FRMD4B

Chr 3

FERM domain containing 4B

Also known as: 6030440G05Rik, GRSP1

The protein functions as a scaffolding protein in epithelial cell polarity regulation, connecting ARF6 activation with the PAR3 complex and participating in GRP1 signaling complexes recruited to plasma membrane ruffles during insulin receptor signaling. Mutations cause neurodevelopmental disorders with intellectual disability and developmental delay, inherited in an autosomal recessive pattern. The gene shows significant constraint against loss-of-function variants, suggesting intolerance to complete protein loss.

Summary from RefSeq, UniProt
Research Assistant →
0
Active trials
3
Pubs (1 yr)
0
P/LP submissions
P/LP missense
0.35
LOEUF· LoF intol.
Multiple*
Mechanism· predicted
Clinical SummaryFRMD4B
Population Constraint (gnomAD)
Constrained for loss-of-function variants (OE-LoF 0.22) despite low pLI — interpret in context.

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

LoF intolerant — likely haploinsufficient
LoF Constraint
0.35LOEUF
pLI 0.454
Z-score 5.71
OE 0.22 (0.150.35)
Highly constrained

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

Missense Constraint
-0.04Z-score
OE missense 1.00 (0.941.08)
547 obs / 544.3 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE0.22 (0.150.35)
00.351.4
Missense OE1.00 (0.941.08)
00.61.4
Synonymous OE1.04
01.21.6
LoF obs/exp: 14 / 62.8Missense obs/exp: 547 / 544.3Syn Z: -0.40
DN
0.6162th %ile
GOF
0.5856th %ile
LOF
0.53top 25%

This gene has evidence for multiple mechanisms of pathogenicity (loss-of-function and dominant-negative). The Badonyi & Marsh model scores dominant-negative 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 0.35
DNprediction 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

0 submitted variants in ClinVar

Protein Context — Lollipop Plot

FRMD4B · 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 →
Key Publications
Landmark & review papers · by relevance
PubMed
Top 1 results · since 2015Search PubMed ↗
Recent Gene-Specific Literature
Gene in title · MEDLINE · newest first
Europe PMC