Add BrightSurf on Google Email

Signaling hope for polycystic kidney disease

Researchers identify hyperactive c-Met protein as key player in ADPKD cyst growth, leading to potential therapeutic target. Pharmacological inhibition of c-Met decreases mTOR activity and blocks cyst formation in mouse model.

SourceJCI Journals·JournalJournal of Clinical Investigation·DateSep 13, 2010

Tips from the American Journal of Pathology

Researchers found that transforming growth factor-β1 contributes to kidney disease by inducing fibrosis and nephron degeneration. Meanwhile, a new diagnostic criteria for T-cell lymphoma was discovered using mast cells and Th17 cells. Additionally, a novel peptide ASARM may implicate in impaired dentin mineralization in rickets.

SourceAmerican Journal of Pathology·JournalAmerican Journal Of Pathology·DateJul 28, 2010

Unraveling how cells respond to low oxygen

Researchers at Burnham Institute for Medical Research discovered that the REDD1 protein is degraded under hypoxic conditions, enabling cells to rapidly restore mTOR signaling. This regulation mechanism plays a crucial role in cellular stress response and may be linked to tumor growth in cancer.

SourceSanford Burnham Prebys·JournalEMBO Reports·DateAug 5, 2009

JCI table of contents: Aug. 21, 2008

Simultaneous inhibition of two signaling pathways, mTOR and MAPK, resulted in enhanced antitumor effects in mouse models of prostate and breast cancer. This combination therapy may improve the treatment of human cancers, particularly for patients with advanced, hormone-refractory prostate cancer.

SourceJCI Journals·JournalJournal of Clinical Investigation·DateAug 21, 2008