NPC2

Chr 14AR

NPC intracellular cholesterol transporter 2

Also known as: EDDM1, HE1

The protein functions as an intracellular cholesterol transporter that works with NPC1 to facilitate cholesterol egress from the lysosomal compartment by transferring unesterified cholesterol from late endosomes/lysosomes to the cholesterol-binding domain of NPC1. Mutations cause Niemann-Pick disease type C2 through an autosomal recessive inheritance pattern, with disease resulting from loss of cholesterol transport function leading to lysosomal cholesterol accumulation.

GeneReviewsOMIMResearchSummary from RefSeq, OMIM, UniProt, Mechanism
LOFmechanismARLOEUF 1.392 OMIM phenotypes
Clinical SummaryNPC2
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Gene-Disease Validity (ClinGen)
Niemann-Pick disease, type C2 · ARDefinitive

Definitive — sufficient evidence for diagnostic panels

Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
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ClinVar Variants
38 unique Pathogenic / Likely Pathogenic· 40 VUS of 200 total submissions
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GeneReview available — NPC2
Authoritative clinical overview · Recommended first read
Open GeneReview ↗

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.39LOEUF
pLI 0.002
Z-score 0.85
OE 0.67 (0.351.39)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
1.30Z-score
OE missense 0.59 (0.470.75)
47 obs / 79.7 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.67 (0.351.39)
00.351.4
Missense OE0.59 (0.470.75)
00.61.4
Synonymous OE1.23
01.21.6
LoF obs/exp: 5 / 7.5Missense obs/exp: 47 / 79.7Syn Z: -1.00
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
definitiveNPC2-related Niemann-Pick diseaseLOFAR
Mechanism Note (expert annotation)
LOF

Cholesterol-binding protein in late endosomes/lysosomes. Biallelic LOF causes Niemann-Pick disease type C2. This is a classic autosomal recessive LOF gene; the DN prediction is incorrect.

References:PMID:10617473

Predictions shown for reference only — model trained on dominant genes, not applicable to AR conditions.

DN
0.6649th %ile
GOF
0.4677th %ile
LOF
0.3162th %ile

The Badonyi & Marsh prediction model was trained exclusively on dominant disease genes. Predictions are not reliable for genes with autosomal recessive inheritance and are shown at reduced opacity for reference only.

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

ClinVar Variant Classifications

200 submitted variants in ClinVar

Classification Summary

Pathogenic16
Likely Pathogenic22
VUS40
Likely Benign98
Benign6
Conflicting9
16
Pathogenic
22
Likely Pathogenic
40
VUS
98
Likely Benign
6
Benign
9
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
9
2
5
0
16
Likely Pathogenic
17
3
2
0
22
VUS
2
28
10
0
40
Likely Benign
0
7
45
46
98
Benign
0
0
6
0
6
Conflicting
9
Total28406846191

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

View in ClinVar →

Protein Context — Lollipop Plot

NPC2 · 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.

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Clinical Literature
Open Research Assistant →