Affinage

FNIP1

Folliculin-interacting protein 1 · UniProt Q8TF40

Length
1166 aa
Mass
130.6 kDa
Annotated
2026-04-28
32 papers in source corpus 22 papers cited in narrative 22 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

FNIP1 is a multifunctional adaptor protein that integrates nutrient sensing, energy homeostasis, and organelle biogenesis by coupling AMPK signaling to mTORC1-TFEB-dependent transcriptional programs and by serving as a co-chaperone of Hsp90. FNIP1 forms a heterodimeric complex with folliculin (FLCN) that acts as a GAP for RagC/D GTPases, promoting mTORC1 lysosomal recruitment; AMPK phosphorylation of FNIP1 on multiple conserved serines (including S220) suppresses this GAP activity, enabling TFEB nuclear translocation and sequential waves of lysosomal and mitochondrial biogenesis (PMID:37079666, PMID:38324677). FNIP1 independently functions as a negative regulator of AMPK in B cells, heart, and skeletal muscle, where its loss causes developmental arrest of B and iNKT cells, cardiomyopathy, and a shift to oxidative slow-twitch fibers via the AMPK–PGC-1α axis (PMID:22608497, PMID:27303042, PMID:25548157). CK2-mediated phosphorylation of FNIP1 promotes its interaction with Hsp90 and incremental inhibition of Hsp90 ATPase activity, while PP5 dephosphorylation and O-GlcNAcylation target FNIP1 for ubiquitin-dependent degradation; additionally, FNIP1 binds SERCA to suppress Ca²⁺-dependent thermogenesis in adipocytes and binds phosphorylated STAT3 to limit its nuclear translocation (PMID:30699359, PMID:35412553, PMID:39262790).

Mechanistic history

Synthesis pass · year-by-year structured walk · 11 steps
  1. 2006 High

    Identifying FNIP1 as a FLCN-binding, AMPK-phosphorylated protein placed it at the intersection of AMPK and mTOR signaling, establishing the molecular framework for all subsequent pathway dissection.

    Evidence Co-immunoprecipitation, in vitro AMPK phosphorylation assay, and pharmacological inhibition in mammalian cells

    PMID:17028174

    Open questions at the time
    • AMPK phosphorylation sites on FNIP1 not mapped
    • functional consequence of phosphorylation unknown
    • no in vivo model
  2. 2008 Medium

    Mapping the FLCN–FNIP1 interaction to C-terminal domains and showing that FNIP1 knockdown reduces S6K1 phosphorylation established the complex as a positive regulator of mTOR signaling.

    Evidence Co-IP domain mapping and siRNA knockdown with S6K1 phosphorylation readout

    PMID:18663353

    Open questions at the time
    • Whether mTOR regulation is direct or indirect was unresolved
    • no structural information
  3. 2012 High

    Fnip1 knockout mice revealed that FNIP1 is essential for B cell and iNKT cell development by maintaining metabolic homeostasis through AMPK/mTOR balance, extending the protein's role from biochemistry to an in vivo developmental checkpoint.

    Evidence Global Fnip1 KO mice, conditional Flcn deletion, Bcl2 transgene rescue, flow cytometry, apoptosis and metabolic assays

    PMID:22608497 PMID:22709692

    Open questions at the time
    • Whether FNIP1 directly suppresses AMPK activity was unclear
    • mechanism linking metabolic dysregulation to apoptosis not defined
  4. 2014 High

    Genetic epistasis in Fnip1/PGC-1α double-knockout mice established that FNIP1 acts upstream of AMPK–PGC-1α to control skeletal muscle fiber type, revealing a tissue-specific metabolic function beyond immune cells; simultaneously, iNKT cell arrest confirmed generalized immune metabolic checkpoint function.

    Evidence Fnip1 KO × PGC-1α KO double mutant mice, fiber type immunostaining, mitochondrial assays; separate iNKT KO with TCR transgene and Bim KO rescue

    PMID:24785297 PMID:25548157

    Open questions at the time
    • Whether muscle fiber phenotype involves mTORC1 or is solely AMPK-dependent was unresolved
    • direct AMPK inhibition mechanism unknown
  5. 2015 High

    Crystal structure of the yeast FNIP1 orthologue Lst4 revealed a DENN/longin domain architecture mediating heterodimer formation with FLCN orthologue Lst7 and nutrient-regulated vacuolar membrane recruitment, providing the first structural framework for the complex.

    Evidence Crystal structure, gel filtration, co-IP, fluorescence microscopy in yeast

    PMID:26631379

    Open questions at the time
    • Mammalian FNIP1 structure not solved
    • GAP activity not yet assigned to the complex
  6. 2016 High

    An ENU-derived Fnip1 loss-of-function allele causing cardiomyopathy with elevated AMPK and autophagy independently confirmed FNIP1 as a negative regulator of AMPK, while miR-499 was identified as an upstream suppressor of Fnip1 mRNA linking muscle gene regulatory networks to AMPK control.

    Evidence ENU mutagenesis mouse, cardiac phenotyping, kinase assays; miR-499 target validation in vivo and in myocytes

    PMID:27303042 PMID:27506764

    Open questions at the time
    • Molecular basis of AMPK inhibition by FNIP1 not defined
    • cardiac pathology mechanism not fully dissected
  7. 2019 High

    Demonstration that CK2 phosphorylates FNIP1 to promote Hsp90 co-chaperone activity, counteracted by PP5 dephosphorylation and O-GlcNAcylation-triggered ubiquitination, revealed a second major molecular function for FNIP1 independent of FLCN and AMPK.

    Evidence In vitro phosphorylation, phospho-site mutagenesis, Hsp90 ATPase assay, ubiquitination assay

    PMID:30699359

    Open questions at the time
    • Physiological client proteins of FNIP1-regulated Hsp90 not identified
    • relationship between Hsp90 co-chaperone and FLCN-AMPK functions unclear
  8. 2021 High

    Transgenic gain- and loss-of-function models showed that FNIP1 regulates mitochondrial oxidative programming through both AMPK-dependent and AMPK-independent mechanisms, resolving earlier ambiguity about pathway dependence; separately, FLCN-FNIP1 loss induced interferon-like STAT1/2 signaling in renal cells.

    Evidence Fnip1 transgenic/KO epistasis in muscle; CRISPR KO in RPTEC/TERT1 cells with ChIP and transcriptomics

    PMID:33459596 PMID:33780446

    Open questions at the time
    • AMPK-independent mechanism not molecularly identified
    • whether STAT1/2 activation contributes to Birt-Hogg-Dubé renal pathology unknown
  9. 2022 High

    Discovery that FNIP1 binds and stimulates SERCA to suppress cytosolic Ca²⁺ and Ca²⁺-dependent thermogenesis in adipocytes identified a third major molecular activity beyond FLCN-GAP and Hsp90 co-chaperone functions.

    Evidence Adipocyte-specific FNIP1 KO mice, co-IP, Ca²⁺ imaging, SERCA activity assays

    PMID:35412553

    Open questions at the time
    • Structural basis of FNIP1-SERCA interaction unknown
    • whether SERCA regulation occurs in non-adipose tissues not tested
  10. 2023 High

    Identification of five conserved AMPK phosphorylation sites on FNIP1 that suppress FLCN-FNIP1 GAP activity toward RagC/D, enabling TFEB nuclear translocation and sequential lysosomal then mitochondrial biogenesis, provided the definitive mechanistic link between AMPK activation and mTORC1-TFEB control; the FLCN-FNIP1/2 complex was confirmed as the RagC/D GAP regulated transcriptionally by MEF2A/D.

    Evidence In vitro AMPK phosphorylation, phospho-site mutagenesis, TFEB nuclear translocation imaging, transcriptional reporters; ChIP for MEF2 at FNIP1 promoter

    PMID:37079666 PMID:37772772

    Open questions at the time
    • Whether all five sites contribute equally is untested
    • structural basis of phosphorylation-dependent GAP inhibition unknown
  11. 2024 High

    Phospho-site-specific knock-in mice (S220A/S220D) demonstrated that AMPK phosphorylation of FNIP1-S220 controls mitochondrial ETC complex assembly and exercise performance independently of mTORC1-TFEB, revealing site-specific bifurcation of FNIP1 signaling outputs; additionally, FNIP1 deficiency drives TFEB-dependent Igf2 secretion mediating muscle-bone crosstalk and binds p-STAT3 to suppress tumorigenesis.

    Evidence Phospho-site transgenic mice with exercise and ETC assays; muscle-specific KO with TFEB ChIP at Igf2 promoter and AAV rescue; Co-IP of FNIP1 with p-STAT3 and STAT3 inhibitor rescue in CRC models

    PMID:38324677 PMID:38838134 PMID:39262790

    Open questions at the time
    • Direct substrate/effector downstream of S220 phosphorylation for ETC assembly unidentified
    • whether p-STAT3 binding involves FLCN is unknown
    • physiological relevance of muscle-bone axis in human disease not established

Open questions

Synthesis pass · forward-looking unresolved questions
  • Major open questions include the structural basis of how AMPK phosphorylation inhibits FLCN-FNIP1 GAP activity, the molecular identity of the AMPK-independent mechanism controlling fiber type, whether the Hsp90 co-chaperone and SERCA-binding functions intersect with the FLCN-AMPK-mTORC1 axis, and the relevance of FNIP1 to Birt-Hogg-Dubé syndrome pathogenesis in humans.
  • No high-resolution structure of mammalian FLCN-FNIP1 in active/inactive states
  • AMPK-independent fiber-type mechanism uncharacterized
  • integration of Hsp90, SERCA, and STAT3 functions with canonical pathway untested

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 6 GO:0060090 molecular adaptor activity 4 GO:0003924 GTPase activity 2 GO:0044183 protein folding chaperone 1
Localization
GO:0005764 lysosome 3 GO:0005829 cytosol 3
Pathway
R-HSA-162582 Signal Transduction 7 R-HSA-1852241 Organelle biogenesis and maintenance 4 R-HSA-8953897 Cellular responses to stimuli 4 R-HSA-1266738 Developmental Biology 3 R-HSA-168256 Immune System 3 R-HSA-9612973 Autophagy 2
Partners
ATP2A2CSNK2A1FLCNHSP90AA1PPP5CPRKAA1PRKAA2STAT3
Complex memberships
FLCN-FNIP1FLCN-FNIP1-AMPK

Evidence

Reading pass · 22 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2006 FNIP1 was identified as a direct binding partner of folliculin (FLCN) and also interacts with AMPK. FNIP1 is phosphorylated by AMPK, and this phosphorylation is reduced by AMPK inhibitors, which also reduce FNIP1 expression. FLCN phosphorylation is diminished by rapamycin and amino acid starvation and facilitated by FNIP1 overexpression, placing FNIP1 in the AMPK and mTOR signaling pathways. Co-immunoprecipitation, pulldown, in vitro phosphorylation assay, pharmacological inhibition Proceedings of the National Academy of Sciences of the United States of America High 17028174
2008 FNIP1 interaction with FLCN is mediated mainly by the C-terminal domains of each protein. Knockdown of FNIP1 decreases S6K1 phosphorylation, indicating that the FLCN-FNIP1 complex positively regulates S6K1 phosphorylation (mTOR signaling). Co-immunoprecipitation, siRNA knockdown, western blot for S6K1 phosphorylation Oncogene Medium 18663353
2012 Fnip1 knockout mice display a complete block in B cell development at the pre-B cell stage. AMPK and mTOR are dysregulated in Fnip1-null pre-B cells, resulting in excessive cell growth and enhanced apoptosis in response to metabolic stress, establishing Fnip1 as a metabolic checkpoint for B lymphocyte development. Genetic knockout mouse model, flow cytometry, immunoglobulin transgene rescue experiment, apoptosis assays Immunity High 22608497
2012 Conditional deletion of Flcn in B cells recapitulates the pro-B cell arrest of Fnip1-null mice. The B cell developmental arrest in Fnip1-null mice results from rapid caspase-induced pre-B cell death, and a Bcl2 transgene reconstitutes mature B-cell populations, demonstrating FLCN-FNIP1 complex functions through both mTOR-dependent and independent pathways in B cell differentiation. Conditional knockout mice, Bcl2 transgene rescue, caspase activity assays, flow cytometry Blood High 22709692
2014 Loss of Fnip1 in mice increases type I slow-twitch muscle fibers, increases AMPK activation, and increases PGC1α expression. Genetic disruption of PGC1α rescues normal levels of type I fiber markers in Fnip1-null mice, placing Fnip1 upstream of AMPK-PGC1α in the control of muscle fiber type specification. Knockout mouse model, genetic epistasis (Fnip1 KO × PGC1α KO double mutant), fiber type immunostaining, mitochondrial assays, biochemical analysis Proceedings of the National Academy of Sciences of the United States of America High 25548157
2014 Fnip1-null mice show arrest of iNKT cell development at stage 2. Fnip1-null iNKT cells exhibit hyperactive mTOR, reduced mitochondrial number despite lower ATP levels, and increased apoptosis sensitivity, indicating Fnip1 maintains metabolic homeostasis required for iNKT cell maturation. Knockout mouse model, flow cytometry, TCR transgene and Bim KO rescue experiments, mitochondrial and metabolic assays Proceedings of the National Academy of Sciences of the United States of America High 24785297
2015 Structural analysis of yeast Fnip1/2 orthologue Lst4 confirms it contains a longin domain (first domain of the DENN module), and the Lst7 (folliculin orthologue)/Lst4 complex exists as a 1:1 heterodimer in solution. The Lst4 DENN domain mediates interaction with Lst7. The Lst7/Lst4 complex relocates to the vacuolar membrane in response to nutrient (carbon) starvation. Crystal structure, biochemical reconstitution, gel filtration, co-immunoprecipitation, fluorescence microscopy Open biology High 26631379
2016 miR-499 directly targets Fnip1 mRNA. Inhibition of Fnip1 reactivates AMPK/PGC-1α signaling and mitochondrial oxidative metabolism in myocytes, establishing a miR-499/Fnip1/AMPK circuit that couples muscle fiber type and mitochondrial function. In vivo mouse models, miRNA target validation, siRNA knockdown in myocytes, metabolic assays, mdx mouse model EMBO molecular medicine High 27506764
2016 A loss-of-function mutation in Fnip1 causes profound B cell deficiency, and FNIP1-deficient mice develop cardiomyopathy with left ventricular hypertrophy and glycogen accumulation. γ2-specific AMPK activity is elevated in neonatal FNIP1-deficient myocardium, and AMPK-dependent ULK1 phosphorylation and autophagy are increased in FNIP1-deficient B cell progenitors, confirming FNIP1 as a negative regulator of AMPK. ENU-mutagenesis mouse model, cardiac phenotyping, kinase activity assays, autophagy assays, BCL2 rescue Proceedings of the National Academy of Sciences of the United States of America High 27303042
2019 CK2 phosphorylates FNIP1 on priming serine-938, triggering relay phosphorylation on S939, S941, S946, and S948, which promotes FNIP1 interaction with Hsp90 and leads to incremental inhibition of Hsp90 ATPase activity and gradual activation of Hsp90 client proteins. PP5 dephosphorylates FNIP1, enabling O-GlcNAc addition to S938 that antagonizes phosphorylation, prevents Hsp90 interaction, and promotes FNIP1 ubiquitination at K1119 and proteasomal degradation. In vitro phosphorylation assay, mutagenesis of phospho-sites, co-immunoprecipitation, ATPase activity assay, ubiquitination assay, client protein activation assays Cell reports High 30699359
2021 FNIP1 controls skeletal muscle mitochondrial oxidative program through AMPK signaling; basal levels of FNIP1 are sufficient to inhibit AMPK but not mTORC1 activity. Surprisingly, FNIP1 actions on type I fiber program are independent of AMPK and its downstream PGC-1α, establishing separable AMPK-dependent and -independent functions of FNIP1. Transgenic and knockout mouse models (Fnip1Tg, Fnip1KO, Fnip1TgKO), primary muscle cell assays, genetic epistasis PLoS genetics High 33780446
2021 Loss of FLCN or its binding partners FNIP1/FNIP2 in human renal tubular epithelial cells induces an interferon response independently of interferon, with STAT2 recruitment to chromatin and slowed cellular proliferation, identifying STAT1/2 signaling as a novel target downstream of the FLCN-FNIP complex in renal cells. CRISPR knockout in RPTEC/TERT1 cells, chromatin immunoprecipitation, transcriptomics, proliferation assays eLife Medium 33459596
2022 FNIP1 binds to and promotes the activity of SERCA (the main Ca2+ pump responsible for cytosolic Ca2+ removal) in adipocytes. Loss of FNIP1 results in enhanced intracellular Ca2+ signals and activation of a Ca2+-dependent thermogenic program, establishing FNIP1 as a negative regulator of beige adipocyte thermogenesis through SERCA-Ca2+ dynamics. Adipocyte-specific FNIP1 knockout mice, co-immunoprecipitation, Ca2+ imaging, SERCA activity assays, mitochondrial respiration assays, metabolic phenotyping The Journal of experimental medicine High 35412553
2023 AMPK directly phosphorylates five conserved serine residues in FNIP1, suppressing the function of the FLCN-FNIP1 complex. FNIP1 phosphorylation by AMPK is required for nuclear translocation of TFEB and TFEB-dependent increases of PGC1α and ERRα mRNAs, linking mitochondrial damage to sequential waves of lysosomal and mitochondrial biogenesis. In vitro AMPK phosphorylation assay, phospho-site mutagenesis, TFEB nuclear translocation imaging, transcriptional reporter assays, mitochondrial biogenesis assays Science (New York, N.Y.) High 37079666
2023 MEF2A and MEF2D transcription factors directly regulate transcription of FNIP1 and FNIP2. The FLCN-FNIP1/2 complex acts as a GTPase-activating protein (GAP) for RRAGC/RRAGD to promote mTORC1 recruitment to lysosomes and activation. SRC kinase phosphorylates MEF2D, enhancing its transcriptional activity and MTORC1 activation through FNIP1/2 upregulation. ChIP, transcriptional reporter assays, knockdown/overexpression, lysosomal fractionation, mTORC1 activity assays Autophagy Medium 37772772
2023 Myofiber-specific FNIP1 deficiency stimulates PGC-1α to activate chemokine gene transcription, driving macrophage recruitment and functional muscle angiogenesis independently of AMPK. Muscle-specific knockout mouse model, hindlimb ischemia model, macrophage depletion, gene expression analysis, blood flow measurement Nature communications Medium 37932296
2023 FNIP1 is a substrate of the FEM1b ubiquitin ligase axis; the FEM1b-FNIP1 interaction is targetable by the small molecule EN106. FNIP1 alters mitochondrial morphology, reduces oxidative phosphorylation, and protects cells from ROS accumulation. In vitro experiments in HUVECs, pharmacological inhibition with EN106, cellular ROS and mitochondrial morphology assays Bioactive materials Low 37521275
2024 AMPK phosphorylation of FNIP1 at serine-220 (S220) controls mitochondrial electron transfer chain complex assembly, fuel utilization, and exercise performance in skeletal muscle. Using nonphosphorylatable (S220A) and phosphomimetic (S220D) transgenic mouse models, S220 phosphorylation was shown to regulate mitochondrial function independently of mTORC1-TFEB signaling. Phospho-site specific transgenic mouse models (S220A/S220D), in vitro AMPK phosphorylation, primary muscle cell biochemistry, exercise performance assays, electron transport chain complex assembly assays Science advances High 38324677
2024 Muscle-specific FNIP1 deficiency stimulates nuclear translocation of TFEB, which activates transcription of Igf2 at a conserved promoter-binding site, leading to IGF2 secretion that stimulates osteoclastogenesis through IGF2 receptor signaling, establishing a muscle-bone cross-talk axis. Muscle-specific FNIP1 knockout and rescue (AAV9-FNIP1), TFEB ChIP at Igf2 promoter, AAV9-IGF2 overexpression, osteoclast assays, bone phenotyping Science translational medicine High 38838134
2024 FNIP1 binds to phosphorylated STAT3 (p-STAT3) and suppresses its expression. Loss of FNIP1 increases STAT3 phosphorylation and nuclear localization, and pharmacological inhibition of p-STAT3 rescues the excessive tumorigenesis caused by FNIP1 deletion in colorectal cancer cells. Co-immunoprecipitation, in vivo and in vitro knockout models, STAT3 phosphorylation western blot, nuclear fractionation, p-STAT3 inhibitor rescue iScience Medium 39262790
2024 MITF suppresses melanoma mesenchymal phenotype by activating expression of FNIP1, FNIP2, and FLCN, components of the non-canonical mTORC1 pathway, thereby promoting cytoplasmic retention and lysosome-mediated degradation of TFE3. Transcriptional reporter assays, TFE3 localization imaging, FNIP1/FNIP2/FLCN expression manipulation in melanoma cell lines bioRxivpreprint Low bio_10.1101_2024.07.11.603140
2026 Fnip1 modulates B cell receptor (BCR) signaling thresholds and metabolic programming by regulating the AMPK/FLCN/TFEB and CD19/PI3K/Akt/mTORC1 pathways, restricting TFEB nuclear access. Loss of Fnip1 in conditional knockout mice causes arrest at the transitional B220+CD93mid stage. Conditional knockout mouse model, BCR signaling assays, TFEB nuclear localization imaging, metabolic assays, MD4/mHEL/sHEL tolerance model bioRxivpreprint Medium 41959523

Source papers

Stage 0 corpus · 32 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2006 Folliculin encoded by the BHD gene interacts with a binding protein, FNIP1, and AMPK, and is involved in AMPK and mTOR signaling. Proceedings of the National Academy of Sciences of the United States of America 395 17028174
2023 Induction of lysosomal and mitochondrial biogenesis by AMPK phosphorylation of FNIP1. Science (New York, N.Y.) 165 37079666
2016 Coupling of mitochondrial function and skeletal muscle fiber type by a miR-499/Fnip1/AMPK circuit. EMBO molecular medicine 111 27506764
2008 Interaction of folliculin (Birt-Hogg-Dubé gene product) with a novel Fnip1-like (FnipL/Fnip2) protein. Oncogene 107 18663353
2014 Fnip1 regulates skeletal muscle fiber type specification, fatigue resistance, and susceptibility to muscular dystrophy. Proceedings of the National Academy of Sciences of the United States of America 98 25548157
2012 Disruption of Fnip1 reveals a metabolic checkpoint controlling B lymphocyte development. Immunity 71 22608497
2012 The folliculin-FNIP1 pathway deleted in human Birt-Hogg-Dubé syndrome is required for murine B-cell development. Blood 60 22709692
2023 Glucose-responsive, antioxidative HA-PBA-FA/EN106 hydrogel enhanced diabetic wound healing through modulation of FEM1b-FNIP1 axis and promoting angiogenesis. Bioactive materials 55 37521275
2019 Post-translational Regulation of FNIP1 Creates a Rheostat for the Molecular Chaperone Hsp90. Cell reports 48 30699359
2016 Mutation of Fnip1 is associated with B-cell deficiency, cardiomyopathy, and elevated AMPK activity. Proceedings of the National Academy of Sciences of the United States of America 47 27303042
2021 AMPK-dependent and -independent coordination of mitochondrial function and muscle fiber type by FNIP1. PLoS genetics 37 33780446
2014 Metabolic regulator Fnip1 is crucial for iNKT lymphocyte development. Proceedings of the National Academy of Sciences of the United States of America 37 24785297
2017 Dihydromyricetin prevents obesity-induced slow-twitch-fiber reduction partially via FLCN/FNIP1/AMPK pathway. Biochimica et biophysica acta. Molecular basis of disease 36 28363698
2015 Lst4, the yeast Fnip1/2 orthologue, is a DENN-family protein. Open biology 28 26631379
2022 FNIP1 regulates adipocyte browning and systemic glucose homeostasis in mice by shaping intracellular calcium dynamics. The Journal of experimental medicine 26 35412553
2020 Mutations of the gene FNIP1 associated with a syndromic autosomal recessive immunodeficiency with cardiomyopathy and pre-excitation syndrome. European journal of immunology 26 32181500
2018 Loss of Fnip1 alters kidney developmental transcriptional program and synergizes with TSC1 loss to promote mTORC1 activation and renal cyst formation. PloS one 26 29897930
2024 Muscle-bone cross-talk through the FNIP1-TFEB-IGF2 axis is associated with bone metabolism in human and mouse. Science translational medicine 24 38838134
2024 AMPK phosphorylation of FNIP1 (S220) controls mitochondrial function and muscle fuel utilization during exercise. Science advances 20 38324677
2021 Loss of FLCN-FNIP1/2 induces a non-canonical interferon response in human renal tubular epithelial cells. eLife 18 33459596
2023 A Neutral Polysaccharide from Spores of Ophiocordyceps gracilis Regulates Oxidative Stress via NRF2/FNIP1 Pathway. International journal of molecular sciences 13 37834168
2023 FNIP1 abrogation promotes functional revascularization of ischemic skeletal muscle by driving macrophage recruitment. Nature communications 13 37932296
2024 FNIP1: A key regulator of mitochondrial function. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 12 39013219
2023 Direct regulation of FNIP1 and FNIP2 by MEF2 sustains MTORC1 activation and tumor progression in pancreatic cancer. Autophagy 11 37772772
2023 Familial multiple discoid fibromas is linked to a locus on chromosome 5 including the FNIP1 gene. Journal of human genetics 10 36599954
2023 AMPK promotes lysosomal and mitochondrial biogenesis via folliculin:FNIP1. Life metabolism 6 37621729
2024 A novel mutation in FNIP1 associated with a syndromic immunodeficiency and cardiomyopathy. Immunogenetics 3 39537849
2024 Clinical and Immunologic Features of a Patient With Homozygous FNIP1 Variant. Journal of pediatric hematology/oncology 2 38748614
2025 Klebsiella pneumoniae causes mammary gland damage via FNIP1-mediated mitochondrial dysfunction. Journal of animal science 1 41206543
2024 FNIP1 suppresses colorectal cancer progression through inhibiting STAT3 phosphorylation and nuclear translocation. iScience 1 39262790
2026 FNIP1 Modulates B Cell Receptor Signaling Strength by Coordinating Metabolism During Development. bioRxiv : the preprint server for biology 0 41959523
2025 FNIP1 Deficiency: Pathophysiology and Clinical Manifestations of a Rare Syndromic Primary Immunodeficiency. Current issues in molecular biology 0 40699689