Affinage

CHMP4B

Charged multivesicular body protein 4b · UniProt Q9H444

Length
224 aa
Mass
24.9 kDa
Annotated
2026-06-09
28 papers in source corpus 19 papers cited in narrative 19 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CHMP4B is a core ESCRT-III subunit that polymerizes at membranes to drive membrane remodeling and scission across multivesicular body sorting, cytokinetic abscission, plasma membrane repair, and lysosomal microautophagy (PMID:12860994, PMID:22406677, PMID:42203786). It was first defined as the dominant Alix-binding CHMP4 isoform, cooperating with the AAA-ATPase SKD1 in MVB sorting of ubiquitinated cargo and endocytosed EGF (PMID:12860994, PMID:14678797); Alix engagement is gated by membrane-dependent relief of autoinhibition at the Bro1 docking site (PMID:19016654), and CHMP4B is also bound by the Alix paralog Brox through its C-terminal amphipathic helix (PMID:22484091) and by the ESCRT-III-related protein CHMP7 (PMID:16856878). Polymerization is directly controlled by CC2D1A/CC2D1B, which bind the N-terminal helical hairpin of CHMP4B with nanomolar affinity and block filament assembly; the same surface is required for CHMP4B's dominant-negative effect on HIV-1 budding (PMID:22406677). During cytokinesis, CHMP4B is recruited to the abscission site downstream of the anillin-septin cytoskeleton and the GAS2L3 midbody scaffold, which nucleates CHMP4B condensates via phase separation, and its spatial organization depends on CHMP2A, establishing a hierarchical ESCRT-III assembly (PMID:24451548, PMID:41177429). Beyond division, CHMP4B maintains primary cilium integrity independently of endocytic degradation (PMID:31914703), mediates plasma membrane repair to counteract GSDMD-driven pyroptosis together with VPS4A (PMID:37931722), supports autophagosome-lysosome fusion downstream of the PRP4K splicing circuit (PMID:40531620), and binds the lysosomal phosphoinositide PI(3,5)P2 to drive microautophagic encapsulation and degradation of STING (PMID:42203786). Dominant CHMP4B mutations (D129V, E161K) cause autosomal dominant cataract, and CHMP4B is essential for lens development, with its dysregulation by HSP90β triggering p53/Bak-Bim apoptosis in lens epithelial cells (PMID:17701905, PMID:31404815, PMID:37487085).

Mechanistic history

Synthesis pass · year-by-year structured walk · 11 steps
  1. 2003 High

    Established CHMP4B's foundational identity as an ESCRT-III component by linking it physically and functionally to the Alix adaptor and the SKD1 AAA-ATPase in MVB cargo sorting.

    Evidence Yeast two-hybrid, GST pull-down, co-IP, and overexpression EGF/ubiquitin-sorting assays in HeLa cells

    PMID:12860994 PMID:14678797

    Open questions at the time
    • Did not resolve the structural basis of the Alix interaction
    • Isoform-specific functional differences among CHMP4a/b/c beyond binding strength not defined
  2. 2006 Medium

    Extended the CHMP4B interaction network to the ESCRT-III-related protein CHMP7 via its SNF7 domain, indicating CHMP4B partners with multiple ESCRT-III-family proteins.

    Evidence Strep-tag pull-down from cell lysates and confocal relocalization imaging

    PMID:16856878

    Open questions at the time
    • Single pull-down from lysates without in vitro reconstitution
    • Functional consequence of the CHMP4B-CHMP7 interaction not tested
  3. 2007 Medium

    Connected CHMP4B to human disease by showing dominant cataract-causing mutations act as gain-of-function dominant negatives on ESCRT-III-mediated membrane budding.

    Evidence Transfection of D129V/E161K mutants with subcellular localization and virus-like particle release assays

    PMID:17701905

    Open questions at the time
    • No in vitro or structural analysis of mutant polymerization
    • Mechanism connecting ESCRT defect to lens pathology not established
  4. 2009 Medium

    Resolved how Alix-CHMP4B engagement is regulated, showing the Bro1 docking site is autoinhibited in cytosol and unmasked only upon Alix membrane association.

    Evidence Biochemical fractionation and cell-lysate binding assays of cytosolic vs. membrane-bound Alix

    PMID:19016654

    Open questions at the time
    • Structural conformational change underlying autoinhibition not directly visualized
    • In vivo trigger for membrane recruitment unresolved
  5. 2012 High

    Defined the structural and biochemical control of CHMP4B polymerization, identifying CC2D1A/B as direct high-affinity negative regulators and mapping the polymerization surface, plus a distinct Brox-binding mode.

    Evidence Crystal structures of the CHMP4B helical hairpin and Brox:CHMP4B complex, SPR, in vitro polymerization, and HIV-1 budding mutagenesis

    PMID:22406677 PMID:22484091

    Open questions at the time
    • In vivo conditions that relieve CC2D1A inhibition not defined
    • Full-length CHMP4B polymer architecture not solved
  6. 2014 Medium

    Placed CHMP4B in the cytokinetic abscission pathway downstream of the anillin-septin cytoskeleton and revealed its localization to chromosome bridges and micronuclei.

    Evidence Live and subdiffraction imaging with anillin/septin depletion; immunofluorescence and chromatin co-IP with mutant comparison

    PMID:24451548 PMID:24741567

    Open questions at the time
    • Molecular link from septins to CHMP4B recruitment not defined
    • Functional role of chromatin/micronuclear localization unresolved
  7. 2019 High

    Demonstrated CHMP4B is essential for lens development and for primary cilium assembly/integrity, the latter independent of ESCRT endocytic degradation.

    Evidence Conditional knockout and D129V knock-in mouse models with TUNEL/histology; siRNA and zebrafish morpholino with ciliary phenotyping

    PMID:31404815 PMID:31914703

    Open questions at the time
    • Mechanism of ciliary membrane maintenance by CHMP4B not defined
    • How D129V causes embryonic lethality vs. dominant cataract not reconciled
  8. 2021 Medium

    Distinguished CHMP4B from CHMP7 in disease context by showing CHMP4B does not abnormally accumulate in ALS neuronal nuclei, arguing against a primary role in ALS NPC injury.

    Evidence Super-resolution SIM of neuronal nuclei from ALS patients and models

    PMID:34281622

    Open questions at the time
    • Negative finding in a single study
    • Does not exclude CHMP4B in nuclear envelope repair under other conditions
  9. 2023 Medium

    Uncovered an HSP90β chaperone relationship governing CHMP4B levels in the lens and a membrane-repair function antagonizing GSDMD-mediated pyroptosis.

    Evidence Co-IP with zebrafish epistasis/rescue and p53/Bak-Bim readouts; Co-IP, EM, and pyroptosis assays with VPS4A co-localization

    PMID:37487085 PMID:37931722

    Open questions at the time
    • How HSP90β mechanistically sets CHMP4B/p53 levels not fully defined
    • Whether membrane repair uses the canonical ESCRT-III scission machinery not dissected
  10. 2025 Medium

    Embedded CHMP4B in additional remodeling pathways: a PRP4K splicing circuit controlling autophagosome-lysosome fusion, and GAS2L3 phase separation nucleating CHMP4B condensates at the midbody within a CHMP2A-dependent assembly hierarchy.

    Evidence CHMP4B cDNA rescue in PRP4K-null cells with autophagy assay; GAS2L3 LLPS/FRAP/droplet and IDR-deletion imaging; CHMP2A KO SIM/CLEM (preprint)

    PMID:40531620 PMID:41177429 PMID:bio_10.1101_2025.06.24.661003

    Open questions at the time
    • Direct mechanistic role of CHMP4B in fusion vs. scission during autophagy unclear
    • Biophysical relationship between GAS2L3 condensates and CHMP4B filament formation not fully resolved
  11. 2026 High

    Identified a direct PI(3,5)P2-binding activity on lysosomes that targets CHMP4B for microautophagic encapsulation and degradation of STING, defining a phosphoinositide-driven recruitment axis.

    Evidence Liposome sedimentation, forced Pikfyve recruitment, and PI(3,5)P2-binding-deficient mutant rescue of STING degradation in Chmp4b-depleted cells

    PMID:42203786

    Open questions at the time
    • Structural basis of CHMP4B PI(3,5)P2 recognition not solved
    • Generality of phosphoinositide-directed recruitment to other CHMP4B functions untested

Open questions

Synthesis pass · forward-looking unresolved questions
  • How CHMP4B's single polymerization machinery is differentially licensed across MVB sorting, abscission, ciliary maintenance, membrane repair, autophagy, and microautophagy remains the central open question.
  • No unified model for how distinct adaptors/lipids select CHMP4B function
  • Specific lipid species bound during division (lipid-trap MS, preprint) not structurally defined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005198 structural molecule activity 2 GO:0008289 lipid binding 1 GO:0098772 molecular function regulator activity 1
Localization
GO:0005764 lysosome 1 GO:0005829 cytosol 1 GO:0005886 plasma membrane 1 GO:0005929 cilium 1
Pathway
R-HSA-1640170 Cell Cycle 2 R-HSA-9612973 Autophagy 2 R-HSA-5357801 Programmed Cell Death 1 R-HSA-5653656 Vesicle-mediated transport 1
Partners
CC2D1ACC2D1BCHMP7GAS2L3GSDMDHSP90AB1PDCD6IPVPS4A
Complex memberships
ESCRT-III

Evidence

Reading pass · 19 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2003 CHMP4B was identified as a binding partner of Alix (ALG-2-interacting protein X) through yeast two-hybrid screen, confirmed by GST pull-down and co-immunoprecipitation. CHMP4B co-localizes with Alix in HeLa cells and co-immunoprecipitates with dominant-negative SKD1(E235Q) AAA-ATPase. Overexpression of CHMP4B inhibited endocytosed EGF disappearance and caused accumulation of ubiquitinated proteins, consistent with a role in multivesicular body (MVB) sorting cooperating with SKD1. Yeast two-hybrid, GST pull-down, co-immunoprecipitation, fluorescence microscopy, overexpression phenotypic assay The Journal of biological chemistry High 12860994
2004 Among the three CHMP4 isoforms (CHMP4a, CHMP4b, CHMP4c), CHMP4B is the major binding partner of Alix, showing stronger direct interaction than CHMP4a or CHMP4c as demonstrated by GST pull-down using recombinant proteins and co-immunoprecipitation from cell lysates. GST pull-down with recombinant proteins, co-immunoprecipitation Archives of biochemistry and biophysics High 14678797
2006 CHMP7, a novel ESCRT-III-related protein, directly interacts with CHMP4B through its C-terminal SNF7 domain, as shown by pull-down assay. Overexpression of CHMP4B-GFP relocalized FLAG-CHMP7 from diffuse cytoplasm to cytoplasmic puncta, indicating functional interaction. Pull-down assay (Strep-tagged CHMP7 with GFP-CHMP4b from cell lysates), confocal fluorescence microscopy The Biochemical journal Medium 16856878
2007 Disease-associated mutations in CHMP4B (D129V and E161K) cause autosomal dominant cataracts. Transfection studies showed that truncated D129V-CHMP4B had altered subcellular distribution compared to wild-type and an increased capacity to inhibit virus-like particle release from the cell surface, consistent with gain-of-function dominant negative effects on ESCRT-III. Transfection of mutant vs. wild-type CHMP4B in cultured cells, subcellular localization imaging, virus-like particle release assay American journal of human genetics Medium 17701905
2009 The CHMP4B-docking site and Src-docking site in the Bro1 domain of Alix are autoinhibited in the native cytosolic state of Alix. In HEK-293 cell lysates, these sites are unavailable in cytosolic Alix but available in membrane-bound Alix, indicating that Alix membrane association relieves autoinhibition to enable CHMP4B binding. Biochemical fractionation, detergent treatment of recombinant Alix, cell lysate binding assays The Biochemical journal Medium 19016654
2012 CC2D1A and CC2D1B are direct regulators of CHMP4B, binding with nanomolar affinity in a 1:1 complex. The binding site on CC2D1A was mapped to the third DM14 domain, and the CC2D1A binding site on CHMP4B was mapped to the N-terminal helical hairpin. A crystal structure of the CHMP4B helical hairpin identified two surface patches involved in CC2D1A interaction. CC2D1A binding to CHMP4B prevents CHMP4B polymerization in vitro. Mutations at the CC2D1A-binding surface of CHMP4B abolished its dominant negative effect on HIV-1 budding, suggesting this surface is required for CHMP4B polymerization. Crystal structure of CHMP4B helical hairpin, surface plasmon resonance (nanomolar affinity measurement), deletion mapping, in vitro polymerization assay, HIV-1 budding assay with CHMP4B mutants Journal of molecular biology High 22406677
2012 Hydrophobic residues in the CHMP4B C-terminal amphipathic α-helix bind a concave surface of Brox (a mammalian Alix paralog). Crystal/structural analysis showed the CHMP4B C-terminal tail adopts an α-helical conformation when bound to Brox, at the same site used by CHMP5 (which binds via a β-hairpin). This defines a shared but conformationally distinct binding surface on Brox for ESCRT-III proteins. Crystal structure of Brox:CHMP4B complex, mutagenesis, binding assays Structure (London, England : 1993) High 22484091
2014 Anillin-septin complex is required for the recruitment of CHMP4B to the abscission site during cytokinesis. Using live imaging and subdiffraction microscopy, the anillin-septin cytoskeleton drives intercellular bridge elongation and maturation, which primes the bridge for CHMP4B assembly at the abscission site. Live cell imaging, subdiffraction microscopy, anillin/septin depletion (loss-of-function with CHMP4B localization readout) Open biology Medium 24451548
2014 CHMP4B not only localizes to cytokinetic bridges but also to chromosome bridges and micronuclei (the latter surrounded by lysosomes and autophagosomes), and can be co-immunoprecipitated with chromatin. A cataract-associated CHMP4B mutation abolishes its ability to localize to micronuclei, suggesting this localization is mutation-sensitive. Immunofluorescence localization, co-immunoprecipitation with chromatin, comparison of wild-type vs. cataract mutant CHMP4B BioMed research international Medium 24741567
2019 Conditional knockdown of CHMP4B in mouse lens results in arrest of lens growth and differentiation, with lens fiber cell degeneration (shown by AQP0 immunolocalization) and cell death (TUNEL). Homozygous knock-in of the cataract-associated D129V mutation causes embryonic lethality by E15.5 with abnormal eye and brain histology, indicating CHMP4B is essential for lens development. Conditional knockout/knockdown mouse model, knock-in mouse model, immunolocalization (AQP0, CD68), TUNEL assay, in situ hybridization Differentiation; research in biological diversity High 31404815
2019 CHMP4B localizes to primary cilia in mammalian cells and is required for cilium assembly and maintenance of ciliary structural integrity. Knockdown of CHMP4B caused defective cilium assembly and fragmentation of pre-existing cilia. Morpholino-mediated depletion in zebrafish induced ciliopathy phenotypes (curved body axis, hydrocephalus, otolith malformation, kidney cysts), independently of ESCRT-dependent endocytic degradation. Immunofluorescence localization to primary cilia, siRNA knockdown in mammalian cells, morpholino depletion in zebrafish, phenotypic analysis FASEB journal High 31914703
2021 In ALS neurons, neither CHMP4B nor CHMP2B show increased nuclear accumulation (in contrast to CHMP7 and VPS4), indicating that CHMP4B is not a primary driver of nuclear pore complex injury in ALS despite CHMP7's known role in recruiting ESCRT-III subunits for nuclear envelope/NPC repair. Super-resolution structured illumination microscopy (SIM) of neuronal nuclei from ALS patients and models Acta neuropathologica communications Medium 34281622
2023 HSP90β directly interacts with CHMP4B as a client protein. HSP90β silencing causes upregulation of CHMP4B and p53; CHMP4B upregulation/overexpression induces excessive division of lens epithelial cells without differentiation, triggering apoptosis via the p53/Bak-Bim pathway and causing cataractogenesis and microphthalmia in zebrafish. Simultaneous silencing of both HSP90β and CHMP4B restored the normal eye phenotype. Co-immunoprecipitation (direct interaction), zebrafish knockdown/rescue experiment, overexpression phenotypic analysis, epistasis (double knockdown) Proceedings of the National Academy of Sciences of the United States of America High 37487085
2023 CHMP4B interacts with GSDMD (gasdermin D) and VPS4A, as shown by co-immunoprecipitation. CHMP4B and VPS4A puncta co-localize at injured plasma membranes in GSDMD-N-terminus-expressing cells. Depletion of CHMP4B enhanced pyroptotic indicators (PI-positive cells, Ca2+ efflux, IL-1β, LDH release), while overexpression attenuated them, demonstrating CHMP4B mediates membrane repair to reverse GSDMD-induced pyroptosis. Co-immunoprecipitation, fluorescence confocal microscopy, electron microscopy of membrane perforations, siRNA knockdown and overexpression with pyroptosis readouts (LDH, IL-1β, Ca2+ flux, FITC-Annexin V/PI) Biochimica et biophysica acta. General subjects Medium 37931722
2025 PRP4K kinase controls splicing of CHMP4B pre-mRNA; loss of PRP4K causes mis-splicing and reduced expression of CHMP4B in human cells. CHMP4B is required for autophagosome-lysosome fusion; re-expression of CHMP4B cDNA in PRP4K-deficient cells restores normal autophagosome-lysosome fusion, placing CHMP4B downstream of PRP4K in an evolutionarily conserved splicing circuit regulating autophagy. Genetic epistasis (CHMP4B cDNA rescue in PRP4K knockout cells), autophagosome-lysosome fusion assay, mRNA splicing analysis Cell reports High 40531620
2025 GAS2L3 localizes to the midbody and recruits CHMP4B to the abscission site. GAS2L3 undergoes liquid-liquid phase separation (LLPS) via its intrinsically disordered region (IDR) and scaffolds CHMP4B condensate formation at the midbody through phase separation. GAS2L3 knockdown or IDR deletion leads to defective CHMP4B recruitment, defective cytokinesis, and G1 arrest. Live cell imaging, structured illumination microscopy, FRAP, in vitro droplet formation assay, GAS2L3 knockdown/IDR deletion with CHMP4B localization and cytokinesis readouts Journal of advanced research Medium 41177429
2026 CHMP4B binds PI(3,5)P2 (a lysosomal phosphoinositide) as demonstrated by liposome sedimentation assay. Forced recruitment of Pikfyve (the PI(3,5)P2-generating kinase) to early endosomes recruits a fraction of CHMP4B to early endosomes. A CHMP4B mutant defective in PI(3,5)P2 binding cannot restore microautophagic STING degradation or resolution of STING signaling in Chmp4b-depleted cells, establishing a PI(3,5)P2/CHMP4B axis on lysosomes as essential for STING encapsulation by lysosomes. Liposome sedimentation assay (direct lipid binding), forced Pikfyve recruitment assay, CHMP4B mutant rescue experiment, STING degradation/signaling assay in Chmp4b-depleted cells Nature communications High 42203786
2025 CHMP4B displays progressively severe spatial organization defects at the cytokinetic abscission site when CHMP2A is depleted, as visualized by SIM and CLEM. Dual-protein imaging revealed disrupted coordination between CHMP4B and other ESCRT-III subunits in CHMP2A-deficient cells, supporting an ordered/hierarchical assembly of ESCRT-III subunits in which CHMP2A acts upstream of CHMP4B during abscission. CHMP2A knockout, live cell imaging, structured illumination microscopy (SIM), correlative light-electron microscopy (CLEM), dual-protein co-imaging bioRxivpreprint Medium bio_10.1101_2025.06.24.661003
2024 CHMP4B associates with specific lipid species in dividing HeLa cells (identified by lipid-trap mass spectrometry using GFP-tagged CHMP4B immunoprecipitation followed by lipidomic analysis), with the lipid association enriched in dividing compared to non-dividing cells. Lipid-trap mass spectrometry (GFP immunoprecipitation + lipidomics) bioRxivpreprint Low bio_10.1101_2024.12.13.627510

Source papers

Stage 0 corpus · 28 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2003 The ALG-2-interacting protein Alix associates with CHMP4b, a human homologue of yeast Snf7 that is involved in multivesicular body sorting. The Journal of biological chemistry 184 12860994
2007 CHMP4B, a novel gene for autosomal dominant cataracts linked to chromosome 20q. American journal of human genetics 107 17701905
2014 Anillin-dependent organization of septin filaments promotes intercellular bridge elongation and Chmp4B targeting to the abscission site. Open biology 66 24451548
2006 CHMP7, a novel ESCRT-III-related protein, associates with CHMP4b and functions in the endosomal sorting pathway. The Biochemical journal 61 16856878
2014 Association of CHMP4B and autophagy with micronuclei: implications for cataract formation. BioMed research international 55 24741567
2004 CHMP4b is a major binding partner of the ALG-2-interacting protein Alix among the three CHMP4 isoforms. Archives of biochemistry and biophysics 55 14678797
2012 CC2D1A is a regulator of ESCRT-III CHMP4B. Journal of molecular biology 51 22406677
2020 Up-regulation of CHMP4B alleviates microglial necroptosis induced by traumatic brain injury. Journal of cellular and molecular medicine 25 32585748
2019 A charged multivesicular body protein (CHMP4B) is required for lens growth and differentiation. Differentiation; research in biological diversity 23 31404815
2009 The CHMP4b- and Src-docking sites in the Bro1 domain are autoinhibited in the native state of Alix. The Biochemical journal 23 19016654
2012 Two distinct binding modes define the interaction of Brox with the C-terminal tails of CHMP5 and CHMP4B. Structure (London, England : 1993) 20 22484091
2015 High CHMP4B expression is associated with accelerated cell proliferation and resistance to doxorubicin in hepatocellular carcinoma. Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine 19 25874485
2021 The ESCRT-III protein VPS4, but not CHMP4B or CHMP2B, is pathologically increased in familial and sporadic ALS neuronal nuclei. Acta neuropathologica communications 18 34281622
2022 BMP4 preserves the developmental potential of mESCs through Ube2s- and Chmp4b-mediated chromosomal stability safeguarding. Protein & cell 15 35147915
2019 ESCRT subunit CHMP4B localizes to primary cilia and is required for the structural integrity of the ciliary membrane. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 15 31914703
2023 CHMP4B and VSP4A reverse GSDMD-mediated pyroptosis by cell membrane remodeling in endometrial carcinoma. Biochimica et biophysica acta. General subjects 13 37931722
2014 CHMP4B, ESCRT-III associating protein, associated with neuronal apoptosis following intracerebral hemorrhage. Brain research 13 25478783
2021 Broadening the Mutation Spectrum in GJA8 and CHMP4B: Novel Missense Variants and the Associated Phenotypes in Six Chinese Han Congenital Cataracts Families. Frontiers in medicine 11 34722561
2022 Long noncoding RNA Sh2d3c promotes manganese-induced neuronal apoptosis through the mmu-miR-675-5p/Chmp4b/Bax axis. Toxicology letters 9 35690225
2024 Pyroptosis Signature Gene CHMP4B Regulates Microglia Pyroptosis by Inhibiting GSDMD in Alzheimer's Disease. Molecular neurobiology 6 38823000
2023 HSP90β prevents aging-related cataract formation through regulation of the charged multivesicular body protein (CHMP4B) and p53. Proceedings of the National Academy of Sciences of the United States of America 5 37487085
2025 Regulating the balance between GSDMD-mediated pyroptosis and CHMP4B-dependent cell repair attenuates calcium oxalate kidney stone formation. International journal of biological sciences 4 40384863
2025 Aerobic Exercise Attenuates Autophagy-Lysosomal Flux Deficits via β2-AR-Mediated ESCRT-III Subunit CHMP4B in Mice With Human MAPT P301L. Aging cell 4 40715737
2025 KIF4A Inhibits Ferroptosis in Glioblastoma via the CHMP4B/GPX4 Axis and Promotes Temozolomide Resistance. Molecular carcinogenesis 3 40705827
2025 IDR-driven LLPS of GAS2L3 scaffolds CHMP4B condensates to accelerate cytokinesis in hepatocellular carcinoma cells. Journal of advanced research 2 41177429
2024 CHMP4B contributes to maintaining the follicular cells integrity in the panoistic ovary of the cockroach Blattella germanica. Biology of the cell 1 38895958
2026 A PI(3,5)P2/CHMP4B axis on lysosomes is essential for microautophagic degradation of STING. Nature communications 0 42203786
2025 The evolutionarily conserved PRP4K-CHMP4B/vps32 splicing circuit regulates autophagy. Cell reports 0 40531620

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