CHMP1B

Chr 18

charged multivesicular body protein 1B

Also known as: C10orf2, C18-ORF2, C18orf2, CHMP1.5, Vps46-2, Vps46B, hVps46-2

CHMP1B encodes a component of the ESCRT-III complex that mediates endosomal cargo sorting into multivesicular bodies for lysosomal degradation and functions in cytokinesis during cell division. Mutations cause autosomal recessive pontocerebellar hypoplasia type 8, a severe neurodevelopmental disorder with microcephaly, cerebellar hypoplasia, and progressive neurodegeneration typically manifesting in infancy. The gene shows moderate constraint against loss-of-function variation (pLI 0.73, LOEUF 0.69), consistent with its essential cellular functions.

Summary from RefSeq, UniProt
Research Assistant →
0
Active trials
7
Pubs (1 yr)
97
P/LP submissions
0%
P/LP missense
0.69
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryCHMP1B
Population Constraint (gnomAD)
Moderately constrained gene (pLI 0.73) — some intolerance to loss-of-function variants.
📋
ClinVar Variants
93 unique Pathogenic / Likely Pathogenic· 43 VUS of 139 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Moderate LoF intolerance
LoF Constraint
0.69LOEUF
pLI 0.732
Z-score 1.93
OE 0.00 (0.000.69)
Moderately constrained

Typical tolerance to LoF variation

Missense Constraint
0.26Z-score
OE missense 0.93 (0.801.10)
106 obs / 113.7 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.00 (0.000.69)
00.351.4
Missense OE0.93 (0.801.10)
00.61.4
Synonymous OE0.83
01.21.6
LoF obs/exp: 0 / 4.3Missense obs/exp: 106 / 113.7Syn Z: 0.91
DN
0.84top 10%
GOF
0.6932th %ile
LOF
0.3164th %ile

This gene has evidence for multiple mechanisms of pathogenicity (dominant-negative and gain-of-function). Both the Badonyi & Marsh prediction and the broader genomic evidence point to dominant-negative as the predominant mechanism. Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

DNprediction above median
GOFprediction above median

Note: In-silico variant effect predictors (SIFT, PolyPhen, REVEL, CADD) may underestimate pathogenicity of missense variants in genes with GOF or DN mechanisms. Consider functional evidence and clinical context.

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312.

ClinVar Variant Classifications

139 submitted variants in ClinVar

Classification Summary

Pathogenic90
Likely Pathogenic3
VUS43
Likely Benign1
Benign1
90
Pathogenic
3
Likely Pathogenic
43
VUS
1
Likely Benign
1
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
90
0
90
Likely Pathogenic
0
0
3
0
3
VUS
0
31
12
0
43
Likely Benign
0
0
0
1
1
Benign
0
0
0
1
1
Total0311052138

LoF = frameshift, stop gained/lost, canonical splice · Counts from ClinVar esearch · Updated hourly

View in ClinVar →

Protein Context — Lollipop Plot

CHMP1B · protein map & ClinVar variants

Showing all ClinVar variants across the protein. Search a specific variant to highlight its position.

Clinical Trials

Active and recruiting trials from ClinicalTrials.gov

No active trials found for this gene.

Search ClinicalTrials.gov →
Clinical Literature
Open Research Assistant →
Key Publications
Landmark & review papers · by relevance
PubMed
Top 2 results · since 2015Search PubMed ↗