Search

everythingexperts & clinicslearnfaqsresearchcommunity

for

Search:↓

This study found that FLCN deficiency in mice muscles led to increased mitochondrial biogenesis and a metabolic shift towards oxidative phosphorylation, with a similar advantage observed in FLCN-null kidney cancer cells.

This study found that autophagy is impaired in Birt-Hogg-Dubé syndrome-associated renal tumors and identified that the FLCN protein interacts with key autophagy components regulated by ULK1.

This study developed a kidney-specific knockout mouse model lacking the Flcn gene, which recapitulates human Birt-Hogg-Dubé kidney tumorigenesis and shows that mTOR pathway inhibition with rapamycin can suppress tumor growth.

This study found that loss of the folliculin protein delays transferrin receptor recycling, leading to iron deficiency and suggesting a role in the mechanisms of Birt-Hogg-Dubé syndrome.

This study found that dysregulation of the folliculin-p0071 interaction may lead to changes in cell adhesion and signaling, contributing to conditions like emphysema and renal cell carcinoma.