matriptase 2

06/15/2007 - "Furthermore, we report that matriptase-2 overexpression dramatically reduced the invasive (P = 0.0001) and migratory properties (P = 0.01) of the breast cancer cells. "
11/15/2013 - "Matriptase-2 (TMPRSS6) has been identified as a breast cancer risk factor. "
06/15/2007 - "Matriptase-2 suppresses breast tumor development in vivo, displays prognostic value for breast cancer patients, inhibits both breast cancer cell invasion and motility in vitro, and may play a contrasting role to matriptase-1 in breast cancer."
06/15/2007 - "Here, we show that reduced matriptase-2 levels in breast cancer tissues correlate with an overall poor prognosis for the breast cancer patient. "
06/15/2007 - "Matriptase-2 was also experimentally overexpressed in the MDA-MB-231 human breast cancer cell line. "

06/01/2020 - "According to our findings, the increase in TMPRSS6 gene expression in cancerous tissues shows that matriptase-2 may be effective in the cancer process. "
06/15/2007 - "This study aimed to provide new insights into the significance of matriptase-2 in cancer. "
01/01/2017 - "These findings suggest that the expression of matriptase-2 may be both a prognostic marker and a potential therapeutic target for this cancer."
01/01/2017 - "Our results demonstrate that the inverse expression of matriptase-2 correlates with tumor progression and an advanced TNM stage, and has a poor prognosis in patients with OSCC. "
01/01/2017 - "The matriptase-2 immunoscore was significantly higher in well-differentiated OSCCs than in poorly differentiated tumors (P=0.001). "

03/31/2017 - "Such compounds represent useful pharmacological tools to test matriptase-2 inhibition in a context of iron overload."
04/01/2016 - "En Route to New Therapeutic Options for Iron Overload Diseases: Matriptase-2 as a Target for Kunitz-Type Inhibitors."
01/01/2019 - "Another related TTSP, matriptase-2 is expressed in the liver and functions by regulating iron homoeostasis through the cleavage of hemojuvelin and thus is implicated in iron overload diseases. "
01/01/2016 - "The serine protease matriptase-2 has attracted much attention as a potential target for the treatment of iron overload diseases. "
11/01/2009 - "Suppression of the hepcidin-encoding gene Hamp permits iron overload in mice lacking both hemojuvelin and matriptase-2/TMPRSS6."

11/01/2017 - "The opportunity to reduce matriptase-2 proteolytic activity may open a novel possibility to treat iron overload diseases, such as hereditary hemochromatosis and thalassemia. "
03/31/2017 - "Matriptase-2 emerges as an attractive target for the treatment of conditions associated with iron overload, such as hemochromatosis or beta-thalassemia. "
01/01/2016 - "Inhibition of matriptase-2 is considered as an attractive strategy for the treatment of iron-overload diseases, such as hemochromatosis and β-thalassemia. "
08/12/2010 - "Thus, matriptase-2 represents a novel target for the development of enzyme inhibitors potentially useful for the treatment of systemic iron overload (hemochromatosis). "
01/01/2017 - "Mutations in the genes HFE, TFR2, HJV, HAMP (encoding hepcidin), and SLC40A1 (encoding ferroportin) cause hereditary hemochromatosis, whereas mutations in TMPRSS6 (which encodes matriptase 2) cause iron-refractory iron deficiency anemia through the upregulation of hepcidin expression. "

06/01/2013 - "Iron refractory iron deficiency anemia is a hereditary recessive anemia due to a defect in the TMPRSS6 gene encoding Matriptase-2. "
01/01/2014 - "The role of TMPRSS6/matriptase-2 in iron regulation and anemia."
06/01/2013 - "In vitro experiments on transfected cells suggest that Matriptase-2 cleaves Hemojuvelin, a major regulator of hepcidin expression and that this function is altered in this genetic form of anemia. "
12/01/2009 - "In mice, defects in the Tmprss6 gene encoding matriptase-2 result in high hepcidin expression and cause severe microcytic anemia. "
12/01/2008 - "The expression of matriptase-2 mutants in zebrafish results in anemia, confirming the matriptase-2 role in iron metabolism and its interaction with HJV."