TLR5-Mediated Phosphoinositide 3-Kinase Activation Negatively Regulates Flagellin-Induced Proinflammatory Gene Expression

نویسندگان
چکیده

برای دانلود باید عضویت طلایی داشته باشید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Lymphocyte Activation Gene-3 (LAG-3) Negatively Regulates Environmentally-Induced Autoimmunity

Environmental factors including drugs, mineral oils and heavy metals such as lead, gold and mercury are triggers of autoimmune diseases in animal models or even in occupationally exposed humans. After exposure to subtoxic levels of mercury (Hg), genetically susceptible strains of mice develop an autoimmune disease characterized by the production of highly specific anti-nucleolar autoantibodies,...

متن کامل

Phosphoinositide 3-kinase p85beta regulates invadopodium formation

The acquisition of invasiveness is characteristic of tumor progression. Numerous genetic changes are associated with metastasis, but the mechanism by which a cell becomes invasive remains unclear. Expression of p85β, a regulatory subunit of phosphoinositide-3-kinase, markedly increases in advanced carcinoma, but its mode of action is unknown. We postulated that p85β might facilitate cell invasi...

متن کامل

berberine induced apoptosis of human osteosarcoma cells by inhibiting phosphoinositide 3 kinase/protein kinase b (pi3k/akt) signal pathway activation

background: osteosarcoma is a malignant tumor with high mortality but effective therapy has not yet been developed. berberine, an isoquinoline alkaloid component in several chinese herbs including huanglian, has been shown to induce growth inhibition and the apoptosis of certain cancer cells. the aim of this study was to determine the role of berberine on human osteosarcoma cell lines u2os and ...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

ژورنال

عنوان ژورنال: The Journal of Immunology

سال: 2006

ISSN: 0022-1767,1550-6606

DOI: 10.4049/jimmunol.176.10.6194