ArticleProceedings of the National Academy of Sciences of the United States of America2015
Folliculin-interacting proteins Fnip1 and Fnip2 play critical roles in kidney tumor suppression in cooperation with Flcn.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 94 citations in OpenAlex.
- Pulmonary Manifestations of Birt-Hogg-Dubé Syndrome: A Single-Centre Retrospective Case Series of Seven Genetically Confirmed Patients.Journal of clinical medicine · 2026Article
- Integrative In Silico mRNA-miRNA Profiling of mTOR Pathway Dysregulation in High-Grade Serous Ovarian Carcinoma.Cancers · 2026Article
- Pellino1-mTOR/S6K1 signaling axis is a key pathogenesis for the development of polycystic kidney disease.Cell death & disease · 2026Article
- Single cell transcriptomic landscape of adult and pediatric non-ischemic cardiomyopathy.Journal of molecular and cellular cardiology · 2026Review
- FNIP1 Deficiency: Pathophysiology and Clinical Manifestations of a Rare Syndromic Primary Immunodeficiency.Current issues in molecular biology · 2025Review
- A novel uORF regulates folliculin to promote cell growth and lysosomal biogenesis during cardiac stress.Scientific reports · 2025Article
- Action and therapeutic targets of folliculin interacting protein 1: a novel signaling mechanism in redox regulation.Frontiers in cell and developmental biology · 2025Review
- Clinic Examination and Gene Diagnosis for a Birt-Hogg-Dubé Syndrome Family With a NovelHuman mutation · 2025Article
- Skeletal muscle of young females under resistance exercise exhibits a unique innate immune cell infiltration profile compared to males and elderly individuals.Journal of muscle research and cell motility · 2024Article
- The impact of aerobic and anaerobic exercise interventions on the management and outcomes of non-alcoholic fatty liver disease.Physiological research · 2024Review
- The Spectrum of Renal "TFEopathies": Flipping the mTOR Switch in Renal Tumorigenesis.Physiology (Bethesda, Md.) · 2024Review
- Review
- FNIP1 suppresses colorectal cancer progression through inhibiting STAT3 phosphorylation and nuclear translocation.iScience · 2024Article
- AMPK phosphorylation of FNIP1 (S220) controls mitochondrial function and muscle fuel utilization during exercise.Science advances · 2024Article
- Comprehensive analysis of transcriptome-wide MEpigenetics · 2023Article
- FNIP1 abrogation promotes functional revascularization of ischemic skeletal muscle by driving macrophage recruitment.Nature communications · 2023Article
- TFEB and TFE3 drive kidney cystogenesis and tumorigenesis.EMBO molecular medicine · 2023Article
- Functional TFEB activation characterizes multiple models of renal cystic disease and loss of polycystin-1.American journal of physiology. Renal physiology · 2023Article
- Imputation-powered whole-exome analysis identifies genes associated with kidney function and disease in the UK Biobank.Nature communications · 2023Article
- Impact of Co-chaperones and Posttranslational Modifications Toward Hsp90 Drug Sensitivity.Sub-cellular biochemistry · 2023Article
1 more citing papers are in PubMed but not listed here.
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Authors and funding
19 authors at 6 institutions in 3 countries.
Funding
Abstract
Folliculin (FLCN)-interacting proteins 1 and 2 (FNIP1, FNIP2) are homologous binding partners of FLCN, a tumor suppressor for kidney cancer. Recent studies have revealed potential functions for Flcn in kidney; however, kidney-specific functions for Fnip1 and Fnip2 are unknown. Here we demonstrate that Fnip1 and Fnip2 play critical roles in kidney tumor suppression in cooperation with Flcn. We observed no detectable phenotype in Fnip2 knockout mice, whereas Fnip1 deficiency produced phenotypes similar to those seen in Flcn-deficient mice in multiple organs, but not in kidneys. We found that absolute Fnip2 mRNA copy number was low relative to Fnip1 in organs that showed phenotypes under Fnip1 deficiency but was comparable to Fnip1 mRNA copy number in mouse kidney. Strikingly, kidney-targeted Fnip1/Fnip2 double inactivation produced enlarged polycystic kidneys, as was previously reported in Flcn-deficient kidneys. Kidney-specific Flcn inactivation did not further augment kidney size or cystic histology of Fnip1/Fnip2 double-deficient kidneys, suggesting pathways dysregulated in Flcn-deficient kidneys and Fnip1/Fnip2 double-deficient kidneys are convergent. Heterozygous Fnip1/homozygous Fnip2 double-knockout mice developed kidney cancer at 24 mo of age, analogous to the heterozygous Flcn knockout mouse model, further supporting the concept that Fnip1 and Fnip2 are essential for the tumor-suppressive function of Flcn and that kidney tumorigenesis in human Birt-Hogg-Dubé syndrome may be triggered by loss of interactions among Flcn, Fnip1, and Fnip2. Our findings uncover important roles for Fnip1 and Fnip2 in kidney tumor suppression and may provide molecular targets for the development of novel therapeutics for kidney cancer.
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