target the SEC-16 gene, dsRNAs that target this sequence were constructed by using DCL3. This method uses TFG-1 hexamers to aid in the assembly of large complexes. The process may be disrupted because dsRNAs are longer than the target gene. To understand the mechanism of processing dsRNAs, we first examined the CCD. The CCD is the central domain that is conserved in all four SEC-16 isoforms.
In the distal germline SEC-16 and TFG-1 are expressed in an exclusive niche. The ER exit sites are comparable to those of the proximal gonad, and immunofluorescence analysis showed that they co-express at distinct ER exit sites. The ratio of SEC-16 and TFG-1 fluorescence intensities was not dramatically different between ER exit sites. In wild-type mice, both genes were strongly connected.
To generate dsRNAs directed against SEC16 In order to do this, we first needed to create a plasmid as well as a cDNA library. First, we isolated DNA fragments. To obtain the highest yield we used cDNAs of Pol IV and RDR2. Then we synthesized the dsRNAs using a dsRNA synthesis kit.
The RNAi library that produced dsRNAs against SEC-16 had CDNA clones that came from 15 different genes. Clones that are clones can promote the degradation of the corresponding mRNA. Additionally screening, we also check mammalian cells for defects using RNAi library clones. This procedure is based on several methods, and is described in the sections below.
We constructed a dsRNA model that was 52-bp long and blunt-ended. The model dsRNA contains three C, G and A residues. From the 3 ends, we have synthesized two functional duplex dsRNAs. These dsRNAs then are used to target SEC-16 as well as other genes. We have also looked into the mechanism of SEC-16 cleavage by dsRNAs.
To prevent interferon-mediated reactions or cellular apoptosis, dsRNAs should be purified before transfection. The RNA Binding Buffer should be used to remove the long dsRNA from the sample. The contaminating dsRNA could be able to bind to the column, when there aren't any particles that resemble viruses. These dsRNAs need to be purified with a high purity.
We also identified the cleavage sites in the sense strand of the target RNA. These cleavage spots are located in the same area of identity as the DsRNAs of the target RNA. A lower-percentage gel was employed to determine the cleavage sites on the antisense strand. The cleavage sites for sense strand, however, are located between 10 and 10 nt downstream from the 5' end within the area covered by dsRNA.
Drosophila Lysate was used to produce 21-nt DsRNAs. This method produced dsRNAs that contained Pp-luc as target RNA. The dsRNAs then were identified and extracted using phosphorimaging. The caps of the sense and antisense dsRNAs are separated to extract the RNA.
The BLOCK iT(tm), Dicer Enzyme is required for high yields of DNA. Lipofectamine(r) 2000 Reagent can be used for transfection in mammalian cells. This kit contains the RNAi-specific Lipofectamine (r) 2000 Reagent. Specific instructions are provided in the user's manual of the BLOCK-iT RNAi TOPO(r) transfection kit.
The dsRNA generated by the RNAi treatment requires a concentration of 250 times greater than the control group. This means that the amount of dsRNA is indefinite and can be increased to compensate. C. cell lines could be affected by RNAi. This can cause toxic effects on the cell targeted. Therefore, it is crucial to understand how to make DsRNAs that are resistant to SEC-16.
After the dsRNAs were synthesized and then oligomers resulting from the process were examined for their capability to target SEC-16. dsRNAs with long 3' staggered ends or single stranded regions block the RNAi. The low siRNA formation rates of short (30-bp dsRNAs may also be responsible for the lack of RNAi.
After being synthesized siRNPs are translated into dsRNAs. The siRNPs are processed by an endonuclease complex. These proteins break down siRNAs at the middle of the region that is identified by the guide siRNA. These dsRNAs can then be utilized to target SEC-16 cells, which is a major step in the development of therapeutics.
PMID: 2927393 by Martin-Zanca D., et al. Molecular and biochemical characterization of the human trk proto- oncogene.
PMID: 7823156 by Shelton D.L., et al. Human trks: molecular cloning, tissue distribution, and expression of extracellular domain immunoadhesins.
*More publications can be found for each product on its corresponding product page