Affinage

INF2

Inverted formin-2 · UniProt Q27J81

Length
1249 aa
Mass
135.6 kDa
Annotated
2026-06-10
84 papers in source corpus 39 papers cited in narrative 39 extracted findings
Cross-family judge vs UniProt: tie faithfulness: 6/7 claims corpus-supported (86%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

INF2 is an ER-anchored formin that uniquely combines actin filament nucleation, processive barbed-end elongation, and filament severing/depolymerization to drive rapid actin turnover at organelle membranes (PMID:19366733, PMID:24412206, PMID:26124273). Its catalytic core nucleates and elongates actin, while the FH2 domain encircles filament sides and, together with a C-terminal WH2/DAD motif, severs filaments after phosphate release (PMID:24412206, PMID:40993919); this generates short, fast-turning-over filaments whose disassembly is rate-limited by nucleotide exchange and accelerated by profilin (PMID:26124273). INF2 is held inactive by intramolecular DID-DAD autoinhibition that selectively suppresses depolymerization (PMID:19366733), and is activated by Ca2+/calmodulin binding to an N-terminal CaM-binding site required for stress-induced actin assembly and MRTF nuclear translocation (PMID:36306014, PMID:41498749). The CAAX/farnesylated isoform anchors to the ER cytoplasmic face, where INF2-driven actin polymerization at ER-mitochondria contacts mediates initial mitochondrial constriction upstream of Drp1 fission (PMID:19366733, PMID:23349293), a function tuned by SPOP/CUL3 and FBXO7 ubiquitination and by AMPK phosphorylation (PMID:28448495, PMID:38233384, PMID:37344480), and extended to endosomal and lysosomal fission and to IP3R cluster organization that supports ER-to-mitochondria calcium transfer (PMID:42259291). INF2 also bundles and stabilizes microtubules through its C-terminus, acting downstream of an mDia1→IQGAP1→INF2 cascade to build detyrosinated microtubules and reorient the centrosome (PMID:21998204, PMID:22986496, PMID:27030671), and regulates polarized membrane trafficking through MAL/MAL2 and Cdc42 (PMID:20493814, PMID:20881207). INF2 functions as a node in Rho/mDia and MRTF-SRF transcriptional signaling, where it inhibits mDia-driven actin polymerization via DID-DAD contacts (PMID:21278336, PMID:26086034). Mutations in the DID cause autosomal-dominant focal segmental glomerulosclerosis and Charcot-Marie-Tooth neuropathy (PMID:20023659, PMID:22187985); these are gain-of-function alleles that escape CAP/acetylated-actin- and mDia-mediated inhibition, constitutively activate actin polymerization, and disrupt DYNLL1-dependent nephrin trafficking, ultimately driving MRTF-SRF reprogramming and mitotic catastrophe (PMID:30962575, PMID:33443052, PMID:39536114, PMID:38916773).

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 2009 High

    Established INF2 as an ER-localized formin whose distinctive depolymerization activity is held in check by an intramolecular DID-DAD interaction, defining its core autoregulatory architecture.

    Evidence Subcellular fractionation, farnesylation inhibition, in vitro binding/Kd measurement, and pyrene-actin assays with DAD/WH2 mutants

    PMID:19366733

    Open questions at the time
    • Did not establish the physiological trigger that relieves autoinhibition
    • Structural basis of FH2-mediated severing not yet defined
  2. 2009 Medium

    Linked INF2 to human disease by showing DID missense mutations cause autosomal-dominant FSGS, focusing attention on the autoregulatory domain in podocyte actin control.

    Evidence Linkage analysis and candidate gene sequencing across 11 FSGS families

    PMID:20023659

    Open questions at the time
    • No in vitro functional consequence of the mutations demonstrated in this study
    • Cell type-specific mechanism not addressed
  3. 2010 High

    Placed INF2 in polarized membrane trafficking by identifying MAL/MAL2 and GTP-Cdc42 as partners required for transcytosis, lumen formation, and Lck-dependent immunological synapse assembly.

    Evidence Reciprocal Co-IP, siRNA knockdown, GTP-loading assays, and activity-dead mutant rescue in epithelial and T cells

    PMID:20493814 PMID:20881207

    Open questions at the time
    • Whether trafficking roles depend on ER versus non-CAAX isoform unresolved
    • Direct substrate filaments for transcytosis not visualized
  4. 2011 High

    Defined INF2's signaling and cytoskeletal cross-talk: its DID binds mDia DADs to restrain Rho/SRF-driven actin polymerization, and its C-terminus bundles and stabilizes microtubules.

    Evidence Yeast two-hybrid, in vitro binding, Co-IP, SRF reporter assays, and microtubule co-sedimentation/bundling assays

    PMID:21278336 PMID:21998196 PMID:21998204

    Open questions at the time
    • How DID-mDia inhibition is integrated with INF2's own actin activity unclear
    • Non-CAAX isoform role at Golgi mechanistically incomplete
  5. 2012 High

    Refined the catalytic mechanism and a microtubule-stabilization function: specific FH2 residues separate capping/severing from elongation, and INF2 is required for detyrosinated microtubule formation and centrosome reorientation.

    Evidence Pyrene-actin and TIRF assays with FH2 point mutants plus knockdown and FH2 rescue in T cells

    PMID:22879592 PMID:22986496

    Open questions at the time
    • Coupling between actin and microtubule activities at the molecular level unresolved
  6. 2013 High

    Identified INF2's signature cellular role: ER-anchored actin polymerization at ER-mitochondria contacts drives initial mitochondrial constriction upstream of Drp1, establishing actin's role in fission.

    Evidence siRNA knockdown, super-resolution and live imaging, and Drp1 epistasis

    PMID:23349293

    Open questions at the time
    • Signal initiating contact-site actin polymerization not defined
    • Quantitative contribution relative to Drp1 not resolved
  7. 2014 High

    Resolved the severing mechanism structurally, showing FH2 encircles filament sides and requires phosphate release, with the WH2/DAD boosting severing potency.

    Evidence 20 Å helical 3D EM reconstruction, two-color TIRF, and phosphate-release/truncation assays

    PMID:24412206

    Open questions at the time
    • Atomic-resolution structure of the severing complex not obtained
  8. 2014 Medium

    Provided in vivo validation that INF2 acts upstream of RhoA/Dia in the glomerulus and that FSGS DID mutants are loss-of-rescue alleles in this context.

    Evidence Zebrafish morpholino knockdown with human INF2 WT/mutant rescue and RhoA/Dia2 genetic epistasis

    PMID:26086034

    Open questions at the time
    • Single model system
    • Mechanistic reconciliation with gain-of-function findings unresolved
  9. 2015 High

    Characterized INF2's rapid filament turnover kinetics, identifying nucleotide exchange as rate-limiting and profilin as an accelerator, and confirmed conserved in vivo function through the C. elegans ortholog.

    Evidence Pyrene/TIRF kinetics with profilin titration and C. elegans exc-6 rescue with human disease variants

    PMID:25771894 PMID:26124273

    Open questions at the time
    • In vivo relevance of short-filament steady state not directly tested
  10. 2016 High

    Defined a formin activation cascade in which IQGAP1 scaffolds mDia1 to INF2 to build stable detyrosinated microtubules, linking actin and microtubule regulation hierarchically.

    Evidence Direct binding assays, Co-IP, knockdown, and MT dynamics measurements with interaction-disrupting mutants

    PMID:27030671

    Open questions at the time
    • Whether INF2 microtubule and actin pools are spatially distinct unclear
  11. 2017 High

    Showed INF2 mitochondrial fission activity is restrained post-translationally by SPOP/CUL3 atypical ubiquitination that controls its ER localization rather than its stability.

    Evidence Co-IP, in-cell ubiquitination assays, ER/DRP1 imaging, and SPOP-binding motif mutagenesis

    PMID:28448495

    Open questions at the time
    • Upstream signals controlling SPOP-INF2 engagement not defined
  12. 2019 High

    Discovered facilitated autoinhibition: a CAP·lysine-acetylated-actin complex bridges DID and DAD to inhibit INF2, relieved by HDAC6 deacetylation, and impaired by disease DID mutants.

    Evidence Endogenous inhibitor purification, in vitro reconstitution with K50/K61 acetylmimetics, HDAC6 treatment, and disease-mutant binding assays

    PMID:30962575 PMID:31871199

    Open questions at the time
    • Cellular dynamics of acetylation-controlled switching not fully mapped
    • Later contradicted regarding CAP requirement for inhibition
  13. 2020 High

    Demonstrated that diverse FSGS/CMT mutations are gain-of-function alleles producing graded constitutive formin activation, and uncovered additional disease-relevant interactions with DYNLL1, CFTR, mDIA1, and a cathepsin-cleaved DID fragment.

    Evidence Quantitative CaAR live imaging across >50 mutants, Y2H, surface trafficking assays, protease inhibition, and a R218Q knockin mouse

    PMID:31924668 PMID:32444357 PMID:32573649 PMID:33443052

    Open questions at the time
    • How a single DID determines both mitochondrial and trafficking phenotypes unresolved
    • Quantitative activation thresholds distinguishing FSGS from CMT not mechanistically explained
  14. 2022 High

    Identified Ca2+/calmodulin binding at an N-terminal site as a direct activating input required for stress-induced actin assembly and MRTF nuclear translocation, and extended INF2 activation to neuronal injury (actinification).

    Evidence NMR structure with 1-4-8 motif mutagenesis, KO complementation, MRTF assays, and neuronal NMDA/ischemia models

    PMID:36229429 PMID:36306014

    Open questions at the time
    • Integration of CaM activation with DID-DAD/CAP autoinhibition not resolved
    • 8S INF2:actin complex stoichiometry resolved only at low EM resolution (#36)
  15. 2024 Medium

    Established R218Q as a gain-of-function allele driving FSGS in vivo and dissected its downstream effects on actin, adhesion, mitochondria, nephrin proteostasis, MRTF-SRF reprogramming, and mitotic catastrophe.

    Evidence Knockin-versus-knockout mouse comparisons, organoids, RNA-seq, Co-IP, DYNLL1-PI31 trafficking dissection with bortezomib rescue, and pathogenic-variant ER/mitochondria imaging

    PMID:38916773 PMID:39337270 PMID:39536114 PMID:39621430

    Open questions at the time
    • Tissue specificity of podocyte/Schwann vulnerability not fully explained
    • Causal ordering of mitochondrial versus adhesion phenotypes unresolved
  16. 2024 Medium

    Expanded regulatory and physiological scope: AMPK phosphorylation and FBXO7 ubiquitination tune INF2-DRP1 fission in cancer, CAP1/CAP2 inhibit INF2 during dendritic spine maturation, and ER-actin marks endosome/lysosome fission.

    Evidence Kinase and ubiquitination assays, neuronal genetic epistasis, and live organelle imaging (one preprint)

    PMID:37344480 PMID:38233384 PMID:39154297 PMID:39184068

    Open questions at the time
    • Whether multiple regulatory inputs converge on the same INF2 pool unknown
    • Organelle-fission generality not yet peer-reviewed (#31)
  17. 2025 Medium

    Connected mechanosensory and meiotic contexts and revised the autoinhibition model, proposing actin buffering by profilin/thymosin rather than CAP is required, alongside refined structural definition of the WH2/DAD helix.

    Evidence Cell-free reconstitution, Piezo1/INF2 confinement migration assays, oocyte knockdown with Co-IP, and NMR of the WH2/DAD

    PMID:40120583 PMID:40180021 PMID:40993919 PMID:41498749

    Open questions at the time
    • CAP-requirement contradiction (#32 vs #17/#18) awaits independent reconciliation
    • Single-study mechanistic claims for migration and meiosis
  18. 2026 Medium

    Defined an INF2-IP3R axis in which INF2 actin activity organizes IP3R clusters to position ER-mitochondria contacts and facilitate calcium transfer, integrating its fission and calcium-handling roles.

    Evidence Co-IP, knockdown, calcium and IP3R cluster imaging, and activity-mutant dissection

    PMID:42259291

    Open questions at the time
    • Single study
    • Whether IP3R clustering precedes or follows fission machinery recruitment unclear

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the multiple activating (Ca2+/CaM, HDAC6, mechanical/ionic) and inhibitory (CAP/acetyl-actin, profilin buffering, ubiquitination, phosphorylation) inputs are integrated in space and time to select between mitochondrial, microtubule, trafficking, and transcriptional outputs remains unresolved.
  • No unified model reconciling CAP-dependent versus actin-buffering-dependent autoinhibition
  • No atomic structure of activated full-length INF2 on a filament
  • Mechanism dictating cell-type-specific disease vulnerability undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0008092 cytoskeletal protein binding 3 GO:0140096 catalytic activity, acting on a protein 3 GO:0098772 molecular function regulator activity 2 GO:0140313 molecular sequestering activity 2
Localization
GO:0005783 endoplasmic reticulum 4 GO:0005815 microtubule organizing center 2 GO:0005829 cytosol 2 GO:0005856 cytoskeleton 2
Pathway
R-HSA-162582 Signal Transduction 4 R-HSA-1643685 Disease 4 R-HSA-1852241 Organelle biogenesis and maintenance 4 R-HSA-9609507 Protein localization 4 R-HSA-74160 Gene expression (Transcription) 3
Partners
CDC42DIAPH1DNM1LDYNLL1IQGAP1ITPR1MALMAL2

Evidence

Reading pass · 39 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2009 INF2 is peripherally bound to the cytoplasmic face of the endoplasmic reticulum (ER) in Swiss 3T3 cells. ER localization requires a C-terminal farnesyl (prenyl) group on INF2, though farnesylation alone is insufficient and ionic interactions also contribute. The WH2 motif of INF2 functions as a diaphanous autoregulatory domain (DAD) that binds to the N-terminal diaphanous inhibitory domain (DID) with an apparent Kd of 1.1 µM. The DID-DAD interaction does not inhibit actin nucleation but does inhibit INF2's depolymerization activity. DAD/WH2 point mutations that disrupt DID-DAD interaction also abolish depolymerization activity, and expression of these mutants causes ER collapse around the nucleus with actin filament accumulation around the collapsed ER. Subcellular fractionation, membrane extraction, immunofluorescence of endogenous and GFP-fusion INF2, farnesylation inhibitor experiments, in vitro binding assays (Kd measurement), pyrene-actin polymerization and depolymerization assays, site-directed mutagenesis Journal of cell science High 19366733
2009 Mutations in the diaphanous inhibitory domain (DID) of INF2 cause autosomal-dominant focal segmental glomerulosclerosis (FSGS). All nine independent disease-causing missense mutations are located within the DID, altering highly conserved residues, implicating this domain in podocyte actin regulation. Linkage analysis, candidate gene sequencing in 11 unrelated FSGS families, segregation analysis Nature genetics Medium 20023659
2010 INF2 is a binding partner of MAL2 in epithelial cells. Cdc42 binds INF2 in a GTP-loaded-dependent manner. Cdc42 and INF2 regulate MAL2 dynamics and are both necessary for basolateral-to-apical transcytosis and lumen formation in HepG2 and MDCK cells. Both the actin polymerization and depolymerization activities of INF2 are required for efficient transcytosis. Co-immunoprecipitation, siRNA knockdown, videomicroscopy, GTP-loading assays, organotypic culture lumen-formation assay Developmental cell High 20493814
2010 INF2 interacts with MAL in Schwann cells and T lymphocytes. In Jurkat T cells, INF2 colocalizes with MAL at the cell periphery and pericentriolar endosomes and along microtubules. Knockdown of INF2 reduces MAL+ transport vesicle formation and Lck levels at the plasma membrane, impairing immunological synapse formation. Cdc42 and Rac1 bind INF2 and regulate Lck transport. Both actin polymerization and depolymerization activities of INF2 are required for Lck targeting. Co-immunoprecipitation, siRNA knockdown, videomicroscopy, flow cytometry (surface Lck), immunological synapse assay, dominant-negative GTPase constructs Blood High 20881207
2011 INF2 mutations cause Charcot-Marie-Tooth neuropathy with FSGS. INF2 colocalizes and physically interacts with MAL in Schwann cells. Disease-causing INF2 DID mutants perturb the INF2-MAL-CDC42 pathway, resulting in cytoskeleton disorganization, enhanced INF2 binding to CDC42, and mislocalization of INF2, MAL, and CDC42. Direct INF2 sequencing in CMT+FSGS patients, immunohistochemistry, co-immunoprecipitation, co-localization imaging, functional cell studies with mutant constructs The New England journal of medicine High 22187985
2011 INF2's DID domain interacts with the DADs of mDia1, mDia2, and mDia3. This interaction was confirmed by yeast two-hybrid, in vitro biochemical assays, and co-immunoprecipitation in cells. INF2_DID/mDia_DAD binding inhibits mDia-mediated, Rho-activated actin polymerization and SRF-responsive gene transcription. Disease-causing INF2 DID mutations (E184K, R218Q) decrease this inhibitory effect, suggesting DID-mDia DAD interaction is disrupted by FSGS mutations. Yeast two-hybrid screen, in vitro binding assays, co-immunoprecipitation, actin polymerization assays, SRF luciferase reporter assays, site-directed mutagenesis Proceedings of the National Academy of Sciences of the United States of America High 21278336
2011 INF2 is expressed as two C-terminal splice variants: CAAX (farnesylated, ER-localized) and non-CAAX. The non-CAAX isoform localizes to an actin-dependent meshwork distinct from ER. Suppression of INF2-non-CAAX causes Golgi fragmentation, an effect counteracted by latrunculin B treatment. Discrete actin filament patches are present in the peri-Golgi region and are reduced upon INF2 suppression. RT-PCR (splice variant expression), siRNA knockdown, fluorescence microscopy (ER and Golgi markers), digitonin extraction (localization), actin drug treatment Molecular biology of the cell High 21998196
2011 INF2, mDia1, and mDia2 all bind microtubules through constructs containing FH1, FH2, and C-terminal domains with Kd < 100 nM. INF2-FH1FH2C is a potent microtubule-bundling protein that reduces catastrophe rate; this bundling activity requires the C-terminus. Actin monomers inhibit microtubule binding/bundling by INF2 but not by mDia1 or mDia2. Microtubules do not inhibit actin polymerization by INF2, unlike mDia2. In vitro microtubule co-sedimentation assays, microtubule bundling assays, stoichiometry measurements, TIRF microscopy, actin competition assays Molecular biology of the cell High 21998204
2012 INF2 FH2 domain mutations I643A and K792A have unexpected effects: neither abolishes barbed-end binding, but I643A causes tight capping of a subset of filaments and almost completely abolishes severing and depolymerization activity. K792A has small effects on polymerization and severing. I643A cannot induce actin polymerization in cells because it cannot promote assembly in the presence of capping protein. Pyrene-actin polymerization assays, TIRF microscopy, barbed-end capping assays, cell imaging with GFP-INF2 mutants, site-directed mutagenesis The Journal of biological chemistry High 22879592
2012 INF2 is required for formation of stabilized, detyrosinated (Glu) microtubules following T cell receptor (TCR) engagement, and is essential for centrosome reorientation to the immunological synapse. The FH2 domain of INF2 mediates centrosome repositioning and can restore centrosome translocation in DIA1-, FMNL1-, Rac1-, and Cdc42-deficient cells. Microtubule stabilization is required for centrosome polarization. siRNA knockdown, immunofluorescence microscopy (Glu-tubulin staining), dominant-negative and constitutively active GTPase constructs, centrosome reorientation assay, FH2 domain rescue experiments The Journal of cell biology High 22986496
2013 ER-localized INF2 drives actin polymerization at ER-mitochondria contact sites, which is required for efficient mitochondrial fission. INF2 functions upstream of Drp1 in fission. Actin filaments accumulate between mitochondria and INF2-enriched ER membranes at constriction sites. INF2-induced actin polymerization drives initial mitochondrial constriction, enabling Drp1-driven secondary constriction. siRNA knockdown, live-cell imaging, super-resolution microscopy (SIM), phalloidin staining, dominant-negative Drp1 epistasis, rescue with INF2 constructs Science (New York, N.Y.) High 23349293
2014 INF2 severs actin filaments via a mechanism in which the FH2 domain encircles the filament (as revealed by 20 Å helical 3D electron microscopy reconstruction). INF2 binds stoichiometrically to filament sides and requires phosphate release. Unlike cofilin, INF2 binds ADP and ADP-Pi filaments equally well. As few as a single INF2 dimer can sever filaments. The C-terminal WH2/DAD motif increases severing potency 40-fold over FH1-FH2 alone. TIRF microscopy (two-color), pyrene-actin assays, electron microscopy (helical 3D reconstruction at 20 Å), phosphate release assays, truncation/domain analysis Current biology : CB High 24412206
2014 INF2 knockdown in zebrafish causes glomerular edema, podocyte dysfunction, and altered glomerular filtration barrier with mistrafficking of slit diaphragm proteins and disinhibited mDia (Dia2) activity. This phenotype is rescued by wild-type human INF2 but not by FSGS-causing DID mutants. The INF2 knockdown phenotype is also rescued by loss of either RhoA or Dia2, placing INF2 functionally upstream of RhoA/Dia signaling in the glomerulus. Morpholino knockdown in zebrafish, rescue with human INF2 WT and mutants, genetic epistasis with RhoA and Dia2, podocyte trafficking assays EBioMedicine Medium 26086034
2015 INF2 creates short actin filaments (<60 nm) that continuously turn over through combined barbed-end elongation, severing, and WH2-mediated depolymerization. The rate-limiting step is nucleotide exchange (ADP→ATP) on actin monomers after release from the INF2/actin complex. Profilin addition accelerates filament turnover 6-fold (by accelerating nucleotide exchange) and shifts equilibrium toward longer filaments. Pyrene-actin assays, TIRF microscopy, nucleotide exchange assays, truncation analysis, profilin competition experiments The Journal of biological chemistry High 26124273
2015 C. elegans EXC-6 (ortholog of human INF2) is required for tubulogenesis of the excretory cell; it regulates microtubule and F-actin accumulation at cell tips and dynamics of basolateral MTs. Activated human INF2 can substitute for EXC-6 in C. elegans, and FSGS/CMT disease-associated INF2 mutations cause constitutive activity in this in vivo assay. C. elegans genetics (exc-6 mutants), live imaging, rescue with human INF2 variants (WT and disease mutants), genetic analysis of cytoskeletal markers Developmental cell Medium 25771894
2016 INF2 is necessary for mDia1-mediated induction of stable detyrosinated microtubules (Glu MTs) in fibroblasts after LPA treatment. mDia1 regulates INF2 localization to MTs. IQGAP1 associates directly with the C-terminus of INF2 and mediates the interaction between mDia1 and INF2, acting as a scaffold in an mDia1→INF2 formin activation cascade. Mutants that disrupt mDia1-INF2 interaction fail to rescue MT stability in cells depleted of the respective formin. siRNA knockdown, immunofluorescence (Glu-tubulin), co-immunoprecipitation, direct binding assays (IQGAP1-INF2 N-terminus), MT dynamics measurements, domain interaction mutants Molecular biology of the cell High 27030671
2017 SPOP (acting as adaptor of the CUL3-RBX1 E3 ubiquitin ligase) recognizes a Ser/Thr-rich motif in the C-terminal region of INF2 and triggers atypical polyubiquitination of INF2. This ubiquitination does not cause INF2 degradation but reduces INF2 ER localization and mitochondrially associated DRP1 puncta formation, thereby inhibiting INF2-mediated mitochondrial fission. INF2 mutants that escape SPOP-mediated ubiquitination promote more mitochondrial fission. Cancer-associated SPOP mutants increase INF2 ER localization and promote fission through dominant-negative inhibition of endogenous SPOP. Co-immunoprecipitation, ubiquitination assays, confocal microscopy (ER localization, DRP1 puncta), site-directed mutagenesis of SPOP-binding motif, SPOP knockout/knockdown PLoS genetics High 28448495
2019 INF2 is inhibited by a complex of cyclase-associated protein (CAP) bound to lysine-acetylated actin (KAc-actin). This inhibition is dependent on the INF2 DID domain. Treatment with HDAC6 releases INF2 inhibition by deacetylating the CAP-KAc-actin complex; HDAC6 inhibitors block cellular INF2 activation. FSGS/CMT disease-associated INF2 DID mutants are poorly inhibited by CAP-KAc-actin, suggesting these diseases result from reduced CAP-KAc-actin binding. Biochemical purification from mouse brain tissue, in vitro actin polymerization assays, HDAC6 enzymatic treatment, HDAC6 inhibitor treatment, disease mutant analysis Nature cell biology High 30962575
2019 Lysine residues K50 and K61 on actin are the relevant acetylation sites for CAP/KAc-actin-mediated INF2 inhibition. K50Q- and K61Q-actin (acetylmimetics), when bound to CAP2, inhibit full-length INF2 but not INF2 lacking DID. The CAP WH2 domain binds INF2-DID with submicromolar affinity. INF2-DAD binds CAP/K50Q-actin 5-fold better than CAP/WT-actin. A model is proposed whereby CAP/KAc-actin bridges INF2 DID and DAD to enforce 'facilitated autoinhibition'. K→Q acetylmimetic mutations in actin, in vitro polymerization assays, direct-binding assays (fluorescence polarization), cell expression of mutant actins, TIRF microscopy Proceedings of the National Academy of Sciences of the United States of America High 31871199
2020 INF2-CAAX is the predominant podocyte isoform and is proteolytically cleaved by cathepsin proteases, liberating the N-terminal DID to function independently. The N-terminal fragment localizes to podocyte foot processes (dependent on cleavage), binds mDIA1, and promotes cell spreading; these functions are impaired by the FSGS-associated R218Q mutation without affecting cleavage itself. Immunoblot (cleavage detection), cathepsin inhibitor treatment, subcellular fractionation, co-immunoprecipitation (mDIA1), cell spreading assay, INF2 disease mutant analysis, human kidney disease tissue immunostaining Journal of the American Society of Nephrology : JASN High 31924668
2020 INF2 mutations cause a deregulated calcium-mediated actin reset (CaAR) stress response in cells, resulting in constitutive formin activation. Mutations linked exclusively to FSGS can be distinguished from those causing FSGS+CMT based on degree of INF2 activation. This was validated in primary patient cells and Drosophila nephrocytes. Quantitative live-cell imaging of CaAR, expression of >50 INF2 mutant variants, validation in primary patient cells and Drosophila nephrocyte model Journal of the American Society of Nephrology : JASN Medium 32444357
2020 INF2 interacts with CFTR and regulates CFTR plasma membrane levels. Reduction of INF2 levels promotes CFTR trafficking to the plasma membrane under EPAC1 activation, indicating INF2 acts as a negative regulator of CFTR PM stability after cAMP/EPAC1 signaling. Protein interaction profiling (Co-IP/pulldown), siRNA knockdown of INF2, surface biotinylation assay for CFTR PM levels, EPAC1 activation with cAMP analog The Biochemical journal Medium 32573649
2020 FSGS-causing INF2 mutation R218Q disrupts an interaction of INF2 with dynein light chain 1 (DYNLL1). This mutation diverts dynein-mediated post-endocytic sorting of nephrin from recycling endosomes to lysosomes for degradation. Antagonizing dynein-mediated transport rescues this effect. Yeast two-hybrid (INF2-DYNLL1 interaction), live cell imaging, fluorescent and surface biotinylation trafficking assays in cultured podocytes, dynein inhibitor treatment, R218Q knockin mouse model with puromycin nephropathy Journal of the American Society of Nephrology : JASN High 33443052
2022 The N-terminal extension of INF2 contains a calmodulin-binding site (CaMBS) organized into two α-helices; the first helix binds Ca2+/calmodulin (CaM) directly through its C-terminal lobe, with residues W11, L14, and L18 (1-4-8 motif) being critical. This CaM interaction is required for INF2 activation: INF2 KO cells lack perinuclear F-actin ring, have low cytosolic F-actin, and do not respond to Ca2+ by making F-actin. Expression of INF2 with inactivated CaMBS fails to restore these defects and fails to translocate MRTF to the nucleus. NMR structure determination, biochemical binding assays, site-directed mutagenesis (W11, L14, L18), INF2 KO cell complementation, F-actin quantification, MRTF localization assay, Ca2+ stimulation experiments Cellular and molecular life sciences : CMLS High 36306014
2022 INF2 activation mediates actin reorganization (actinification) in neurons in response to NMDA receptor hyperactivation and ischemia: F-actin depolymerizes from dendritic spines and polymerizes into stable filaments in dendrite shafts and soma within <5 min. INF2 silencing renders neurons vulnerable to cell death; INF2 overexpression is protective against ischemia-induced death. Na+, Cl-, water, and Ca2+ influx combined with spine F-actin depolymerization are required together to activate INF2. siRNA knockdown of INF2 in cultured neurons, INF2 overexpression, bath-applied NMDA, photothrombotic stroke in mice, live F-actin imaging, cell viability assays Nature communications High 36229429
2024 INF2 R218Q is a gain-of-function mutation: R218Q knockin mice develop FSGS upon PAN injury while INF2 knockout mice show minimal phenotype. Co-immunoprecipitation and cellular actin measurements show R218Q INF2 confers increased actin cytoskeleton activity. RNA expression analysis shows adhesion and mitochondria-related pathways are enriched in R218Q PAN-treated mice. Both R218Q mouse podocytes and human INF2-S186P organoid podocytes recapitulate adhesion and mitochondrial phenotypes. Knockin vs knockout mouse comparison with PAN-induced injury model, co-immunoprecipitation, actin content measurement, RNA-seq, human kidney organoids with INF2 patient mutation Science advances High 39536114
2024 AMPK phosphorylates INF2 at Ser1077 under energy stress conditions, leading to increased INF2 localization to the ER and enhanced DRP1 recruitment to mitochondria, thereby promoting mitochondrial fission and cancer cell growth. In vitro kinase assay, phosphorylation site mutagenesis (S1077A), confocal microscopy (ER localization, DRP1 puncta), immunohistochemistry of patient specimens correlating AMPK activity with phospho-INF2 Cell death & disease Medium 38233384
2024 FBXO7 E3 ubiquitin ligase mediates ubiquitination and degradation of INF2, thereby restraining INF2-mediated DRP1 recruitment and mitochondrial division. Cancer-associated FBXO7 mutants are defective in INF2 ubiquitination and degradation, promoting mitochondrial hyper-division. The FBXO7-INF2-DRP1 axis controls endometrial cancer cell proliferation and apoptosis. Co-immunoprecipitation, in-cell ubiquitination assays, INF2 and DRP1 knockdown, DRP1 inhibitor Mdivi-1, immunohistochemistry of patient specimens Cell death & disease Medium 37344480
2024 Pathogenic INF2 variants disrupt ER continuity by altering interactions between the ER and the cytoskeleton (both F-actin and microtubules). FSGS variants induce sheet-like ER, while CMT-FSGS variants cause severe ER dysmorphism with fragmented ER and INF2 aggregates. Pathogenic variants also induce mitochondrial fragmentation and dysregulate mitochondrial distribution, more severely in CMT-FSGS than FSGS-only variants. High-resolution live imaging in HeLa cells expressing WT and pathogenic INF2 variants, actin and microtubule inhibitor treatment, quantification of ER tubule/sheet ratio, mitochondrial morphology analysis International journal of molecular sciences Medium 39337270
2024 Pathogenic INF2 DID variants trigger translocation of the transcriptional cofactor MRTF into the nucleus, causing profound transcriptome reprogramming primarily through sustained MRTF-SRF complex activation. This leads to surplus microtubule-organizing centers, multipolar spindle assembly, multi-micronucleation, mitotic catastrophe, and cell death. Inactivation of INF2's catalytic domain prevents aberrant nuclei formation; reducing MRTF-SRF activation mitigates multi-micronucleation. Retrovirus and plasmid expression of WT and pathogenic INF2 variants, immunofluorescence microscopy, RNA sequencing, MRTF localization assay, INF2 catalytic domain inactivation, MRTF-SRF pathway inhibition Cellular and molecular life sciences : CMLS Medium 38916773
2024 The R218Q INF2 mutation disrupts sequestration of DYNLL1 by INF2, allowing DYNLL1 to interact with PI31, which promotes dynein-mediated transport of nephrin to the proteasome for degradation. Knockdown of DYNLL1 or PI31, dynein inactivation, or proteasome inhibition (bortezomib) each restore nephrin proteostasis in R218Q knockin podocytes. Bortezomib ameliorates R218Q podocytopathy and FSGS in vivo. Co-immunoprecipitation (DYNLL1-INF2, DYNLL1-PI31), siRNA knockdown (DYNLL1, PI31), dynein inhibitor, bortezomib treatment, R218Q knockin mouse PAN model, nephrin trafficking assays Kidney360 High 39621430
2024 INF2-mediated actin polymerization at ER-organelle contacts regulates morphology and mobility of mitochondria, endosomes, and lysosomes. ER-associated actin consistently marks mitochondrial, endosomal, and lysosomal fission sites. INF2 (ER-anchored isoform) is a key regulator of morphology and mobility of these organelles. Live-cell imaging, INF2 knockdown/knockout, ER and organelle co-localization analysis, organelle morphology and motility quantification Research square (preprint)preprint Medium 39184068
2025 INF2 is activated by calcium-bound calmodulin (CALM) through binding to the N-terminus. INF2 inhibition does not require CAP proteins (contradicting prior reports) but does require actin 'buffering' by monomer-binding proteins such as profilin or thymosin. The N-terminus plays roles in INF2 regulation beyond CALM binding. Novel cell-free reconstitution assay, calmodulin binding assays, actin polymerization assays with profilin/thymosin, CAP protein titration, N-terminal deletion mutants The Journal of cell biology Medium 41498749
2025 Piezo1-mediated Ca2+ influx activates INF2, causing widespread actin cytoskeletal remodeling that promotes de-adhesion and drives mesenchymal-to-amoeboid transition (MAT) in confined environments in melanoma cells. Piezo1 knockdown/inhibition, INF2 knockdown, intracellular Ca2+ measurement, confinement assays (microchannels), cell migration quantification, actin staining Current biology : CB Medium 40120583
2025 INF2 co-localizes with HDAC6 and interacts with it, affecting tubulin acetylation and microtubule stability for mitochondrial transport during oocyte meiosis. INF2 co-localizes with cytoplasmic actin and its depletion reduces actin polymerization, causing spindle migration failure in mouse and porcine oocytes. INF2 associates with DRP1 and depletion disturbs mitochondrial distribution and fission. Exogenous INF2 mRNA rescues meiotic maturation defects in obese mouse oocytes. siRNA/morpholino knockdown in mouse and porcine oocytes, immunofluorescence microscopy, co-immunoprecipitation (INF2-HDAC6, INF2-DRP1), mRNA rescue experiment, JC-1 mitochondrial potential assay Free radical biology & medicine Medium 40180021
2026 INF2-mediated actin filaments facilitate agonist-induced IP3R activity and regulate the formation and/or stability of IP3R clusters on the ER. INF2 physically interacts with IP3R isoforms, often at IP3R clusters. INF2-IP3R interaction is independent of INF2 actin polymerization activity, but the ability of INF2 to mediate IP3R clusters requires its actin polymerization activity. INF2 on the ER regulates IP3R cluster positioning to mediate ER-mitochondrial contacts and facilitate ER-to-mitochondrial calcium transfer. Co-immunoprecipitation (INF2-IP3R), INF2 knockdown, live-cell calcium imaging, IP3R cluster imaging, ER-mitochondria contact site analysis, INF2 activity mutants Current biology : CB Medium 42259291
2022 INF2 and actin form an 8S complex (4 actin monomers : 2 INF2 dimer molecules) in which actin monomers are in a parallel orientation, as shown by chemical crosslinking and negative-staining electron microscopy 2D class averages. 8S particles can seed rapid actin assembly. INF2 also accelerates disassembly of oxidized Mox-F-actin. Negative-staining electron microscopy (2D class averages), chemical crosslinking, pyrene-actin assembly/disassembly assays, stoichiometry determination Journal of biomolecular structure & dynamics Medium 35343388
2024 CAP1 and CAP2 inhibit INF2 to induce dendritic spine maturation in hippocampal neurons. INF2 overactivation causes an impaired spine maturation phenotype similar to CAP1/CAP2 double KO. INF2 inactivation largely rescues spine maturation defects in CAP-deficient neurons. CAPs act as a molecular switch controlling the transition from filopodia-like to mature spines partly by inhibiting INF2. Genetic inactivation of CAP1 and/or CAP2 in hippocampal neurons, INF2 overexpression and inactivation constructs, dendritic spine morphology analysis, epistasis experiments Cellular and molecular life sciences : CMLS Medium 39154297
2025 The WH2/DAD motif of INF2 forms a single α-helix (determined by NMR in H2O and TFE). The hydrophobic N-terminal region of the WH2/DAD is essential for INF2-mediated actin polymerization; cells expressing INF2 with only the hydrophobic region of WH2/DAD show higher F-actin and nuclear abnormalities phenocopying pathogenic DID variants. Deletion of the entire WH2/DAD or hydrophobic region alone abolishes INF2 activity. NMR structure determination, site-directed deletion/truncation of WH2/DAD subregions, cell F-actin quantification, nuclear abnormality scoring The FEBS journal Medium 40993919

Source papers

Stage 0 corpus · 84 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2013 An actin-dependent step in mitochondrial fission mediated by the ER-associated formin INF2. Science (New York, N.Y.) 674 23349293
2009 Mutations in the formin gene INF2 cause focal segmental glomerulosclerosis. Nature genetics 361 20023659
2011 INF2 mutations in Charcot-Marie-Tooth disease with glomerulopathy. The New England journal of medicine 219 22187985
2011 Mutations in INF2 are a major cause of autosomal dominant focal segmental glomerulosclerosis. Journal of the American Society of Nephrology : JASN 126 21258034
2011 Differential interactions of the formins INF2, mDia1, and mDia2 with microtubules. Molecular biology of the cell 114 21998204
2009 INF2 is an endoplasmic reticulum-associated formin protein. Journal of cell science 114 19366733
2012 Mutations in the INF2 gene account for a significant proportion of familial but not sporadic focal and segmental glomerulosclerosis. Kidney international 104 23014460
2010 The formin INF2 regulates basolateral-to-apical transcytosis and lumen formation in association with Cdc42 and MAL2. Developmental cell 83 20493814
2018 INF2 regulates oxidative stress-induced apoptosis in epidermal HaCaT cells by modulating the HIF1 signaling pathway. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 80 30579254
2011 Splice variant-specific cellular function of the formin INF2 in maintenance of Golgi architecture. Molecular biology of the cell 73 21998196
2012 INF2 promotes the formation of detyrosinated microtubules necessary for centrosome reorientation in T cells. The Journal of cell biology 72 22986496
2011 Rho activation of mDia formins is modulated by an interaction with inverted formin 2 (INF2). Proceedings of the National Academy of Sciences of the United States of America 72 21278336
2017 Dysregulation of INF2-mediated mitochondrial fission in SPOP-mutated prostate cancer. PLoS genetics 64 28448495
2019 A complex containing lysine-acetylated actin inhibits the formin INF2. Nature cell biology 60 30962575
2014 INF2-mediated severing through actin filament encirclement and disruption. Current biology : CB 56 24412206
2010 Formin INF2 regulates MAL-mediated transport of Lck to the plasma membrane of human T lymphocytes. Blood 55 20881207
2016 An mDia1-INF2 formin activation cascade facilitated by IQGAP1 regulates stable microtubules in migrating cells. Molecular biology of the cell 49 27030671
2012 Mutations to the formin homology 2 domain of INF2 protein have unexpected effects on actin polymerization and severing. The Journal of biological chemistry 45 22879592
2019 Regulation of INF2-mediated actin polymerization through site-specific lysine acetylation of actin itself. Proceedings of the National Academy of Sciences of the United States of America 44 31871199
2015 The disease-associated formin INF2/EXC-6 organizes lumen and cell outgrowth during tubulogenesis by regulating F-actin and microtubule cytoskeletons. Developmental cell 43 25771894
2016 Mice with mutant Inf2 show impaired podocyte and slit diaphragm integrity in response to protamine-induced kidney injury. Kidney international 42 27350175
2020 The formin INF2 in disease: progress from 10 years of research. Cellular and molecular life sciences : CMLS 40 32451589
2018 Tanshinone IIA promotes IL2-mediated SW480 colorectal cancer cell apoptosis by triggering INF2-related mitochondrial fission and activating the Mst1-Hippo pathway. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 40 30372868
2013 De novo INF2 mutations expand the genetic spectrum of hereditary neuropathy with glomerulopathy. Neurology 37 24174593
2015 Assembly and turnover of short actin filaments by the formin INF2 and profilin. The Journal of biological chemistry 31 26124273
2020 A Deregulated Stress Response Underlies Distinct INF2-Associated Disease Profiles. Journal of the American Society of Nephrology : JASN 30 32444357
2014 Neuropathologic characterization of INF2-related Charcot-Marie-Tooth disease: evidence for a Schwann cell actinopathy. Journal of neuropathology and experimental neurology 27 24487800
2014 Novel INF2 mutations in an Italian cohort of patients with focal segmental glomerulosclerosis, renal failure and Charcot-Marie-Tooth neuropathy. Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association 27 25165188
2022 INF2-mediated actin filament reorganization confers intrinsic resilience to neuronal ischemic injury. Nature communications 26 36229429
2014 Human Kidney Disease-causing INF2 Mutations Perturb Rho/Dia Signaling in the Glomerulus. EBioMedicine 24 26086034
2010 Variable renal phenotype in a family with an INF2 mutation. Pediatric nephrology (Berlin, Germany) 24 20803156
2020 FSGS-Causing INF2 Mutation Impairs Cleaved INF2 N-Fragment Functions in Podocytes. Journal of the American Society of Nephrology : JASN 22 31924668
2018 Formin Proteins FHOD1 and INF2 in Triple-Negative Breast Cancer: Association With Basal Markers and Functional Activities. Breast cancer : basic and clinical research 22 30158824
2012 Novel INF2 mutation p. L77P in a family with glomerulopathy and Charcot-Marie-Tooth neuropathy. Pediatric nephrology (Berlin, Germany) 22 22961558
2020 Dysregulated Dynein-Mediated Trafficking of Nephrin Causes INF2-related Podocytopathy. Journal of the American Society of Nephrology : JASN 21 33443052
2024 Phosphorylation of INF2 by AMPK promotes mitochondrial fission and oncogenic function in endometrial cancer. Cell death & disease 19 38233384
2020 Cytoskeleton regulators CAPZA2 and INF2 associate with CFTR to control its plasma membrane levels under EPAC1 activation. The Biochemical journal 19 32573649
2018 Nur77 promotes cerebral ischemia-reperfusion injury via activating INF2-mediated mitochondrial fragmentation. Journal of molecular histology 19 30298449
2019 Suppression of Tafazzin promotes thyroid cancer apoptosis via activating the JNK signaling pathway and enhancing INF2-mediated mitochondrial fission. Journal of cellular physiology 18 30741413
2018 Nurr1 exacerbates cerebral ischemia-reperfusion injury via modulating YAP-INF2-mitochondrial fission pathways. The international journal of biochemistry & cell biology 17 30267803
2016 Diagnosing FSGS without kidney biopsy - a novel INF2-mutation in a family with ESRD of unknown origin. BMC medical genetics 14 27733133
2016 INF2- and FHOD-related formins promote ovulation in the somatic gonad of C. elegans. Cytoskeleton (Hoboken, N.J.) 14 27770600
2014 A novel INF2 mutation in a Korean family with autosomal dominant intermediate Charcot-Marie-Tooth disease and focal segmental glomerulosclerosis. Journal of the peripheral nervous system : JPNS 14 24750328
2015 INF2 mutations associated with dominant inherited intermediate Charcot-Marie-Tooth neuropathy with focal segmental glomerulosclerosis in two Chinese patients. Clinical neuropathology 11 25943269
2023 FBXO7, a tumor suppressor in endometrial carcinoma, suppresses INF2-associated mitochondrial division. Cell death & disease 10 37344480
2024 INF2 mutations cause kidney disease through a gain-of-function mechanism. Science advances 9 39536114
2019 A cryptic splicing mutation in the INF2 gene causing Charcot-Marie-Tooth disease with minimal glomerular dysfunction. Journal of the peripheral nervous system : JPNS 9 30680856
2024 Altered Endoplasmic Reticulum Integrity and Organelle Interactions in Living Cells Expressing INF2 Variants. International journal of molecular sciences 7 39337270
2024 Regulation of formin INF2 and its alteration in INF2-linked inherited disorders. Cellular and molecular life sciences : CMLS 7 39586895
2017 Mutations in INF2 may be associated with renal histology other than focal segmental glomerulosclerosis. Pediatric nephrology (Berlin, Germany) 7 29038887
2025 The activation of INF2 by Piezo1/Ca2+ is required for mesenchymal-to-amoeboid transition in confined environments. Current biology : CB 6 40120583
2022 Structure and function of the N-terminal extension of the formin INF2. Cellular and molecular life sciences : CMLS 6 36306014
2016 Reduced INF2 expression in nephrotic syndrome is possibly related to clinical severity of steroid resistance in children. Nephrology (Carlton, Vic.) 6 26383224
2024 Cyclase-associated protein (CAP) inhibits inverted formin 2 (INF2) to induce dendritic spine maturation. Cellular and molecular life sciences : CMLS 5 39154297
1996 Photodissimilation of Fructose to H(inf2) and CO(inf2) by a Dinitrogen-Fixing Cyanobacterium, Anabaena variabilis. Applied and environmental microbiology 5 16535288
2024 Functional genetic variants of the disulfidptosis-related INF2 gene predict survival of hepatitis B virus-related hepatocellular carcinoma. Carcinogenesis 4 38270181
2021 INF2 p.Arg214Cys mutation in a Chinese family with rapidly progressive renal failure and follow-up of renal transplantation: case report and literature review. BMC nephrology 4 33541266
1996 Biosynthesis of Poly(3-Hydroxyalkanoic Acid) Copolymer from CO(inf2) in Pseudomonas acidophila through Introduction of the DNA Fragment Responsible for Chemolithoautotrophic Growth of Alcaligenes hydrogenophilus. Applied and environmental microbiology 4 16535252
2025 De novo somatic mosaicisms of INF2 and TRPV4 in patients with Charcot-Marie-Tooth disease. Genes & genomics 3 40257654
2024 INF2 formin variants linked to human inherited kidney disease reprogram the transcriptome, causing mitotic chaos and cell death. Cellular and molecular life sciences : CMLS 3 38916773
2023 Characterization of Expression and Function of the Formins FHOD1, INF2, and DAAM1 in HER2-Positive Breast Cancer. Journal of breast cancer 3 37985384
2022 Parallel actin monomers in the 8S complex of actin-INF2. Journal of biomolecular structure & dynamics 3 35343388
2024 Missense Mutant Gain-of-Function Causes Inverted Formin 2 (INF2)-Related Focal Segmental Glomerulosclerosis (FSGS). bioRxiv : the preprint server for biology 2 38915495
2021 Enterovirus 71 Induces INF2 Cleavage via Activated Caspase-2 in Infected RD Cells. Frontiers in microbiology 2 34046026
2026 Regulation of the formin INF2 by actin monomers and calcium/calmodulin. The Journal of cell biology 1 41498749
2025 Formin INF2 supplementation alleviates cytoskeleton-based mitochondria defects for oocyte quality under obesity. Free radical biology & medicine 1 40180021
2025 Structural and functional dissection of the WH2/DAD motif of INF2, a formin linked to human inherited degenerative disorders. The FEBS journal 1 40993919
2024 The activation of INF2 by Piezo1/Ca2+ is required for mesenchymal to amoeboid transition in confined environments. bioRxiv : the preprint server for biology 1 37745412
2024 INF2-mediated actin polymerization at ER-organelle contacts regulates organelle size and movement. Research square 1 39184068
2024 Dynll1-PI31 Interaction Enhances Proteolysis Through the Proteasome, Representing a Novel Therapeutic Target for INF2-Related FSGS. Kidney360 1 39621430
2023 INF2 and ROBO2 gene mutation in an Indian family with end stage renal failure and follow-up of renal transplantation. Nephrology (Carlton, Vic.) 1 37772439
2023 Drebrin Protects Assembled Actin from INF2-FFC-mediated Severing and Stabilizes Cell Protrusions. Journal of molecular biology 1 38158176
2010 The inverted Formin INF2 sorts it out. Developmental cell 1 20493801
1994 Selection of soybean plant leaves which yield mesophyll cell isolates with maximal rates of CO2 and NO inf2 (sup-) photoassimilation. Photosynthesis research 1 24311219
2026 A very rare case report with INF2 gene mutation related sporadic FSGS and response to treatment. Nefrologia 0 41997690
2026 An INF2-dependent actin-mediated step in inositol 1,4,5-trisphosphate receptor cluster formation and activity. Current biology : CB 0 42259291
2025 Nerve Enlargement in Patients with INF2 Variants Causing Peripheral Neuropathy and Focal Segmental Glomerulosclerosis. Biomedicines 0 39857711
2025 Targeting INF2 with DiosMetin 7-O-β-D-Glucuronide: a new stratagem for colorectal cancer therapy. BMC cancer 0 40452021
2025 INF2-Related Charcot-Marie-Tooth Disease in a Japanese Cohort: Genetic and Clinical Insights. Annals of clinical and translational neurology 0 40985697
2025 Generation of a human iPSC line (NUMNi002-A) from a patient with nephrotic syndrome harboring an INF2 gene variant. Stem cell research 0 40992252
2025 Autosomal dominant focal segmental glomerulosclerosis by INF2 p.Arg218Trp and p.Ser186Pro mutations: three case reports and literature review. BMC nephrology 0 41094651
2025 Regulation of the formin INF2 by actin monomers and calcium-calmodulin. bioRxiv : the preprint server for biology 0 41279891
2025 High Diagnostic Yield of Genetic Screening in Autosomal Dominant Steroid-Resistant Nephrotic Syndrome: Predominance of INF2 and TRPC6 and Identification of a Novel Gene. Nephrology (Carlton, Vic.) 0 41326026
2024 Co-occurrence of Charcot-Marie-Tooth disease type 1 and glomerulosclerosis in a patient with a de novo INF2 variant. BMC nephrology 0 39609740

Missed literature

Know a paper Affinage missed for INF2? Flag it for the maintainers and the community.

No submissions yet.