This website uses cookies to ensure you get the best experience on our website.
- Table of Contents
14 Citations 9 Q&As
6 Citations 10 Q&As
7 Citations 7 Q&As
16 Citations
7 Citations 4 Q&As
1 Citations 1 Q&As
Facts about Metalloproteinase inhibitor 2.
.
Human | |
---|---|
Gene Name: | TIMP2 |
Uniprot: | P16035 |
Entrez: | 7077 |
Belongs to: |
---|
protease inhibitor I35 (TIMP) family |
CSC-21Ktissue inhibitor of metalloproteinase 2; metalloproteinase inhibitor 2; TIMP metallopeptidase inhibitor 2; TIMP2; TIMP-2; Tissue inhibitor of metalloproteinases 2
Mass (kDA):
24.399 kDA
Human | |
---|---|
Location: | 17q25.3 |
Sequence: | 17; NC_000017.11 (78852977..78925387, complement) |
Secreted.
Researchers can submit their findings from various species or applications or samples for credit and special product features. These credits for products can be used by scientists across the globe. Boster scientists are allowed to submit their findings from any species or application in order to be qualified for a prize. Boster scientists' results are also published in numerous scientific publications. Below are some of the most popular applications for the TIMP2 Marker.
Boster Bio's TIMP-2 inhibitor blocks MMPs' proteolytic function. The compound was found to completely block MMP-2 enzyme activity at a concentration of 10 nanomol. The IC50 value of 1.39 nM was 1,000 times higher than NNGH which is a common compound. This study is backed by published results from Boster Bio as well as the University of California San Francisco.
The inhibitor TIMP-2 is highly specific for MMP9 and MMP14. In the present study N-TIMP2WT blocked MMP9 gelatinolysis more than other clones. MMP14 binding clones did not hinder MMP9 gelatinolytic activity. N-TIMP2WT thus blocks MMPs' proteolytic activity in MMP9 cells.
TIMP-2 A 21-kDa multifunctional protein that inhibits matrix metaloproteinases, is known as. It blocks MMPs proteolytic activity and stops their degradation of extracellular matrix. It is a promising candidate for biologic treatments against cancer because it inhibits the development of neoangiogenesis aswell as tumor growth in vitro. TIMP-2 recombinant proteins may be created from HEK-293F cells.
The TIMP-2 cDNA has a high GC content. This makes it more likely that stem-loop structures develop. These structures are likely to be discovered in mRNAs that have been converted. This mechanism may allow TIMP-2 inhibition of MMPs' activities. The TIMP-2 inhibitor of the future is a promising compound that targets MMPs that are found in cancer cells.
The peptides that are bound to MMP-2 are crucial in the growth of tumors. MMP-9 is part of the MMP family however its latent form is 92 kmDa. Furthermore that, in human SKHep1 HCC cells, MMP9 is highly expressed in the basement membrane as well as ECM. To assess its proteolytic activities Gelatin zymography was employed. Boster Bio's TIMP-2 inhibitor impedes the proteolytic activity of MMPs in humans.
The library was tested using yeast cells expressing MMP9CAT and MMP14CAT catalytic domains. In vitro testing of the inhibitor TIMP-2 demonstrated binding to both proteins when in the presence MMP-14CAT and MMP9CAT, which are targets that are soluble. In the analysis of flow cytometry the inhibitor was found to be bound to both MMPs however at different levels.
Recent research has proven that TIMP2 is a vital biomarker that can be used to detect severe sepsis. If it is measured early in the course of the disease, the TIMP2 marker can indicate the mortality rate in the early stages, thus improving the outcomes of patients. Boster Bio's research led to the discovery of TIMP2 genes. The research provides a step-by-step guide to its clinical application and can be found here.
The TIMP2 expression of mRNA was substantially greater than that of other TIMPs in all cell lines. Three cell lines were able to detect the expression of the TIMP-2 protein using immunofluorescence. OVCAR4 cells expressed TIMP-2 in higher amounts than JHOS2 and FT282 cells. TIMP-2 expression may be a viable target for achieving resistance to chemotherapy in ovarian cancer.
TIMP2 is an enzyme that is present in nearly all cells. It functions as an inhibitor of MMPs. It interacts with MMPs via cell-surface receptors and regulates their activity. TIMP-2 inhibits MMP-2 activity, which could be essential for tissue homeostasis. The presence of TIMP-2 in tubular cells has also been shown to indicate cell cycle arrest. In addition to blocking the angiogenic effect of MMPs TIMP-2 can also be an inhibitor of MMP-2 activity.
In addition to cancer cell survival TIMP-2 is also an essential protein that plays a role in the progression of various cancers. This is evident by the increased expression of OVCAR4 cells when TIMP-2 is insufficient. It does not mean TIMP-2 is a poor drug. TIMP-2 can also be used to diagnose an unidentified tumor.
Among other biomarkers, TIMP-2 is a promising biomarker to detect early signs of AKI. It is a key trigger of G1 cell-cycle stop, which is a protective mechanism that prevents damaged cells from dividing. In reality the damage to cells caused by TIMP-2 in AKI patients is often irreversible. TIMP-2 has been recommended to be an early AKI biomarker.
Boster Bio: TIMP2 In Critically Ill Patients highlights the best uses of TIMP2 marker in critically sick patients
Patients suffering from acute renal injury of stage 3 (AKI) have a great chance to benefit from TIMP-2 as a biomarker for kidney damage. However, there are limitations to this marker. In particular the biomarker's reliability was challenged by comorbid conditions like diabetes. However the TIMP-2 marker is a reliable biomarker used to detect AKI.
In a recent study researchers evaluated the effectiveness of TIMP-2 for stage 3 AKI among patients in the intensive care unit. They found that most patients in the intervention group had a one-hour turnaround time at the clinical lab. The results will be used to help doctors develop new quality improvement metrics for TIMP-2. Researchers will now examine a broader range of patients to find the most effective method to utilize the biomarker TIMP-2.
The TIMP-2 and IGFBP7 levels in the urine and blood were significantly related to RRT need in this study. The TIMP-2 levels prior to and during surgery were also highly predictive of mortality after surgery. A simple model of baseline serum creatinine was better at predicting RRT demands. It also demonstrated excellent discriminative power and C-statistics on mortality at 30 days and superior discriminative power.
TIMP-2 levels did not distinguish between patients who receive RRT or not. IGFBP7 and serum creatinine levels, however, did a reasonable job. A single biomarker can't predict the need for RRT, while IGFBP7 does not. Moreover, the TIMP-2 level and serum creatinine levels were the only variables that accurately predicted RRT in this study.
TIMP-2 is a novel gene signature that has demonstrated an excellent clinical correlation with the sensitivity to chemotherapy in cancer of the ovary. This gene is expressed in the stroma and the tumor compartments and is linked to overall survival. Additionally, it could be a helpful prognostic marker for predicting the response to chemotherapy. However, the effect of topography on survival remains unclear. To understand the biologic role that TIMP-2 plays in ovarian cancergenesis more research is needed.
In the first clinical trials, the levels of expression of the TIMP-2 gene of patients suffering from cancer of the ovary were assessed. The highest levels of sensitivity and specificity were found in patients with stage II and III disease and women suffering from any AKI. In addition, gene expression levels were significantly higher in women who had advanced stage ovarian cancer than women with a stage that is more advanced.
This gene expression pattern was discovered at Zhongshan Hospital. Before surgery, all patients who were participating signed an informed consent form. The study was conducted only for adults and was conducted at a single hospital. The researchers excluded patients under 18 years old and those with prior renal transplantation or chronic dialysis. The researchers took urine samples prior to surgery and at intervals of 2 hours. Overall Boster Bio's TIMP-2 expression pattern was significantly higher than the ones in the control group.
The researchers studied the TIMP-2 gene expression level in a variety of human cell lines. The ES-2 and EFO-21 cell lines were completely resistant to all chemotherapeutic drugs, whereas the OVCAR-3 cell line showed a moderate response to topotecan and paclitaxel. Boster Bio's TIMP-2 gene expression increased sensitivity in ovarian cancer in a rat model.
The trial's results were encouraging. Boster Bio's TIMP-2 gene expression profile increases the sensitivity to chemotherapy in ovarian cancer. This gene signature has many potential applications in the treatment of ovarian cancer. While further research is required to establish the clinical relevance the gene expression profile could be helpful in discovering new strategies for treating cancer. Patients can begin treatment using Boster Bio's TIMP-2 expression profiles.
PMID: 2380196 by Stetler-Stevenson W.G., et al. Tissue inhibitor of metalloproteinases-2 (TIMP-2) mRNA expression in tumor cell lines and human tumor tissues.
PMID: 2157214 by Boone T.C., et al. cDNA cloning and expression of a metalloproteinase inhibitor related to tissue inhibitor of metalloproteinases.
*Showing only the more recent 20. More publications can be found for each product on its corresponding product page