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FLCN is located within the Smith-Magenis syndrome region on chromosome 17. Additionally we are shipping FLCN Antibodies (85) and FLCN Proteins (6) and many more products for this protein.
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mTOR (show FRAP1 ELISA Kits) inhibitor, sirolimus, suppresses the tumor's growth, suggesting that mTOR (show FRAP1 ELISA Kits) inhibitors might be effective in control of FLCN-deficient RCC (show XRCC1 ELISA Kits).
we show that glycogen (show GYS1 ELISA Kits) accumulates in kidneys from mice lacking FLCN and in renal tumors from a BHD patient
Fnip1 (show FNIP1 ELISA Kits) and Fnip2 play critical roles in kidney tumor suppression in cooperation with Flcn
Folliculin (Flcn) inactivation leads to murine cardiac hypertrophy through mTORC1 deregulation.
The FLCN-GABARAP (show GABARAP ELISA Kits) association is modulated by the presence of either folliculin-interacting protein (FNIP)-1 (show FNIP1 ELISA Kits) or FNIP2 and further regulated by ULK1 (show ULK1 ELISA Kits).
Flcn regulates apoptosis in lung epithelium via E-cadherin (show CDH1 ELISA Kits)-LKB1 (show STK11 ELISA Kits)-AMPK (show PRKAA1 ELISA Kits) axis.
loss of FLCN constitutively activates AMPK (show PRKAA1 ELISA Kits), resulting in PGC-1alpha (show PPARGC1A ELISA Kits)-mediated mitochondrial biogenesis and increased ROS (show ROS1 ELISA Kits) production
These data support a model in which dysregulation of the FLCN-p0071 (show PKP4 ELISA Kits) interaction leads to alterations in cell adhesion, cell polarity, and RhoA (show RHOA ELISA Kits) signaling.
FLCN deficiency and subsequent increased PPARGC1A (show PPARGC1A ELISA Kits) expression result in increased mitochondrial function and oxidative metabolism as the source of cellular energy, which may drive hyperplastic transformation.
The involvement of the AMPK (show PRKAA1 ELISA Kits)-MAPO1-FLCN complex in the signaling pathway of apoptosis, is described.
We identified a hitherto unreported pathogenic FLCN frameshift deletion c.563delT (p.Phe188Serfs*35) in a family of a 46-year-old woman presented with macrohematuria due to bilateral chromophobe renal carcinomas
FLCN irregulation in lung cysts of primary spontaneous pneumothorax is not associated with promoter methylation.
Case Report: FLCN deletion mutation in members of Indian Birt-Hogg-Dube syndrome family.
This report documents the first identification of founder mutations in FLCN, as well as expands mutation spectrum of the gene
FLCN-related renal cell carcinomas showed overexpression of GPNMB and underexpression of FLCN, whereas sporadic tumors showed inverted patterns.
Two predominant genes, ephrin type A receptor 6 (EPHA6 (show Epha6 ELISA Kits)) and folliculin (FLCN), with mutations exclusive to African American CRCs, are by genetic and biological criteria highly likely African American CRC (show CALR ELISA Kits) driver genes.
Findings suggest that folliculin deficient renal cell carcinoma cells are highly sensitive to irradiation due to increased autophagic cell death, unlike other types of renal cell carcinoma.
This gene is located within the Smith-Magenis syndrome region on chromosome 17. Mutations in this gene are associated with Birt-Hogg-Dube syndrome, which is characterized by fibrofolliculomas, renal tumors, lung cysts, and pneumothorax. Alternative splicing of this gene results in two transcript variants encoding different isoforms.
, birt-Hogg-Dube syndrome protein homolog
, BHD skin lesion fibrofolliculoma protein
, birt-Hogg-Dube syndrome protein