NECAB1

Chr 8

N-terminal EF-hand calcium binding protein 1

Also known as: EFCAB1, EFCBP1, STIP-1

The NECAB1 protein enables identical protein binding and is predicted to regulate amyloid precursor protein biosynthetic processes. Mutations cause autosomal recessive developmental and epileptic encephalopathy with onset in infancy, characterized by severe intellectual disability, refractory seizures, and progressive microcephaly. The gene shows moderate constraint against loss-of-function variants, consistent with recessive inheritance where both copies must be disrupted to cause disease.

Summary from RefSeq
Research Assistant →
0
Active trials
4
Pubs (1 yr)
34
P/LP submissions
0%
P/LP missense
0.58
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryNECAB1
Population Constraint (gnomAD)
Constrained for loss-of-function variants (OE-LoF 0.31) despite low pLI — interpret in context.
📋
ClinVar Variants
34 unique Pathogenic / Likely Pathogenic· 43 VUS of 88 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Moderate LoF intolerance
LoF Constraint
0.58LOEUF
pLI 0.025
Z-score 3.04
OE 0.31 (0.170.58)
Moderately constrained

More LoF-intolerant than ~75% of genes

Missense Constraint
1.14Z-score
OE missense 0.75 (0.650.87)
128 obs / 169.9 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.31 (0.170.58)
00.351.4
Missense OE0.75 (0.650.87)
00.61.4
Synonymous OE0.82
01.21.6
LoF obs/exp: 7 / 22.6Missense obs/exp: 128 / 169.9Syn Z: 1.11
DN
0.6939th %ile
GOF
0.6541th %ile
LOF
0.3260th %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

88 submitted variants in ClinVar

Classification Summary

Pathogenic34
VUS43
Likely Benign4
34
Pathogenic
43
VUS
4
Likely Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
34
0
34
Likely Pathogenic
0
0
0
0
0
VUS
0
39
4
0
43
Likely Benign
0
2
1
1
4
Benign
0
0
0
0
0
Total04139181

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

View in ClinVar →

Protein Context — Lollipop Plot

NECAB1 · 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.

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Clinical Literature
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