MME

Chr 3ADAR

membrane metalloendopeptidase

Also known as: CALLA, CD10, CMT2T, NEP, SCA43, SFE

The encoded neutral endopeptidase cleaves and inactivates multiple neuropeptides including enkephalins, substance P, bradykinin, and natriuretic peptides. Mutations cause spinocerebellar ataxia 43 and Charcot-Marie-Tooth disease type 2T, affecting both central and peripheral nervous systems with both autosomal dominant and recessive inheritance patterns reported. The gene shows tolerance to loss-of-function variants (LOEUF 0.923), suggesting different pathogenic mechanisms may underlie the distinct neurological phenotypes.

GeneReviewsOMIMResearchSummary from RefSeq, OMIM, UniProt
MultiplemechanismAD/ARLOEUF 0.922 OMIM phenotypes
Clinical SummaryMME
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Gene-Disease Validity (ClinGen)
Charcot-Marie-Tooth disease axonal type 2T · 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
22 unique Pathogenic / Likely Pathogenic· 31 VUS of 100 total submissions
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Clinical Trials
4 active or recruiting trials — potential therapeutic options may be available
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GeneReview available — MME
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
0.92LOEUF
pLI 0.000
Z-score 2.00
OE 0.70 (0.540.92)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
0.36Z-score
OE missense 0.95 (0.871.03)
374 obs / 394.0 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.70 (0.540.92)
00.351.4
Missense OE0.95 (0.871.03)
00.61.4
Synonymous OE0.93
01.21.6
LoF obs/exp: 36 / 51.5Missense obs/exp: 374 / 394.0Syn Z: 0.67
DN
0.5772th %ile
GOF
0.6735th %ile
LOF
0.2582th %ile

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

GOFprediction above median
LOF1 literature citation · 91% of P/LP variants are LoF

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.

Literature Evidence

LOFTransfection of the mutation into HEK293 cells showed that the mutant protein had significantly decreased neprilysin activity, consistent with a loss of function and haploinsufficiency.PMID:27588448

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

100 submitted variants in ClinVar

Classification Summary

Pathogenic11
Likely Pathogenic11
VUS31
Likely Benign45
Benign2
11
Pathogenic
11
Likely Pathogenic
31
VUS
45
Likely Benign
2
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
9
0
2
0
11
Likely Pathogenic
11
0
0
0
11
VUS
0
27
4
0
31
Likely Benign
0
1
21
23
45
Benign
0
0
2
0
2
Total20282923100

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

View in ClinVar →

Protein Context — Lollipop Plot

MME · protein map & ClinVar variants

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

3D Protein StructureAlphaFold
Clinical Literature
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