CYRIB

Chr 8

CYFIP related Rac1 interactor B

Also known as: BM-009, CYRI, CYRI-B, FAM49B, L1

The CYRIB protein negatively regulates RAC1 signaling and controls cytoskeletal remodeling, cell migration, and mitochondrial dynamics while also protecting against bacterial infections. Mutations cause autosomal dominant developmental and epileptic encephalopathy with microcephaly, affecting the brain and resulting in seizures and developmental delays typically beginning in infancy. The gene is highly constrained against loss-of-function variants, indicating that such mutations are likely to be pathogenic.

Summary from RefSeq, UniProt
Research Assistant →
0
Active trials
1
Pubs (1 yr)
54
P/LP submissions
0%
P/LP missense
0.31
LOEUF· LoF intol.
Multiple*
Mechanism· predicted
Clinical SummaryCYRIB
Population Constraint (gnomAD)
Highly constrained gene — heterozygous loss-of-function variants are very rare in the population (pLI 0.98). One damaged copy is likely sufficient to cause disease.
📋
ClinVar Variants
54 unique Pathogenic / Likely Pathogenic· 21 VUS of 96 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Dual constrained — LoF & missense intolerant
LoF Constraint
0.31LOEUF
pLI 0.976
Z-score 3.76
OE 0.10 (0.040.31)
Highly constrained

Highly LoF-intolerant (top ~10% of genes)

Missense Constraint
3.21Z-score
OE missense 0.30 (0.240.38)
51 obs / 168.2 exp
Constrained

Highly missense-constrained (top ~0.1%)

Observed / Expected Ratios
LoF OE0.10 (0.040.31)
00.351.4
Missense OE0.30 (0.240.38)
00.61.4
Synonymous OE0.73
01.21.6
LoF obs/exp: 2 / 20.3Missense obs/exp: 51 / 168.2Syn Z: 1.60
DN
0.5477th %ile
GOF
0.71top 25%
LOF
0.51top 25%

This gene has evidence for multiple mechanisms of pathogenicity (loss-of-function and gain-of-function). The Badonyi & Marsh model scores gain-of-function highest among its predictions, but genomic evidence (constraint, ClinVar variant spectrum, and literature) most strongly supports loss-of-function (haploinsufficiency). Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

LOFLOEUF 0.31
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. Mechanism ranking also informed by gnomAD constraint, ClinVar, and ClinGen data.

ClinVar Variant Classifications

96 submitted variants in ClinVar

Classification Summary

Pathogenic53
Likely Pathogenic1
VUS21
Likely Benign1
Benign1
53
Pathogenic
1
Likely Pathogenic
21
VUS
1
Likely Benign
1
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
53
0
53
Likely Pathogenic
0
0
1
0
1
VUS
0
12
9
0
21
Likely Benign
0
0
1
0
1
Benign
0
0
1
0
1
Total01265077

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

View in ClinVar →

Protein Context — Lollipop Plot

CYRIB · protein map & ClinVar variants

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

3D Protein StructureAlphaFold

Clinical Trials

Active and recruiting trials from ClinicalTrials.gov

No active trials found for this gene.

Search ClinicalTrials.gov →
Clinical Literature
Open Research Assistant →
Recent Gene-Specific Literature
Gene in title · MEDLINE · newest first
Europe PMC

No open access results found