| http://purl.uniprot.org/citations/27303042 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/27303042 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/27303042 | http://www.w3.org/2000/01/rdf-schema#comment | "Folliculin (FLCN) is a tumor-suppressor protein mutated in the Birt-Hogg-Dubé (BHD) syndrome, which associates with two paralogous proteins, folliculin-interacting protein (FNIP)1 and FNIP2, forming a complex that interacts with the AMP-activated protein kinase (AMPK). Although it is clear that this complex influences AMPK and other metabolic regulators, reports of its effects have been inconsistent. To address this issue, we created a recessive loss-of-function variant of Fnip1 Homozygous FNIP1 deficiency resulted in profound B-cell deficiency, partially restored by overexpression of the antiapoptotic protein BCL2, whereas heterozygous deficiency caused a loss of marginal zone B cells. FNIP1-deficient mice developed cardiomyopathy characterized by left ventricular hypertrophy and glycogen accumulation, with close parallels to mice and humans bearing gain-of-function mutations in the γ2 subunit of AMPK. Concordantly, γ2-specific AMPK activity was elevated in neonatal FNIP1-deficient myocardium, whereas AMPK-dependent unc-51-like autophagy activating kinase 1 (ULK1) phosphorylation and autophagy were increased in FNIP1-deficient B-cell progenitors. These data support a role for FNIP1 as a negative regulator of AMPK."xsd:string |
| http://purl.uniprot.org/citations/27303042 | http://purl.org/dc/terms/identifier | "doi:10.1073/pnas.1607592113"xsd:string |
| http://purl.uniprot.org/citations/27303042 | http://purl.org/dc/terms/identifier | "doi:10.1073/pnas.1607592113"xsd:string |
| http://purl.uniprot.org/citations/27303042 | http://purl.uniprot.org/core/author | "Carling D."xsd:string |
| http://purl.uniprot.org/citations/27303042 | http://purl.uniprot.org/core/author | "Carling D."xsd:string |
| http://purl.uniprot.org/citations/27303042 | http://purl.uniprot.org/core/author | "Woods A."xsd:string |
| http://purl.uniprot.org/citations/27303042 | http://purl.uniprot.org/core/author | "Woods A."xsd:string |
| http://purl.uniprot.org/citations/27303042 | http://purl.uniprot.org/core/author | "Ashrafian H."xsd:string |
| http://purl.uniprot.org/citations/27303042 | http://purl.uniprot.org/core/author | "Ashrafian H."xsd:string |
| http://purl.uniprot.org/citations/27303042 | http://purl.uniprot.org/core/author | "Watkins H."xsd:string |
| http://purl.uniprot.org/citations/27303042 | http://purl.uniprot.org/core/author | "Watkins H."xsd:string |
| http://purl.uniprot.org/citations/27303042 | http://purl.uniprot.org/core/author | "Davies B."xsd:string |
| http://purl.uniprot.org/citations/27303042 | http://purl.uniprot.org/core/author | "Davies B."xsd:string |
| http://purl.uniprot.org/citations/27303042 | http://purl.uniprot.org/core/author | "Beutler B."xsd:string |
| http://purl.uniprot.org/citations/27303042 | http://purl.uniprot.org/core/author | "Beutler B."xsd:string |
| http://purl.uniprot.org/citations/27303042 | http://purl.uniprot.org/core/author | "Crawford G."xsd:string |
| http://purl.uniprot.org/citations/27303042 | http://purl.uniprot.org/core/author | "Crawford G."xsd:string |
| http://purl.uniprot.org/citations/27303042 | http://purl.uniprot.org/core/author | "Siggs O.M."xsd:string |
| http://purl.uniprot.org/citations/27303042 | http://purl.uniprot.org/core/author | "Siggs O.M."xsd:string |
| http://purl.uniprot.org/citations/27303042 | http://purl.uniprot.org/core/author | "Ghaffari S."xsd:string |
| http://purl.uniprot.org/citations/27303042 | http://purl.uniprot.org/core/author | "Ghaffari S."xsd:string |
| http://purl.uniprot.org/citations/27303042 | http://purl.uniprot.org/core/author | "Kingston B.L."xsd:string |
| http://purl.uniprot.org/citations/27303042 | http://purl.uniprot.org/core/author | "Kingston B.L."xsd:string |