Affinage

RIMOC1

RAB7A-interacting MON1-CCZ1 complex subunit 1 · UniProt A6NDU8

Length
294 aa
Mass
33.6 kDa
Annotated
2026-06-10
2 papers in source corpus 1 papers cited in narrative 3 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 3/3 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

RIMOC1 (C5orf51) is a positive regulator of RAB7A-dependent mitophagy that functions as a component of the MON1-CCZ1 RAB7A guanine nucleotide exchange factor complex (PMID:34432599). It associates specifically with GDP-locked (inactive) RAB7A and with the MON1 and CCZ1 subunits of the GEF complex (PMID:34432599), and is required for RAB7A stability and its translocation from late endosomes to the surface of depolarized mitochondria: in its absence RAB7A fails to localize to damaged mitochondria and is instead degraded by the proteasome (PMID:34432599). Through this control of RAB7A, RIMOC1 acts upstream of the core autophagy machinery, being required for recruitment of ATG9A to depolarized mitochondria (PMID:34432599). Beyond these roles in the RAB7A mitophagy pathway, no further mechanistic detail has been characterized in the available corpus.

Mechanistic history

Synthesis pass · year-by-year structured walk · 3 steps
  1. 2021 High

    Establishing that the uncharacterized protein C5orf51/RIMOC1 physically associates with the RAB7A GEF machinery defined its molecular context as a component of the MON1-CCZ1 complex.

    Evidence Proximity-dependent biotinylation (miniTurbo BioID) and co-IP with nucleotide-locked RAB7A mutants, showing interaction with GDP-locked RAB7A, MON1 and CCZ1

    PMID:34432599

    Open questions at the time
    • Stoichiometry and whether RIMOC1 is an obligate versus accessory subunit of MON1-CCZ1 not defined
    • Whether RIMOC1 directly contacts RAB7A or is bridged through MON1-CCZ1 not resolved
    • No structural model of the RIMOC1-containing complex
  2. 2021 High

    Loss-of-function showed that RIMOC1 is functionally required for RAB7A stability and its delivery to depolarized mitochondria, explaining why it matters for the pathway rather than merely being an interactor.

    Evidence C5orf51 knockout cells with RAB7A localization microscopy and MG132 proteasome-inhibitor rescue of RAB7A levels

    PMID:34432599

    Open questions at the time
    • Mechanism by which RIMOC1 protects RAB7A from proteasomal turnover unknown
    • Whether the stabilization defect is direct or a consequence of failed translocation not separated
  3. 2021 Medium

    Placing RIMOC1 upstream of ATG9A recruitment connected its RAB7A function to engagement of the core autophagy machinery during mitophagy.

    Evidence C5orf51 depletion with ATG9A localization microscopy after CCCP-induced mitochondrial depolarization

    PMID:34432599

    Open questions at the time
    • Single method and single lab for this specific readout
    • Whether ATG9A recruitment defect is solely downstream of lost RAB7A or an independent RIMOC1 role not distinguished
    • Impact on mitophagic flux and clearance endpoints not quantified

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unknown whether RIMOC1 functions outside the RAB7A mitophagy pathway and what its enzymatic or structural contribution to the MON1-CCZ1 complex is.
  • No biochemical assay of any RIMOC1 catalytic activity
  • No characterization in conventional (non-mitochondrial) endolysosomal trafficking
  • Findings derive from a single study and single lab

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 3
Localization
GO:0005739 mitochondrion 2 GO:0005768 endosome 1
Pathway
R-HSA-9612973 Autophagy 2
Partners
CCZ1MON1RAB7A
Complex memberships
MON1-CCZ1 complex

Evidence

Reading pass · 3 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2021 C5orf51 (RIMOC1) was identified as a specific interactor of GDP-locked (inactive) RAB7A using proximity-dependent biotinylation (miniTurbo), and also interacts with MON1 and CCZ1, the components of the RAB7A guanine nucleotide exchange factor complex, placing C5orf51 as a component of the MON1-CCZ1 complex. Proximity-dependent biotinylation (miniTurbo BioID), co-immunoprecipitation Autophagy High 34432599
2021 In the absence of C5orf51 (RIMOC1), RAB7A fails to localize to depolarized mitochondria during mitophagy and is instead degraded by the proteasome, demonstrating that C5orf51 is required for RAB7A stability and correct subcellular translocation from late endosomes to the mitochondrial surface. C5orf51 knockout cells, fluorescence microscopy (RAB7A localization), proteasome inhibitor rescue (MG132) Autophagy High 34432599
2021 Depletion of C5orf51 (RIMOC1) inhibited ATG9A recruitment to depolarized mitochondria, establishing C5orf51 as an upstream positive regulator required for the mitophagy autophagy machinery to engage at the mitochondrial surface. C5orf51 knockout/depletion, fluorescence microscopy of ATG9A localization after mitochondrial depolarization (CCCP treatment) Autophagy Medium 34432599

Source papers

Stage 0 corpus · 2 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2021 C5orf51 is a component of the MON1-CCZ1 complex and controls RAB7A localization and stability during mitophagy. Autophagy 35 34432599
2026 Transcriptional and Alternative Splicing Regulation of Autophagy and Vesicle Transport Pathways in Large Yellow Croaker Cells During Megalocytivirus Infection. Animals : an open access journal from MDPI 0 42072025

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