Affinage

CHMP1B

Charged multivesicular body protein 1b · UniProt Q7LBR1

Length
199 aa
Mass
22.1 kDa
Annotated
2026-06-09
43 papers in source corpus 26 papers cited in narrative 26 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CHMP1B is an ESCRT-III subunit that, with IST1, builds a one-start double-stranded helical copolymer in which 'open' interlocked CHMP1B subunits form the inner strand and 'closed' IST1 subunits form the outer strand, an arrangement that uniquely coats positively curved membranes and thereby drives normal-topology membrane remodeling events (PMID:26634441). Activation of CHMP1B for assembly involves release of an autoinhibitory α5 helix from the ESCRT-III core, and the resulting IST1–CHMP1B interaction is required for cytokinetic abscission (PMID:19525971). At constricted membranes the copolymer imposes leaflet-level lipid asymmetry, with two CHMP1B phenylalanines creating a helical hydrophobic defect on the outer leaflet that recruits polyunsaturated lipid tails (PMID:36624348). CHMP1B performs scission across multiple normal-topology sites: it scissions early endosomal tubular carriers to recycle transferrin and mannose-6-phosphate receptors, with SNX15 and CHMP1B alternately recruiting IST1 to distinct endosomal subdomains (PMID:37926552, PMID:38635626), and is recruited by spastin to lipid droplets to support fatty acid transfer to peroxisomes (PMID:31227594). Its C-terminal MIM1 motif is a high-affinity docking site for MIT-domain proteins, including spastin—for which CHMP1B is the midbody-targeting signal (PMID:18997780, PMID:15537668)—VPS4A, whose ATPase it stimulates (PMID:16174732, PMID:20805225), LIP5 (PMID:23105106, PMID:25637630), the deubiquitinases AMSH and UBPY/USP8 (PMID:16760479, PMID:17711858, PMID:35995394), and MITD1 (PMID:23015756), while calpain-7 binds a noncanonical second α-helical region (PMID:21616915, PMID:18316332). CHMP1B is itself dynamically ubiquitinated within a polymerization-sensitive loop—written by the LZTR1-CUL3 ligase and erased by USP8—and this modification governs its membrane recruitment and ESCRT-III assembly during EGF and VEGFR2 receptor trafficking; LZTR1 mutations that reduce CHMP1B ubiquitination cause endosomal accumulation and sustained VEGFR2 signaling in the context of Noonan syndrome (PMID:29933386, PMID:32175818, PMID:35995394). ESCRT-III subunit order also constrains CHMP1B function, as CHMP2A acts upstream to position CHMP1B correctly at the abscission site (PMID:40928930).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 2004 High

    Established the first functional partner of CHMP1B by showing it binds and modulates the microtubule-severing ATPase spastin, linking an ESCRT-III protein to membrane trafficking and microtubule regulation.

    Evidence Yeast two-hybrid, Co-IP, in vitro pull-down, fragment complementation and dominant-negative spastin rescue in Cos-7/PC12 cells

    PMID:15537668

    Open questions at the time
    • Structural basis of the interaction not yet resolved
    • Did not define the spastin recruitment site or in vivo cytokinesis role
  2. 2005 High

    Defined the molecular logic of MIT-domain recognition by showing the VPS4A MIT domain binds the CHMP1B C-terminus with a conserved leucine, framing ESCRT-III tails as TPR-completing ligands.

    Evidence NMR solution structure of VPS4A MIT domain, SPR affinity measurement and mutagenesis

    PMID:16174732

    Open questions at the time
    • Modest ~20 µM affinity leaves cellular avidity contributors undefined
    • Did not address how binding triggers VPS4 disassembly activity
  3. 2006 Medium

    Showed that VPS4 and the deubiquitinase AMSH compete for the CHMP1B C-terminus, suggesting coordinated control of ESCRT-III disassembly and cargo deubiquitination.

    Evidence Co-IP and competitive binding assay

    PMID:16760479

    Open questions at the time
    • Single lab, no structure of the competitive interface
    • Functional consequence of competition not directly tested
  4. 2007 Medium

    Identified UBPY/USP8 as a CHMP1B-binding deubiquitinase whose MIT domain is required for endosomal localization and EGFR degradation, placing CHMP1B in receptor downregulation.

    Evidence Co-IP, UBPY MIT-deletion localization and EGFR degradation rescue

    PMID:17711858

    Open questions at the time
    • Did not map the CHMP1B residues required for binding
    • Direct role of CHMP1B (vs CHMP1A) in EGFR degradation not isolated
  5. 2008 High

    Resolved the structural basis for CHMP1B as the midbody-targeting signal for spastin and mapped overlapping LIP5/VPS4 binding regions on the CHMP1B C-terminus.

    Evidence 2.5 Å crystal structure of CHMP1B tail/spastin MIT, spastin point mutants and cytokinesis assays; separate in vitro LIP5 binding/truncation analysis

    PMID:18385515 PMID:18997780

    Open questions at the time
    • Whether a true second VPS4 site exists on CHMP1B remained inferential
    • Conformational dependence of LIP5 binding only partially defined
  6. 2009 High

    Demonstrated that CHMP1B autoinhibition by the α5 helix gates polymerization and that IST1–CHMP1B assembly is required for abscission, establishing the activation switch for this copolymer.

    Evidence In vitro helical assembly, core-α5 interface mutagenesis, abscission assay and crystal structures of IST1/CHMP3 cores

    PMID:19525971

    Open questions at the time
    • Trigger that releases autoinhibition in vivo not identified
    • Copolymer architecture not yet resolved
  7. 2010 Medium

    Provided a mechanistic model for how CHMP1B activates VPS4A, showing its C-terminal fragment threads into the VPS4A pore to stimulate ATPase activity.

    Evidence In vitro ATPase assays with purified proteins, VPS4A pore-loop mutagenesis and liposome oligomerization

    PMID:20805225

    Open questions at the time
    • Single lab reconstitution without structure of the threaded state
    • Relevance to full-length polymerized CHMP1B not tested
  8. 2011 Medium

    Identified calpain-7 as a noncanonical CHMP1B partner binding a second α-helical region, and showed CHMP1B/IST1 form a ternary complex regulating calpain-7 autolysis and membrane partitioning.

    Evidence Recombinant pull-down with truncation mutants, Co-IP, autolysis assay and subcellular fractionation

    PMID:18316332 PMID:21616915

    Open questions at the time
    • Physiological substrate of calpain-7 at ESCRT sites unknown
    • Single lab, no structure of the noncanonical interface
  9. 2012 High

    Refined LIP5 and MITD1 recognition of CHMP1B, showing LIP5 uses canonical MIM1 contacts but requires simultaneous CHMP5 binding to assemble stable VPS4 complexes, while MITD1 is recruited to the midbody by CHMP1B to regulate IST1-VPS4.

    Evidence NMR structures, SPR, cellular Co-IP (LIP5); Co-IP and siRNA abscission assays (MITD1)

    PMID:23015756 PMID:23105106

    Open questions at the time
    • How these competing adaptors are temporally ordered at one site unclear
    • MITD1 study was single-lab Medium confidence
  10. 2015 High

    Delivered the atomic architecture of the CHMP1B/IST1 copolymer and an atomic-resolution LIP5–CHMP1B/CHMP5 structure, revealing a unique positive-curvature external coat and the conformational coupling of ESCRT-III binding to LIP5/VPS4 stimulation.

    Evidence 4 Å cryo-EM of the copolymer plus membrane assays; 1 Å crystal structure of LIP5NTD with CHMP5/CHMP1B MIMs and ATPase assay

    PMID:25637630 PMID:26634441

    Open questions at the time
    • In vivo membrane substrates of the external coat not yet enumerated
    • How curvature sensing selects sites in cells unresolved
  11. 2018 High

    Established dynamic ubiquitination of CHMP1B—erased by USP8 within a polymerization-sensitive loop—as a regulatory switch for membrane recruitment and EGFR trafficking conserved into Drosophila.

    Evidence Ubiquitination assays, USP8 Co-IP, size-exclusion of a 500 kDa IST1 complex, EGF pulse-chase and Drosophila loss-of-function

    PMID:29933386

    Open questions at the time
    • The ligase writing the modification was not yet identified
    • Quantitative stoichiometry of ubiquitin on polymer vs soluble CHMP1B unclear
  12. 2019 Medium

    Extended CHMP1B function to interorganelle lipid transfer and to endosomal motility control, showing spastin recruits CHMP1B/IST1 to lipid droplets for fatty acid trafficking and that loss of CHMP1B produces protrudin/KIF5-dependent protrusions.

    Evidence Live imaging, loss-of-function, fatty acid trafficking and peroxidation assays; siRNA epistasis with spastin/protrudin/KIF5 and BMP receptor distribution

    PMID:31227594 PMID:31587092

    Open questions at the time
    • Whether scission per se mediates FA transfer not directly proven
    • Both single-lab studies without structural correlates
  13. 2020 Medium

    Identified the LZTR1-CUL3 ligase as the writer of CHMP1B ubiquitination controlling recycling-endosome dynamics, and linked Noonan-syndrome LZTR1 mutations to reduced CHMP1B ubiquitination, endosomal accumulation and sustained VEGFR2 signaling.

    Evidence Co-IP, ubiquitination assays, LZTR1 knockout mouse and endothelial knockdown with trafficking imaging and VEGFR2 readout

    PMID:32175818

    Open questions at the time
    • Direct ubiquitination sites and chain type on CHMP1B by LZTR1 not mapped
    • Single lab; vascular phenotype mechanism partly correlative
  14. 2022 Medium

    Refined CHMP1B–USP8 recognition to specific MIM leucines independent of ubiquitin status, and showed pathogen and host ubiquitin signals on VPS4A tune CHMP1B engagement.

    Evidence HTRF with CHMP1B L192A/L195A and MIM-deletion mutants (USP8); HCV-induced VPS4A K23/K121 ubiquitylation, Co-IP, ATPase and infectivity assays

    PMID:35044214 PMID:35995394

    Open questions at the time
    • Whether USP8 recognition mode differs across MIT proteins not resolved
    • Generality of VPS4A ubiquitin-gated CHMP1B binding beyond HCV unknown
  15. 2023 Medium

    Defined the membrane-physical mechanism and the cargo-specific, ubiquitin-independent scission roles of the CHMP1B/IST1 copolymer at endosomes and exosomes, with a chemical tool isolating the recycling function from cytokinesis and MVB sorting.

    Evidence Cryo-EM of brominated lipids plus MD; live-imaging siRNA of SNX15/CHMP1B endosomal subdomains; small-molecule IST1-CHMP1B disruptor with transferrin recycling and LC3 readouts; Drosophila/HCT116 Rab11a-exosome ILV assays

    PMID:36624348 PMID:36872252 PMID:37926552 PMID:38635626

    Open questions at the time
    • How distinct subdomain recruitment cues (SNX15 vs CHMP1B) are coordinated unclear
    • Trigger for noncanonical LC3 lipidation on stalled endosomes undefined
  16. 2023 Low

    Reported a nuclear/chromatin-associated property of CHMP1B mediated by its N-terminal region, raising a possible role outside membrane scission.

    Evidence Fluorescence microscopy of nuclear foci, N-terminal mutagenesis and interspecies VPS4 recruitment

    PMID:36221007

    Open questions at the time
    • No biochemical or structural validation of chromatin binding
    • Functional consequence of nuclear localization untested
    • Single lab, not independently confirmed
  17. 2025 Medium

    Established that CHMP1B positioning at the abscission site is hierarchically controlled, with CHMP2A acting upstream to organize correct CHMP1B localization.

    Evidence CHMP2A knockout with live imaging, SIM and correlative light-electron microscopy of ESCRT-III subunits

    PMID:40928930

    Open questions at the time
    • Molecular interface by which CHMP2A directs CHMP1B not defined
    • Whether the same hierarchy operates at endosomes unknown

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the various competing MIT-domain effectors and the ubiquitination cycle are temporally choreographed to select among CHMP1B's distinct scission sites (abscission, endosomal tubules, lipid-droplet contacts, exosome biogenesis) remains unresolved.
  • No unified in vivo model coupling ubiquitination state to site selection
  • Site-specific determinants distinguishing normal-topology scission contexts undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005198 structural molecule activity 3 GO:0060090 molecular adaptor activity 3 GO:0098772 molecular function regulator activity 3 GO:0008289 lipid binding 1
Localization
GO:0005768 endosome 3 GO:0005829 cytosol 2 GO:0005886 plasma membrane 2 GO:0005811 lipid droplet 1
Pathway
R-HSA-1640170 Cell Cycle 4 R-HSA-5653656 Vesicle-mediated transport 4 R-HSA-9609507 Protein localization 3 R-HSA-162582 Signal Transduction 2
Partners
AMSHCAPN7IST1LIP5MITD1SPASTUSP8VPS4A
Complex memberships
CHMP1B-IST1 ESCRT-III copolymerESCRT-IIIcalpain-7/CHMP1B/IST1 ternary complex

Evidence

Reading pass · 26 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2015 CHMP1B and IST1 form a one-start, double-stranded helical copolymer resolved at 4 Å resolution by cryo-EM. The inner strand comprises 'open' CHMP1B subunits that interlock in an elaborate domain-swapped architecture, encircled by an outer strand of 'closed' IST1 subunits. Unlike other ESCRT-III proteins, this CHMP1B/IST1 polymer forms external coats on positively curved membranes in vitro and in vivo, indicating a distinct membrane curvature-sensing and -stabilizing mechanism. 4 Å cryo-EM reconstruction of helical copolymer; in vitro and in vivo membrane-binding assays Science (New York, N.Y.) High 26634441
2008 The C-terminal tail of CHMP1B binds the MIT domain of spastin through a noncanonical site between the first and third helices of the MIT domain, forming a high-affinity complex (2.5 Å crystal structure). Point mutations in the CHMP1B-binding site of spastin block spastin recruitment to the midbody and impair cytokinesis, establishing CHMP1B as the midbody-targeting signal for spastin. 2.5 Å X-ray crystal structure of CHMP1B C-terminal tail / spastin MIT domain complex; spastin point mutants; fluorescence microscopy of midbody localization; cytokinesis assay Nature structural & molecular biology High 18997780
2004 CHMP1B interacts with spastin via the spastin MIT domain (residues 80–196). Co-immunoprecipitation, in vitro pull-down, beta-lactamase protein fragment complementation, and co-localization in Cos-7 and PC12 cells confirmed the interaction. Expression of CHMP1B prevented the abnormal microtubule phenotype caused by ATPase-defective spastin, indicating CHMP1B functionally modulates spastin activity in membrane trafficking. Yeast two-hybrid; co-IP; in vitro pull-down; beta-lactamase fragment complementation; immunofluorescence co-localization; dominant-negative spastin phenotype rescue Human molecular genetics High 15537668
2009 CHMP1B forms higher-order helical structures in vitro and interacts with IST1; IST1-CHMP1B interactions are required for cytokinetic abscission. The autoinhibitory alpha5 helix folds back against the ESCRT-III core domain, and its dissociation activates ESCRT-III proteins for membrane assembly. In vitro helical polymer assembly; biochemical interaction assays; mutagenesis of CHMP3 core-alpha5 interface; abscission functional assay; crystal structures of IST1 and CHMP3 N-terminal core domains Nature structural & molecular biology High 19525971
2005 The VPS4A MIT domain binds the C-terminal half of CHMP1B with a Kd of ~20 µM. NMR solution structure of VPS4A MIT domain shows that a conserved leucine (Leu-64) on the third helix, which normally binds a fourth helix in TPR motifs, is used to bind CHMP1B, suggesting ESCRT-III proteins complete the TPR motif. NMR solution structure; surface plasmon resonance / binding affinity measurement; mutational analysis Proceedings of the National Academy of Sciences of the United States of America High 16174732
2006 CHMP1B is a direct binding partner of the deubiquitinating enzyme AMSH; VPS4 and AMSH compete for binding to the C-terminal regions of CHMP1B, suggesting coordinated regulation of ESCRT-III disassembly and endosomal cargo deubiquitination. Co-immunoprecipitation; competitive binding assay between VPS4 and AMSH for CHMP1B C-terminus The Journal of biological chemistry Medium 16760479
2007 The MIT domain of UBPY/USP8 binds CHMP1B (and CHMP1A) among the 11 human CHMP family members. The UBPY MIT domain is essential for endosomal localization and for its functional role in EGF receptor degradation. Co-immunoprecipitation; UBPY MIT-deletion mutant localization and functional assay; EGFR degradation rescue assay The Journal of biological chemistry Medium 17711858
2008 LIP5 binds CHMP1B; in CHMP1B (and CHMP2A), the LIP5 binding site encompasses C-terminal sequences that overlap with MIT-interacting motifs (MIMs) used by VPS4, but evidence for a second VPS4-binding site in CHMP1B suggests LIP5 and VPS4 can bind simultaneously. LIP5 preferentially binds polymerized CHMP2A but soluble CHMP5, indicating conformation-dependent regulation. In vitro binding assays; pull-down with truncation mutants; analysis of MIM overlap Molecular biology of the cell Medium 18385515
2010 C-terminal fragments of CHMP1B (along with other ESCRT-III proteins) activate purified human VPS4A ATPase activity; this activation requires both the MIT-interacting motif and ~50 adjacent amino acids, and mutating VPS4A pore loops alters the response, supporting a model where ESCRT-III proteins thread into the VPS4A pore to stimulate oligomerization and catalysis. In vitro ATPase activity assay with purified proteins; VPS4A pore-loop mutagenesis; liposome-based oligomerization assay The Journal of biological chemistry Medium 20805225
2012 The first MIT module of the tandem LIP5 MIT domain binds CHMP1B through canonical type 1 MIT-interacting motif (MIM1) interactions. LIP5 can bind MIM1-containing ESCRT-III proteins (including CHMP1B), CHMP5, and VPS4 independently in vitro, but in cells stable VPS4 complex assembly requires LIP5 to simultaneously contact both a MIM1-containing protein and CHMP5. Solution NMR structure of LIP5-CHMP5 complex; SPR binding measurements; co-immunoprecipitation in cells The Journal of biological chemistry High 23105106
2012 MITD1 interacts strongly with CHMP1B (and CHMP2A and IST1); CHMP1B and these ESCRT-III subunits are required for recruitment of MITD1 to the midbody, and MITD1 participates in the abscission phase of cytokinesis by negatively regulating IST1-VPS4 interaction. Co-immunoprecipitation; siRNA knockdown with midbody localization readout; cytokinesis abscission assay Molecular biology of the cell Medium 23015756
2015 Crystal structure at 1 Å resolution of the LIP5 N-terminal domain (LIP5NTD) in complex with MIM motifs of both CHMP5 and CHMP1B reveals that ESCRT-III binding induces a conformational change in LIP5NTD via insertion of CHMP5 Tyr182 at the LIP5 core; mutation of Tyr182 partially relieves CHMP5-dependent inhibition of LIP5-mediated VPS4 stimulation. 1 Å X-ray crystal structure; mutagenesis; VPS4 ATPase stimulation assay The Journal of biological chemistry High 25637630
2018 CHMP1B is ubiquitinated within a flexible loop that undergoes conformational changes during polymerization; it is deubiquitinated by USP8/UBPY and found fully devoid of ubiquitin in a ~500 kDa complex containing IST1. EGF stimulation transiently increases ubiquitinated CHMP1B on cell membranes. CHMP1B ubiquitination is required for EGFR trafficking in human cells and wing development in Drosophila. Ubiquitination assay; co-immunoprecipitation with USP8; size-exclusion chromatography (500 kDa complex); EGF stimulation pulse-chase; Drosophila genetic loss-of-function; EGFR trafficking assay PLoS genetics High 29933386
2019 M1 Spastin recruits ESCRT-III proteins IST1 and CHMP1B to lipid droplets via its MIT domain to facilitate fatty acid trafficking from lipid droplets to peroxisomes. Loss of IST1 or CHMP1B impairs LD-to-peroxisome FA trafficking and lipid peroxidation relief. Fluorescence live imaging; co-localization; loss-of-function (siRNA/KO); fatty acid trafficking assay; lipid peroxidation assay The Journal of cell biology Medium 31227594
2019 HeLa cells lacking CHMP1B (or IST1) develop cellular protrusions, a phenotype also seen in spastin-null cells. The protrusion phenotype requires protrudin and KIF5, placing CHMP1B in the ESCRT-III/spastin axis that limits polarised protrudin-dependent endosomal motility to cell protrusions. siRNA knockdown in HeLa cells; epistasis with spastin/IST1/protrudin/KIF5 knockdown; fluorescence microscopy of protrusion phenotype; BMP receptor distribution assay Cellular and molecular life sciences : CMLS Medium 31587092
2020 LZTR1 (a CUL3 ubiquitin ligase adaptor) controls ubiquitination of CHMP1B and thereby regulates dynamics of fusion and fission of recycling endosomes; Noonan syndrome-associated LZTR1 mutations reduce CHMP1B ubiquitination, leading to endosomal accumulation and sustained VEGFR2 signaling. Co-immunoprecipitation; ubiquitination assay; LZTR1 knockout mouse and endothelial cell knockdown; endosomal trafficking imaging; VEGFR2 signaling readout Circulation research Medium 32175818
2011 Calpain-7 binds CHMP1B at its second α-helical region (not the canonical C-terminal MIM1) via its tandem MIT domain (CL7MIT). Coexpression of CHMP1B enhances calpain-7 autolysis, and further coexpression of IST1 forms a ternary calpain-7/CHMP1B/IST1 complex. Overexpression of CHMP1B and IST1 together increases calpain-7 in membrane/organelle fractions. In vitro pull-down with truncation mutants; co-immunoprecipitation; calpain-7 autolysis assay; subcellular fractionation Journal of biochemistry Medium 21616915
2023 A small-molecule pseudonatural product that specifically disrupts IST1-CHMP1B interaction inhibits IST1-CHMP1B copolymer formation, blocks transferrin receptor recycling (causing transferrin accumulation in stalled sorting endosomes), and triggers noncanonical LC3 lipidation on stalled endosomes. The compound does not affect cytokinesis, MVB sorting, or extracellular vesicle biogenesis. Chemical inhibitor screen; Co-IP/interaction assay; transferrin receptor recycling assay; LC3 lipidation assay; cytokinesis and MVB assays as negative controls Proceedings of the National Academy of Sciences of the United States of America Medium 38635626
2023 IST1 and CHMP1B together contribute to scission of early endosomal tubular carriers; SNX15 and CHMP1B alternately recruit IST1 to distinct subdomains of sorting endosomes (clathrin subdomain vs. base of endosomal tubules), regulating transferrin receptor and mannose-6-phosphate receptor recycling. Live-cell microscopy; siRNA depletion; kinetic and spatial trafficking assays for transferrin receptor and M6PR; co-localization with endosomal markers Traffic (Copenhagen, Denmark) Medium 37926552
2023 CHMP1B exhibited nuclear localization in mammalian cells and recruited both human and Asgard VPS4 to nuclear foci; mutation of the ESCRT-III N-terminal region abolished these nuclear properties, indicating the N-terminal domain mediates nuclear targeting and chromatin association. Fluorescence microscopy of nuclear localization; mutagenesis of N-terminal region; interspecies VPS4 recruitment assay The ISME journal Low 36221007
2023 Cryo-EM of brominated lipids within CHMP1B/IST1-coated membrane nanotubes revealed leaflet-level structural asymmetries: constricted membranes show altered lipid diffusion, leaflet thinning, lipid compositional/conformational asymmetry, and two CHMP1B phenylalanine residues create a helical hydrophobic defect on the outer leaflet where polyunsaturated docosahexaenoyl tails accumulate. Cryo-EM with brominated lipid contrast probes; molecular dynamics simulation; reconstituted CHMP1B/IST1 nanotubes Nature structural & molecular biology High 36624348
2022 HCV infection enhances the interaction between CHMP1B and VPS4A (but not VPS4B) via HCV-induced polyubiquitylation of VPS4A at K23 and K121; VPS4A K23R/K121R mutant fails to interact with CHMP1B and has reduced ATPase activity, indicating that VPS4A ubiquitylation promotes CHMP1B binding and VPS4A activation for HCV particle release. Co-immunoprecipitation; site-directed mutagenesis (VPS4A K23R/K121R); ATPase activity assay; siRNA knockdown; viral infectivity titer Journal of virology Medium 35044214
2025 CHMP2A knockout reveals an ordered, hierarchical assembly of ESCRT-III at the cytokinetic abscission site: IST1 and CHMP2B are minimally disrupted, while CHMP1B (along with CHMP4B and CHMP3) shows progressively severe mislocalization, establishing CHMP2A as an upstream organizer required for correct CHMP1B positioning during abscission. CHMP2A knockout; live-cell imaging; structured illumination microscopy (SIM); correlative light-electron microscopy; dual-protein imaging of ESCRT-III subunits Molecular biology of the cell Medium 40928930
2022 Conserved leucine residues L192 and L195 within the MIM (MIT-interacting motif) domain of CHMP1B are required for interaction with USP8/UBPY, whereas the ubiquitination status of CHMP1B does not affect this interaction; deletion of the MIM domain abolishes binding. HTRF interaction assay; CHMP1B point-mutant and deletion analysis (L192A/L195A and MIM deletion); comparison of ubiquitin-deficient CHMP1B mutant (4K→R) vs wild-type binding to USP8 SLAS discovery : advancing life sciences R & D Medium 35995394
2011 Calpain-7 N-terminal tandem MIT domain directly interacts with CHMP1B; the interaction was confirmed by pulldown assay using recombinant proteins. Overexpression of GFP-CHMPs or dominant-negative VPS4B caused calpain-7 accumulation in perinuclear puncta overlapping with endocytosed EGF, and endogenous calpain-7 partitions largely to cytosol with a small fraction in particulate fractions. Strep-tag pulldown from stable HEK293T transfectants; recombinant protein pulldown; fluorescence microscopy; subcellular fractionation Journal of biochemistry Medium 18316332
2023 CHMP1B (along with CHMP1A, CHMP5, and IST1 as accessory ESCRT-III proteins) is required for intraluminal vesicle formation in Drosophila recycling endosomes but, unlike core ESCRTs, is not involved in degradation of ubiquitinated proteins in late endosomes, revealing a specific ubiquitin-independent role in Rab11a-exosome generation. Drosophila genetic knockdown; comparative proteomics of Rab11a-enriched vs. total exosome preparations; CHMP5 siRNA knockdown in HCT116 cells; ILV formation assay Journal of extracellular vesicles Medium 36872252

Source papers

Stage 0 corpus · 43 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2007 Molecular genetics of bipolar disorder and depression. Psychiatry and clinical neurosciences 214 17239033
2015 Structure and membrane remodeling activity of ESCRT-III helical polymers. Science (New York, N.Y.) 212 26634441
2008 Structural basis for midbody targeting of spastin by the ESCRT-III protein CHMP1B. Nature structural & molecular biology 205 18997780
2009 Structural basis for ESCRT-III protein autoinhibition. Nature structural & molecular biology 184 19525971
2019 Spastin tethers lipid droplets to peroxisomes and directs fatty acid trafficking through ESCRT-III. The Journal of cell biology 164 31227594
2004 The hereditary spastic paraplegia protein spastin interacts with the ESCRT-III complex-associated endosomal protein CHMP1B. Human molecular genetics 160 15537668
2005 Structure and ESCRT-III protein interactions of the MIT domain of human VPS4A. Proceedings of the National Academy of Sciences of the United States of America 156 16174732
2007 The MIT domain of UBPY constitutes a CHMP binding and endosomal localization signal required for efficient epidermal growth factor receptor degradation. The Journal of biological chemistry 140 17711858
2006 Interaction of AMSH with ESCRT-III and deubiquitination of endosomal cargo. The Journal of biological chemistry 111 16760479
2008 Novel interactions of ESCRT-III with LIP5 and VPS4 and their implications for ESCRT-III disassembly. Molecular biology of the cell 69 18385515
2023 Accessory ESCRT-III proteins are conserved and selective regulators of Rab11a-exosome formation. Journal of extracellular vesicles 65 36872252
2010 Two genes on A/J chromosome 18 are associated with susceptibility to Staphylococcus aureus infection by combined microarray and QTL analyses. PLoS pathogens 60 20824097
2010 Activation of human VPS4A by ESCRT-III proteins reveals ability of substrates to relieve enzyme autoinhibition. The Journal of biological chemistry 54 20805225
2012 Interactions of the human LIP5 regulatory protein with endosomal sorting complexes required for transport. The Journal of biological chemistry 39 23105106
2018 CHMP1B is a target of USP8/UBPY regulated by ubiquitin during endocytosis. PLoS genetics 38 29933386
2012 MITD1 is recruited to midbodies by ESCRT-III and participates in cytokinesis. Molecular biology of the cell 37 23015756
2020 Impact of the Endosomal Escape Activity of Cell-Penetrating Peptides on the Endocytic Pathway. ACS chemical biology 31 32786263
2019 iTRAQ-based quantitative proteomics analysis of the spleen reveals innate immunity and cell death pathways associated with heat stress in broilers (Gallus gallus). Journal of proteomics 31 30664952
2015 A novel mechanism of regulating the ATPase VPS4 by its cofactor LIP5 and the endosomal sorting complex required for transport (ESCRT)-III protein CHMP5. The Journal of biological chemistry 30 25637630
2023 Brominated lipid probes expose structural asymmetries in constricted membranes. Nature structural & molecular biology 28 36624348
2019 ESCRT-III-associated proteins and spastin inhibit protrudin-dependent polarised membrane traffic. Cellular and molecular life sciences : CMLS 27 31587092
2008 Human calpain 7/PalBH associates with a subset of ESCRT-III-related proteins in its N-terminal region and partly localizes to endocytic membrane compartments. Journal of biochemistry 27 18316332
2022 Hepatitis C Virus-Induced ROS/JNK Signaling Pathway Activates the E3 Ubiquitin Ligase Itch to Promote the Release of HCV Particles via Polyubiquitylation of VPS4A. Journal of virology 24 35044214
2019 Spastin MIT Domain Disease-Associated Mutations Disrupt Lysosomal Function. Frontiers in neuroscience 24 31787869
2020 The Noonan Syndrome Gene Lztr1 Controls Cardiovascular Function by Regulating Vesicular Trafficking. Circulation research 21 32175818
2023 Selective cargo sorting in stem cell-derived small extracellular vesicles: impact on therapeutic efficacy for intervertebral disc degeneration. Clinical and translational medicine 15 38037469
2023 Isolation and proteomic profiling of urinary exosomes from patients with colorectal cancer. Proteome science 14 36759883
2019 Structural Insights into AQP2 Targeting to Multivesicular Bodies. International journal of molecular sciences 14 31661793
2018 Quantitative Proteomics Identify the Possible Tumor Suppressive Role of Protease-Activated Receptor-4 in Esophageal Squamous Cell Carcinoma Cells. Pathology oncology research : POR 14 29502225
2024 A chemical inhibitor of IST1-CHMP1B interaction impairs endosomal recycling and induces noncanonical LC3 lipidation. Proceedings of the National Academy of Sciences of the United States of America 11 38635626
2011 Calpain-7 binds to CHMP1B at its second α-helical region and forms a ternary complex with IST1. Journal of biochemistry 11 21616915
2023 IST1 regulates select recycling pathways. Traffic (Copenhagen, Denmark) 10 37926552
2022 Asgard ESCRT-III and VPS4 reveal conserved chromatin binding properties of the ESCRT machinery. The ISME journal 10 36221007
2024 The characteristics and functional significance of disulfidptosis-related genes in head and neck squamous cell carcinoma. Discover oncology 5 39625660
2025 Corneal stromal cells from patients with keratoconus exhibit alterations in the ESCRT-dependent machinery responsible for multivesicular body formation. Experimental eye research 4 39890050
2022 Identification of chemicals breaking the USP8 interaction with its endocytic substrate CHMP1B. SLAS discovery : advancing life sciences R & D 3 35995394
2005 Association analysis of CHMP1.5 genetic variation and bipolar disorder. Psychiatric genetics 3 16094257
2025 Comparative transcriptome analysis identified genes involved in testicular development in Takifugu rubripes. Fish physiology and biochemistry 2 39757246
2025 Classical swine fever virus hijacks ESCRT-III and VPS4A to promote phagophore closure for accelerating mitophagy. Autophagy 2 40574328
2025 Microscale Proteomic Analysis of the Endolymphatic Sac in Menière's Disease Patients. Otology & neurotology : official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology 1 40062362
2025 Loss of CHMP2A implicates an ordered assembly of ESCRT-III proteins during cytokinetic abscission. Molecular biology of the cell 1 40928930
2025 Hyperlipidemia-associated specific modules and hub genes revealed by integrative methods of WGCNA and MetaDE. Frontiers in genetics 0 41446394
2023 IST1 regulates select endosomal recycling pathways. bioRxiv : the preprint server for biology 0 37577466

Missed literature

Know a paper Affinage missed for CHMP1B? Flag it for the maintainers and the community.

No submissions yet.