Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
FLCN is located within the Smith-Magenis syndrome region on chromosome 17. Additionally we are shipping FLCN Kits (8) and FLCN Proteins (6) and many more products for this protein.
Showing 10 out of 86 products:
Human Polyclonal FLCN Primary Antibody for EIA, WB - ABIN453652
Khoo, Giraud, Kahnoski, Chen, Motorna, Nickolov, Binet, Lambert, Friedel, Lévy, Ferlicot, Wolkenstein, Hammel, Bergerheim, Hedblad, Bradley, Teh, Nordenskjöld, Richard: Clinical and genetic studies of Birt-Hogg-Dubé syndrome. in Journal of medical genetics 2002
Show all 2 references for ABIN453652
Human Polyclonal FLCN Primary Antibody for ELISA, WB - ABIN531278
Nahorski, Reiman, Lim, Nookala, Seabra, Lu, Fenton, Boora, Nordenskjöld, Latif, Hurst, Maher: Birt Hogg-Dubé syndrome-associated FLCN mutations disrupt protein stability. in Human mutation 2011
Tfe3 (show TFE3 Antibodies) 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 Antibodies) 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 Antibodies) inhibitor, sirolimus, suppresses the tumor's growth, suggesting that mTOR (show FRAP1 Antibodies) inhibitors might be effective in control of FLCN-deficient RCC (show XRCC1 Antibodies).
we show that glycogen (show GYS1 Antibodies) accumulates in kidneys from mice lacking FLCN and in renal tumors from a BHD patient
Fnip1 (show FNIP1 Antibodies) and Fnip2 (show FNIP2 Antibodies) 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 Antibodies) association is modulated by the presence of either folliculin-interacting protein (FNIP)-1 (show FNIP1 Antibodies) or FNIP2 (show FNIP2 Antibodies) and further regulated by ULK1 (show ULK1 Antibodies).
Flcn regulates apoptosis in lung epithelium via E-cadherin (show CDH1 Antibodies)-LKB1 (show STK11 Antibodies)-AMPK (show PRKAA1 Antibodies) axis.
loss of FLCN constitutively activates AMPK (show PRKAA1 Antibodies), resulting in PGC-1alpha (show PPARGC1A Antibodies)-mediated mitochondrial biogenesis and increased ROS (show ROS1 Antibodies) production
These data support a model in which dysregulation of the FLCN-p0071 (show PKP4 Antibodies) interaction leads to alterations in cell adhesion, cell polarity, and RhoA (show RHOA Antibodies) signaling.
FLCN deficiency and subsequent increased PPARGC1A (show PPARGC1A Antibodies) expression result in increased mitochondrial function and oxidative metabolism as the source of cellular energy, which may drive hyperplastic transformation.
We report Smith-Magenis syndrome who presents bilateral renal tumors. This is most likely related to haploinsufficiency of FLCN gene, located in the deleted region
For patients whose clinical features are atypical, detection of germline mutation in FLCN gene would help confirm diagnosis. The 2 mutations we reported would expand the mutation spectrum of FLCN gene associated with BHD syndrome
DNA sequence analyses determined that there was a two base pair deletion in exon 4 of the FLCN gene, confirming the diagnosis of BHD syndrome.
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.
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