chr11-47342611-C-T
Variant summary
The NM_000256.3(MYBPC3):c.1591G>A (p.Gly531Arg) variant causes a missense change involving the alteration of a conserved nucleotide. The variant allele was found at a cumulative frequency of 0.0000211 (AC=34) in the gnomAD database across 1,612,338 control chromosomes (no homozygotes observed). The grpmax filtering allele frequency (95% CI) is 0.0000335. In-silico predictor (REVEL) classifies this variant as likely damaging/oncogenic. Splicing prediction tools (SpliceAI) predict no significant impact on normal splicing. The affected nucleotide is highly conserved across species (PhyloP 100-way vertebrate score: 7.50). Variant has been reported in ClinVar as Pathogenic/Likely Pathogenic (★★). ClinVar reports functional evidence for this variant: "SCV000317768: "In a functional study utilizing engineered heart tissue derived from MYBPC3 knockout cardiomyocytes, c.1591G>C p.G531R was unable to completely rescue the hypercontractile phenotype of the knockout tissue" and additional evidence is available in ClinVar. Other variants at the same amino acid position have been reported in ClinVar (not pathogenic): p.G531= (synonymous): Likely_benign (ClinVar VariationId 1603907, 1 star); p.G531= (synonymous): Likely_benign (ClinVar VariationId 164108, 2 stars); p.G531W: Conflicting_classifications_of_pathogenicity (ClinVar VariationId 810736)
Frequency
Consequence
NM_000256.3 missense
Scores
Clinical Significance
Conservation
Publications
- hypertrophic cardiomyopathyInheritance: AD Classification: DEFINITIVE Submitted by: ClinGen
- hypertrophic cardiomyopathy 4Inheritance: AD, AR Classification: DEFINITIVE, STRONG Submitted by: Labcorp Genetics (formerly Invitae), G2P, Ambry Genetics
- left ventricular noncompaction 10Inheritance: AD, AR Classification: DEFINITIVE, MODERATE, LIMITED Submitted by: Ambry Genetics
- familial isolated dilated cardiomyopathyInheritance: AD Classification: SUPPORTIVE Submitted by: Orphanet
- arrhythmogenic right ventricular cardiomyopathyInheritance: AD Classification: LIMITED Submitted by: ClinGen, G2P
- atrial fibrillationInheritance: AD Classification: LIMITED Submitted by: Ambry Genetics
- congenital heart diseaseInheritance: AD Classification: LIMITED Submitted by: ClinGen
- dilated cardiomyopathyInheritance: AD, AR Classification: LIMITED Submitted by: ClinGen
- familial dilated cardiomyopathyInheritance: AD Classification: LIMITED Submitted by: G2P
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Classification according to ACMG Germline Pathogenicity v2019
Our verdict: Pathogenic. The variant received 19 points.
| Apply | Criterion Code & Title / Strength | Rationale / Clinical Context | |
|---|---|---|---|
| PS1Same amino acid change as known pathogenic | Same AA change, ≥2-star ClinVar pathogenic — very strong (PS1); ClinVar contains 1 P/LP entry with the same amino acid change (highest review level: 2 stars). | ||
| PS3Functional studies show damaging effect | Well-established functional study supports damaging effect (PS3); SCV000317768: "In a functional study utilizing engineered heart tissue derived from MYBPC3 knockout cardiomyocytes, c.1591G>C p.G531R was unable to completely rescue the hypercontractile phenotype of the knockout tissue; however, the physiological relevance of this result is unclear (Wijnker PJ et al. J. Mol. Cell. Cardiol. 2016;97:82-92)."; SCV000208035: Published functional studies suggest a damaging effect in mouse engineered heart tissue (PMID: 27108529);; SCV000198900: A functional study in which the c.1591G>C (p.Gly531Arg) variant was transfected into MYBPC3 knockout mouse cardiomyocytes alone and in combination with wild-type MYBPC3 (to represent homozygous and heterozygous disease states) revealed abnormal contractile force in both scenarios compared to wild-type (Wijnker 2016 PMID: 27108529).; SCV004842468: A functional study has shown that a different nucleotide change with the same protein effect (c.1591G>C; p.Gly531Arg) does not fully rescue the hypercontractile phenotype of heart tissue from Mybpc3 knockout mouse (PMID: 27108529).; SCV005045728: A functional study in which the c.1591G>C (p.Gly531Arg) variant was transfected into MYBPC3 knockout mouse cardiomyocytes alone and in combination with wild-type MYBPC3 (to represent homozygous and heterozygous disease states) revealed abnormal contractile force in both scenarios compared to wild-type (PMID: 27108529).; SCV001351745: A functional study has shown that a different nucleotide change with the same protein effect (c.1591G>C; p.Gly531Arg; ClinVar variation ID: 164109) was unable to rescue the hypercontractile phenotype of heart tissue from Mybpc3 knockout mouse (PMID: 27108529).; SCV004014718: Functional studies demonstrated that the c.1591G>A (p.Gly531Arg) variant was unable to restore maximal force to the wild-type level when it was co-expressed with the wild-type protein in engineered heart tissue from MYBPC3 knock-out mice. PMID:27108529; SCV005400439: "This variant has moderate functional evidence supporting abnormal protein function. Mutant constructs (c.1591G>C; p.(Gly531Arg)) transfected into knockout engineered heart cells mice tissues and expressed either as heterozygous or homozygous demonstrated abnormal force and contraction velocity compared to WT (PMID: 27108529)." | ||
| PM2Absent/extremely low in population databases | Rare in gnomAD for AD/XL gene (popmax AF below threshold) — PM2 Supporting; GnomAD popmax AF = 0.0000335 — borderline rare for AD+AR gene (base 0.0001, raised to 0.000144 by highest known P/LP ClinVar AF 0.000144) — PM2 supporting. | ||
| PP3Computational evidence supports damaging effect | Germline meta computational scorer (REVEL/MetaRNN/BayesDel) predicts damaging effect — moderate evidence (PP3); Splicing verdict: not pathogenic.; Germline computational verdict: pathogenic (Moderate). | ||
| PP5Reputable source reports pathogenic | ClinVar 2-star pathogenic — strong (PP5); ClinVar submissions overwhelmingly pathogenic (≥10 total, ≥80% P/LP, <10% B/LB) — strong (PP5, count-based); ClinVar germline classification: Pathogenic/Likely Pathogenic, 2 star(s). ClinVar submissions strongly and reliably favor pathogenicity (23/23 total P/LP). |
Variant Effect in Transcripts
Automated classification analysis was done for transcript: NM_000256.3. You can select a different transcript below to see updated classification assignments.
RefSeq Transcripts
| Sel. | Gene / Transcript | Tags | HGVSc / HGVSp | Effect | Exon rank | Protein / UniProt |
|---|---|---|---|---|---|---|
MYBPC3 | MANE Select | c.1591G>A p.Gly531Arg | missense | Exon 17 of 35 | Prot: NP_000247.2 |
Ensembl Transcripts
| Sel. | Gene / Transcript | Tags | HGVSc / HGVSp | Effect | Exon rank | Protein / UniProt |
|---|---|---|---|---|---|---|
MYBPC3 | TSL:5MANE Select | c.1591G>A p.Gly531Arg | missense | Exon 17 of 35 | Prot: ENSP00000442795.1 UniProt: | |
MYBPC3 | TSL:5 | c.1591G>A p.Gly531Arg | missense | Exon 16 of 34 | Prot: ENSP00000382193.2 UniProt: | |
MYBPC3 | TSL:5 | n.1591G>A | non_coding_transcript_exon | Exon 17 of 27 | Prot: ENSP00000444259.1 UniProt: |
Frequencies
Allele frequencies (AF), counts (AC/AN), homozygotes and coverage
| Source / population | AF | AC | Hom | AN | Coverage |
|---|---|---|---|---|---|
Global population databases 6 sources | |||||
GnomAD3 genomes | AF: 0.0000263 | AC:4 | Hom:0 | AN:152208 | Cov:33 |
GnomAD2 exomes | AF: 0.0000324 | AC:8 | AN:247086 | ||
GnomAD4 exome | AF: 0.0000205 | AC:30 | Hom:0 | AN:1460130 | Cov:31 |
GnomAD4 genome | AF: 0.0000263 | AC:4 | Hom:0 | AN:152208 | Cov:33 |
TOPMed (Bravo) | AF: 0.0000416 | ||||
ALFA (dbGaP/dbSNP Allele Frequency Aggregator) | AF: 0.0000442 | AC:4 | Hom:0 | AN:90460 | |
Local & regional cohorts 1 source | |||||
ChinaMAP Phase 1 | AF: 0.0000492 | ||||
Case/control cohorts
| Cohort | Cases | Controls | ||||
|---|---|---|---|---|---|---|
| AF | AC | AN | AF | AC | AN | |
Epi25 | 0.0000715 | 3 | 41950 | 0.0000449 | 3 | 66812 |
SCHEMA | 0.0000581 | 6 | 103206 | 0.0000272 | 5 | 183972 |
ClinVar
Computational Scores
| Algorithm | Calibrated pred. | Score | Prediction |
|---|---|---|---|
AlphaGenome AVI | Pathogenic | 23 | |
AlphaMissense | Benign | 0.24 | |
BayesDel_addAF | Pathogenic | 0.31 | D |
BayesDel_noAF | Pathogenic | 0.38 | |
CADD | Uncertain | 24 | |
CardioboostCm | Uncertain | 0.38 | |
DANN | Pathogenic | 1.0 | |
DEOGEN2 | Uncertain | 0.78 | D |
Eigen | Pathogenic | 0.71 | |
Eigen_PC | Uncertain | 0.60 | |
FATHMM_MKL | Pathogenic | 0.97 | D |
GPN-Star LLR | N/A | -5.0 | |
GPN-Star score | N/A | 5.0 | |
LIST_S2 | Uncertain | 0.90 | D |
M_CAP | Pathogenic | 0.67 | D |
MetaRNN | Pathogenic | 0.96 | D |
MetaSVM | Uncertain | 0.53 | D |
Mutation Taster | N/A | 0/100 | disease causing (ClinVar) |
MutationAssessor | Uncertain | 2.5 | M |
PhyloP100 | Uncertain | 7.5 | |
popEVE | Benign | -3.4 | |
PrimateAI | Uncertain | 0.74 | T |
PROVEAN | Pathogenic | -7.0 | D |
REVEL | Pathogenic | 0.85 | |
Sift | Pathogenic | 0.0 | D |
Sift4G | Pathogenic | 0.0 | D |
Varity_R | N/A | 0.61 | |
VESM-3B | Benign | -11 |
Splicing Scores
| Algorithm | Calibrated pred. | Score | Prediction |
|---|---|---|---|
Pangolin (max) | Benign | 0.010 | |
SpliceAI score (max) | Benign | 0.0 | Details are displayed if max score is > 0.2 |
Find out detailed SpliceAI scores and Pangolin per-transcript scores at
MaxEntScan Visualizer can be used to analyze the impact of this mutation on the neighboring sequence.