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Facts about Metalloproteinase inhibitor 3.
Known to act on MMP-1, MMP-2, MMP-3, MMP-7, MMP-9, MMP-13, MMP-14 and MMP-15. .
Human | |
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Gene Name: | TIMP3 |
Uniprot: | P35625 |
Entrez: | 7078 |
Belongs to: |
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protease inhibitor I35 (TIMP) family |
HSMRK222; K222; K222TA2; metalloproteinase inhibitor 3; MIG-5 protein; Protein MIG-5; pseudoinflammatory); SFD; TIMP metallopeptidase inhibitor 3; TIMP3; TIMP-3; tissue inhibitor of metalloproteinase 3 (Sorsby fundus dystrophy; Tissue inhibitor of metalloproteinases 3
Mass (kDA):
24.145 kDA
Human | |
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Location: | 22q12.3 |
Sequence: | 22; NC_000022.11 (32801705..32863041) |
Secreted, extracellular space, extracellular matrix.
What is TIMP3 and what is its function? How is it used in immunohistochemistry? What are the potential uses? These and other questions will be answered as you read on. We'll go over the mechanism of action as well as how Boster scientists can benefit from the TIMP3 marker. These answers are available to scientists across the globe. And, of course, we'll touch on some applications of TIMP3 in immunohistochemistry.
Boster Bio's Anti-Metalloproteinase Inhibitor 3 TIMP3 Antibody reacts with Human, Mouse and Rat samples in WB. This antibody can be used to study the expression of genes in specific cells. This antibody is approved for use in animal and plant research. It can also be employed in research in veterinary medicine. Download the Boster Bio TIMP3 Marker Technical Information Sheet to find out more.
Researchers have discovered that TIMP3 gene-methylation is an important component of tumor-metastasis. The TIMP3 CpG methylation rate was significantly higher in patients with advanced metastatic disease. The significance of this marker in cancer research includes predicting the potential for metastatic spread of a cancer. The study has its drawbacks. The study also found that higher levels of MMP3 could lead to worse prognosis.
TIMP3 expression is negatively related to the density of tumor-blood vessels. In human colon cancer cell lines, TIMP3 expression was low. These tumors aren't able to enter mitosis. TNF-a antibody as a treatment, blocked mitotic arrest in 70% of the cases. The study also showed that TIMP3 is a useful biomarker for breast cancer.
The expression of the TIMP3 gene is mediated by hypermethylation of the promoter region, a CpG island. The expression of the protein may assist with stage evaluation and molecular diagnosis. Boster Bio: The Best Benefits of the TIMP3 Marker
The TIMP3 gene encodes the metalloproteinase inhibitor 3 protein. It is part of the tissue inhibitor of metalloproteinases gene family. It inhibits the function of matrix metalloproteinases (MMMPs). It is found in the extracellular matrix. Sorsby's fundus Dystrophy can be described as an illness that is found in patients who have mutations in TIMP3 gene.
A TIMP3 marker is a biomarker of TIMP3 expression in cancer cells It is a biomarker. It is a tumor suppressor and can affect a variety of physiological processes. TIMP3 is often found in the body and may have anticancer properties and an apoptosis-inducing function. Clinical applications of TIMP3 include cancer diagnosis as well as the prediction of tumor progression and cancer therapy. However, more studies are needed to fully assess its benefits.
TIMP3 has been demonstrated to be associated with kidney disease in humans. A recent study examined the expression of 115 candidate genes, and discovered that the presence of polymorphisms in TIMP3 were significantly associated with the development diabetic nephropathy. Thus, allelic variations in this gene may be contributing to DKD risk. In kidney biopsies there was evidence that the TIMP3 marker was also found to be lower in kidney biopsies. This indicates that the gene plays a different role in the tubuli than the glomeruli.
The methylation of TIMP3 in cancer cells has been discovered to be a significant prognostic factor in the survival of patients suffering from advanced stage or metastasis. These findings suggest that TIMP3 expression may be a significant treatment for osteosarcoma. These findings are in line other studies suggesting that TIMP3 expression levels are associated with prognosis for patients suffering from advanced lung cancer.
The expression of TIMP3 is ininversely related to miR-21 levels in the glomeruli of patients suffering from DN. In DN rats, miR-21 levels were downregulated , which decreased kidney inflammation and pro-inflammatory response. TIMP3 increased expression reduced the inflammatory response in diabetic rats. MiR-21 inhibition blocked the development of DN in hg-treated mice.
Researchers found that overexpression of TIMP3 in oral cancer cells prevented their migration and invasion of the tumor. TIMP3 overexpression also slowed lymph node metastasis. These findings support the notion that TIMP3 regulates the epithelial-mesenchymal transition and promotes the expression of prognostic markers in the oral cancer. However, the mechanisms that TIMP3 promoter hypermethylation affects oral cancer cells are still unclear.
TIMP3 regulates expression of T cell adhesion protein Snail, and Twist. TIMP3 also inhibits p ERK and E-cadherin. These three proteins are involved in EMT, one of the pathways controlled by the PI3K/AKT signaling pathway. 30 percent of CRC cells have the gene TIMP3. It is therefore expected that the TIMP3 promoter will be methylated in order to inhibit its expression.
Knockdown of TIMP3 impaired cell adhesion, reducing the expression of E-cadherin and fibronectin. TIMP3 knockdown decreased levels of mesenchymal and epithelial markers. The knockdown of TIMP3 also decreased cell adhesion. This suggests that TIMP3 plays a role in the progression of tumors to more aggressive phenotypes.
Furthermore, TIMP3 inhibits VEGF receptor-2 expression. This reduces downstream signalling and angiogenesis. Furthermore, VEGF plays a critical role in the homeostasis of the kidney. Its absence can cause the dysfunction of the glomerulus and proteinuria. Additionally, TIMP3 is involved in interaction with the Notch pathway in the diabetic kidney disease. This research was supported by the National Natural Science Foundation of China.
DNMT1A and DNMT3B epigenetically silent genes that affect the expression of TIMP3 cells are epigenetically silenced. The knockdown of DNMT1 and DNMT3B significantly enhanced the expression of TIMP3 in oral cancer cell lines. The DNMT inhibitors also enhanced the ability of Sp1 to bind to the promoter of TIMP3. Furthermore, TIMP3 knockdown improves the activity of the tumor suppressor gene RSP1 in oral cancer cell lines.
Wilde et. and. developed a molecular diagnosis by using the TIMP3 marker. Wilde et al. sequenced the TIMP3 gene in phorbol esters-differentiated cells following stimulation with lipopolysaccharide. The gene encodes the precursor of amino acids 211 with a 23-residue molecule. The molecular weight of the mature polypeptide was determined to be 21.6 kD.
Of the cases examined, all 78 samples were positive for TIMP3 protein and methylation. The level of methylation in cases of cancer metastasis was 89.7%. The TIMP3 gene was reduced in non-neoplastic tissues. The results indicated that TIMP3 genes were not altered by cancer cells. It may however be a marker for stage-related diagnosis in patients with high levels TIMP3 methylation.
TIMP3 and TNFa levels that are elevated in mice have been linked to a higher incidence of acute and chronic kidney injury. TNFa levels that are higher in these patients could accelerate the development of kidney damage. TIMP3 deficiency can also increase the risk of recurrence and the progression of renal failure. Mice with TIMP3 deficiency should undergo a sensitivity test in order to detect this protein to determine if they have kidney disease.
TIMP3 is a tissue inhibitor of matrix metalloproteinases. It also acts as a regulator of cell development and growth. It is essential to control metastasis, invasion, growth and other epigenetic changes. TIMP3 hypermethylation in cancer cells has been linked to local lymph node metastaticsis, local and the expression of macrophages. While these findings are encouraging however, further research is needed to confirm its role as a predictor of prognosis.
The use of TIMP3 to assess diabetic kidney disease is gaining popularity, especially for patients with advanced kidney disease. The absence of TIMP3 causes the development of diabetic nephropathy and increases the risk of cardiovascular disease. While this is still an experimental studies, the findings from these studies point to its role in diabetic kidney disease. A recent study also found that TIMP3 deficiency can cause kidney damage in diabetic patients.
TIMP3 is an ECM-bound proteins that are expressed in mice and humans. It regulates matrix composition and plays a role in many physiological processes. It regulates the expression and function of the other proteins that regulate our immune system. For this reason, TIMP3 has been the focus of many different studies. In addition to its function in determining the prognosis for diabetic patients, TIMP3 also influences the level of blood cholesterol in diabetics.
The TIMP3 gene was removed in diabetic mice. Deletion of the gene significantly caused the diabetic renal injury to be worsened, as evidenced by an increased amount of albuminuria and an expansion of mesangial matrix. TIMP3-deficient mice also had higher levels of inflammatory and fibrotic markers. This could indicate that TIMP3 overexpression could decrease the chance of developing diabetes kidney disease.
A peptide that has a similar structure to the TIMP3 structure is extremely sensitive and precise. Its ability to detect the renal cortex using a sensitivity test been demonstrated. The peptide was soluble in renal cortex and it was detected in serum for 24 hours after injection. TIMP3 expression increased significantly at 10' following injection. ProteoGenix SAS synthesized the peptides and then they were conjugated with a G3C12 carrier protein.
PMID: 8174111 by Uria J.A., et al. Structure and expression in breast tumors of human TIMP-3, a new member of the metalloproteinase inhibitor family.
PMID: 7772252 by Wilde C.G., et al. Cloning and characterization of human tissue inhibitor of metalloproteinases-3.
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