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Facts about Mitogen-activated protein kinase kinase kinase 7.
Ceramides are also able to activate MAP3K7/TAK1. Once activated, acts as an upstream activator of the MKK/JNK signal transduction cascade and the p38 MAPK signal transduction cascade through the phosphorylation and activation of several MAP kinase kinases such as MAP2K1/MEK1, MAP2K3/MKK3, MAP2K6/MKK6 and MAP2K7/MKK7.
Human | |
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Gene Name: | MAP3K7 |
Uniprot: | O43318 |
Entrez: | 6885 |
Belongs to: |
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protein kinase superfamily |
EC 2.7.11; EC 2.7.11.25; MAP3K7; MEKK7; mitogen-activated protein kinase kinase kinase 7; TAK1; TAK1/MAP3K7; TAK1TGF1a; TGF1a; TGF-beta activated kinase 1; TGF-beta-activated kinase 1; Transforming growth factor-beta-activated kinase 1
Mass (kDA):
67.196 kDA
Human | |
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Location: | 6q15 |
Sequence: | 6; NC_000006.12 (90513579..90587072, complement) |
Isoform 1A is the most abundant in ovary, skeletal muscle, spleen and blood mononuclear cells. Isoform 1B is highly expressed in brain, kidney and small intestine. Isoform 1C is the major form in prostate. Isoform 1D is the less abundant form.
Cytoplasm. Cell membrane; Peripheral membrane protein; Cytoplasmic side. Although the majority of MAP3K7/TAK1 is found in the cytosol, when complexed with TAB1/MAP3K7IP1 and TAB2/MAP3K7IP2, it is also localized at the cell membrane.
There are many advantages to MAP3K7 ELISA kit. The kits allow for the production of precise results . They also provide product credits that can be used to fund scientific research. These credits are accessible to Boster scientists who are able to submit results for specific species, samples and applications. These credits are available to all researchers from around the globe.
The Boster Bio MAP3K7 Cell Based ELISA Kit is a convenient, lysate-free solution to identify this protein. It utilizes a picogram-scale immunohistochemistry-based method to measure the target protein levels. These kits are great for screening inhibitors and activators. These kits are backed by technical support. Here are some of its important features.
The MAP3K7 gene encodes MAP3K7, which regulates the activity of p53. Prostate cancer cells lacking the gene show higher levels of p53. This gene is highly expressed in prostate cancer cells and is linked to higher Gleason scores. In a recent study, we proved that MAP3K7 gene expression is associated with less-grade tumors, while mutated cells show higher-grade tumors.
By using qPCR Utilizing a qPCR technique, the MAP3K7 gene was removed in 22 out of 77 prostate cancer samples. By analyzing the signal of 200 prostatic cells in interphase can determine this marker. Both G8-005 (tumor) and G9-003 (tumor) displayed hemizygous interstitial deleterious. The LSI MYB probe detected MAP3K7 in both tumors. Normal prostate control had a normal signal pattern.
Mutated MAP3K7 in prostate cancer cells is associated with a negative ERG fusion. Similarly, overexpression of MAP3K7 significantly inhibited the growth of BPH-1 and the prostate cancer cells DU145. However knockdown of the gene didn't significantly hinder the growth of cells. These results suggest that MAP3K7 is playing an anti-tumor function in prostate cancer.
The MAP3K7 protein is a key regulator of cell invasion and migration and its coexpression with the anti-Vimentin marker has been linked with longer disease-free and overall survival for patients suffering from HCC. Other factors may interfere with the signaling of this protein, preventing the cells from being able to colonize their surroundings and migrate. Further research is required to better understand this.
The overexpression of CRABP2 within C643 cells increased expression of E-cadherin as well as vimentin. CRABP2 also increased the expression of vimentin and N-cadherin. These results suggest that CRABP2 can be overexpressed in order to improve the cell's process. This is consistent with previous studies that indicated that MAP3K7 was linked to the progression of cancer.
In a previous study, siRNAs targeted at MAP3K7 were transfected into SK-HEP-1 and Huh7 cells. The cells were then subjected to cell-migration assays. ImageJ software was used to measure the results. The proliferation of HCC primary cells was also decreased by the knockdown of MAP3K7. The cells were then given to mice and studied for proliferation and migration.
Gene silencing of MAP3K7 increases sensitivity to chemotherapeutic drugs in human cancer cells. Inhibition of MAP3K7's function in pancreatic cancer cells enhanced the effectiveness of chemotherapeutics. In mice, the conditional knockout of MAP3K7 causes hepatocyte dysplasia and early hepatocarcinogenesis. In patients suffering from HCC, the protein was significantly higher in tumors than normal tissue adjacent to it.
Boster Bio Anti-AMF makes use of MAP3K7 antibody as part of their Picoband(tm). This antibody reacts to both human and rat protein and can be kept at -20°C for one year and 4°C for one month. This product comes packaged with 5 mg of BSA and also contains recombinant proteins. For more information, please look up the manual for the product.
PMID: 9480845 by Sakurai H., et al. TGF-beta-activated kinase 1 stimulates NF-kappa B activation by an NF-kappa B-inducing kinase-independent mechanism.
PMID: 11118615 by Dempsey C.E., et al. Alternative splicing and gene structure of the transforming growth factor beta-activated kinase 1.