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FLCN is located within the Smith-Magenis syndrome region on chromosome 17. Additionally we are shipping FLCN Antibodies (87) and FLCN Kits (8) and many more products for this protein.
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Tfe3 (show TFE3 Proteins) overexpression in HSPCs impaired long-term hematopoietic reconstitution in vivo, recapitulating the Flcn KO phenotype, and supporting the notion that abnormal activation of Tfe3 (show TFE3 Proteins) contributes to the Flcn KO phenotype. Flcn KO mice develop an acute histiocytic hyperplasia in multiple organs, suggesting a novel function for Flcn in macrophage development
mTOR (show FRAP1 Proteins) inhibitor, sirolimus, suppresses the tumor's growth, suggesting that mTOR (show FRAP1 Proteins) inhibitors might be effective in control of FLCN-deficient RCC (show XRCC1 Proteins).
we show that glycogen (show GYS1 Proteins) accumulates in kidneys from mice lacking FLCN and in renal tumors from a BHD patient
Fnip1 and Fnip2 (show FNIP2 Proteins) 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 Proteins) association is modulated by the presence of either folliculin-interacting protein (FNIP)-1 or FNIP2 (show FNIP2 Proteins) and further regulated by ULK1 (show ULK1 Proteins).
Flcn regulates apoptosis in lung epithelium via E-cadherin (show CDH1 Proteins)-LKB1 (show STK11 Proteins)-AMPK (show PRKAA1 Proteins) axis.
loss of FLCN constitutively activates AMPK (show PRKAA1 Proteins), resulting in PGC-1alpha-mediated mitochondrial biogenesis and increased ROS (show ROS1 Proteins) production
These data support a model in which dysregulation of the FLCN-p0071 (show PKP4 Proteins) interaction leads to alterations in cell adhesion, cell polarity, and RhoA (show RHOA Proteins) signaling.
FLCN deficiency and subsequent increased PPARGC1A expression result in increased mitochondrial function and oxidative metabolism as the source of cellular energy, which may drive hyperplastic transformation.
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 Proteins)) and folliculin (FLCN), with mutations exclusive to African American CRCs, are by genetic and biological criteria highly likely African American CRC (show CALR Proteins) driver genes.
Findings suggest that folliculin deficient renal cell carcinoma (show MOK Proteins) cells are highly sensitive to irradiation due to increased autophagic cell death, unlike other types of renal cell carcinoma (show MOK Proteins).
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