NM_000257.4:c.1491G>T

Variant names:

Variant summary

Our verdict is Pathogenic. The variant received 15 ACMG points: 15P and 0B. PM1PP2PP3_StrongPP5_Very_Strong

The NM_000257.4(MYH7):c.1491G>T(p.Glu497Asp) variant causes a missense change involving the alteration of a non-conserved nucleotide. The variant allele was found at a frequency of 0.00000496 in 1,614,094 control chromosomes in the GnomAD database, with no homozygous occurrence. In-silico tool predicts a pathogenic outcome for this variant. Variant has been reported in ClinVar as Likely pathogenic (★★). Another variant affecting the same amino acid position, but resulting in a different missense (i.e. E497G) has been classified as Uncertain significance.

Frequency

Genomes: 𝑓 0.0000066 ( 0 hom., cov: 32)

Exomes 𝑓: 0.0000048 ( 0 hom. )

Consequence

MYH7
NM_000257.4 missense

Scores

Clinical Significance

Pathogenic/Likely pathogenic criteria provided, multiple submitters, no conflicts P:13

Conservation

PhyloP100: 2.72

Publications

13 publications found

Variant links:

Genes affected

MYH7 (HGNC:7577): (myosin heavy chain 7) Muscle myosin is a hexameric protein containing 2 heavy chain subunits, 2 alkali light chain subunits, and 2 regulatory light chain subunits. This gene encodes the beta (or slow) heavy chain subunit of cardiac myosin. It is expressed predominantly in normal human ventricle. It is also expressed in skeletal muscle tissues rich in slow-twitch type I muscle fibers. Changes in the relative abundance of this protein and the alpha (or fast) heavy subunit of cardiac myosin correlate with the contractile velocity of cardiac muscle. Its expression is also altered during thyroid hormone depletion and hemodynamic overloading. Mutations in this gene are associated with familial hypertrophic cardiomyopathy, myosin storage myopathy, dilated cardiomyopathy, and Laing distal myopathy. [provided by RefSeq, May 2022]

MYH7 Gene-Disease associations (from GenCC):

dilated cardiomyopathy
Inheritance: AD Classification: DEFINITIVE Submitted by: ClinGen
dilated cardiomyopathy 1S
Inheritance: AD Classification: DEFINITIVE, STRONG Submitted by: Labcorp Genetics (formerly Invitae), G2P, Ambry Genetics
hypertrophic cardiomyopathy
Inheritance: AD Classification: DEFINITIVE Submitted by: ClinGen
hypertrophic cardiomyopathy 1
Inheritance: AD Classification: DEFINITIVE, STRONG Submitted by: PanelApp Australia, Labcorp Genetics (formerly Invitae), G2P, Ambry Genetics
MYH7-related skeletal myopathy
Inheritance: AD Classification: DEFINITIVE, STRONG, SUPPORTIVE Submitted by: Orphanet, Labcorp Genetics (formerly Invitae), ClinGen, Ambry Genetics
myopathy, myosin storage, autosomal recessive
Inheritance: AR Classification: STRONG, MODERATE Submitted by: Ambry Genetics, Labcorp Genetics (formerly Invitae)
myopathy, myosin storage, autosomal dominant
Inheritance: AD Classification: MODERATE Submitted by: Ambry Genetics
congenital myopathy 7A, myosin storage, autosomal dominant
Inheritance: AD Classification: SUPPORTIVE Submitted by: Orphanet
Ebstein anomaly
Inheritance: AD Classification: SUPPORTIVE Submitted by: Orphanet
familial isolated dilated cardiomyopathy
Inheritance: AD Classification: SUPPORTIVE Submitted by: Orphanet
hyaline body myopathy
Inheritance: AD Classification: SUPPORTIVE Submitted by: Orphanet
left ventricular noncompaction
Inheritance: AD Classification: SUPPORTIVE Submitted by: Orphanet
arrhythmogenic right ventricular cardiomyopathy
Inheritance: AD Classification: LIMITED Submitted by: ClinGen
congenital heart disease
Inheritance: AD Classification: LIMITED Submitted by: ClinGen

MYH7 links:

Genome browser will be placed here

ACMG classification

Classification was made for transcript

Our verdict: Pathogenic. The variant received 15 ACMG points.

PM1

In a hotspot region, there are 7 aminoacids with missense pathogenic changes in the window of +-8 aminoacids around while only 0 benign, 19 uncertain in NM_000257.4

PP2

Missense variant in the MYH7 gene, where missense mutations are typically associated with disease (based on misZ statistic). The gene has 341 curated pathogenic missense variants (we use a threshold of 10). The gene has 16 curated benign missense variants. Gene score misZ: 3.9329 (above the threshold of 3.09). Trascript score misZ: 6.7889 (above the threshold of 3.09). GenCC associations: The gene is linked to myopathy, myosin storage, autosomal recessive, MYH7-related skeletal myopathy, congenital myopathy 7A, myosin storage, autosomal dominant, Ebstein anomaly, hyaline body myopathy, left ventricular noncompaction, hypertrophic cardiomyopathy 1, dilated cardiomyopathy 1S, dilated cardiomyopathy, congenital heart disease, familial isolated dilated cardiomyopathy, myopathy, myosin storage, autosomal dominant, arrhythmogenic right ventricular cardiomyopathy, hypertrophic cardiomyopathy.

PP3

MetaRNN computational evidence supports a deleterious effect, 0.976

PP5

Variant 14-23428587-C-A is Pathogenic according to our data. Variant chr14-23428587-C-A is described in ClinVar as Pathogenic/Likely_pathogenic. ClinVar VariationId is 14124.Status of the report is criteria_provided_multiple_submitters_no_conflicts, 2 stars.

Transcripts

RefSeq

Gene	Transcript	HGVSc	HGVSp	Effect	Exon rank	MANE	Protein	UniProt
MYH7	NM_000257.4 link	c.1491G>T	p.Glu497Asp	missense_variant	Exon 15 of 40	ENST00000355349.4	NP_000248.2
MYH7	NM_001407004.1 link	c.1491G>T	p.Glu497Asp	missense_variant	Exon 14 of 39		NP_001393933.1

Ensembl

Gene	Transcript	HGVSc	HGVSp	Effect	Exon rank	TSL	MANE	Protein
MYH7	ENST00000355349.4 link	c.1491G>T	p.Glu497Asp	missense_variant	Exon 15 of 40	1	NM_000257.4	ENSP00000347507.3
MYH7	ENST00000713768.1 link	c.1491G>T	p.Glu497Asp	missense_variant	Exon 15 of 41			ENSP00000519070.1
MYH7	ENST00000713769.1 link	c.1491G>T	p.Glu497Asp	missense_variant	Exon 14 of 39			ENSP00000519071.1

Frequencies

GnomAD3 genomes

AF:

0.00000657

AC:

AN:

152206

Hom.:

Cov.:

show subpopulations

Gnomad AFR

AF:

0.00

Gnomad AMI

AF:

0.00

Gnomad AMR

AF:

0.00

Gnomad ASJ

AF:

0.000288

Gnomad EAS

AF:

0.00

Gnomad SAS

AF:

0.00

Gnomad FIN

AF:

0.00

Gnomad MID

AF:

0.00

Gnomad NFE

AF:

0.00

Gnomad OTH

AF:

0.00

GnomAD2 exomes

AF:

0.00000795

AC:

AN:

251488

AF XY:

0.00

show subpopulations

Gnomad AFR exome

AF:

0.00

Gnomad AMR exome

AF:

0.00

Gnomad ASJ exome

AF:

0.000198

Gnomad EAS exome

AF:

0.00

Gnomad FIN exome

AF:

0.00

Gnomad NFE exome

AF:

0.00

Gnomad OTH exome

AF:

0.00

GnomAD4 exome

AF:

0.00000479

AC:

AN:

1461888

Hom.:

Cov.:

AF XY:

0.00000550

AC XY:

AN XY:

727244

show subpopulations

African (AFR)

AF:

0.00

AC:

AN:

33480

American (AMR)

AF:

0.00

AC:

AN:

44724

Ashkenazi Jewish (ASJ)

AF:

0.000230

AC:

AN:

26136

East Asian (EAS)

AF:

0.00

AC:

AN:

39700

South Asian (SAS)

AF:

0.00

AC:

AN:

86258

European-Finnish (FIN)

AF:

0.00

AC:

AN:

53420

Middle Eastern (MID)

AF:

0.00

AC:

AN:

5766

European-Non Finnish (NFE)

AF:

0.00

AC:

AN:

1112010

Other (OTH)

AF:

0.0000166

AC:

AN:

60394

Allele Balance Distribution

Red line indicates average allele balance

Average allele balance: 0.439

Heterozygous variant carriers

0.00

0.20

0.40

0.60

0.80

0.95

Allele balance

Age Distribution

Exome Het

Variant carriers

<30

30-35

35-40

40-45

45-50

50-55

55-60

60-65

65-70

70-75

75-80

>80

Age

GnomAD4 genome

AF:

0.00000657

AC:

AN:

152206

Hom.:

Cov.:

AF XY:

0.00

AC XY:

AN XY:

74364

show subpopulations

⚠️ The allele balance in gnomAD version 4 Genomes is significantly skewed from the expected value of 0.5.

African (AFR)

AF:

0.00

AC:

AN:

41450

American (AMR)

AF:

0.00

AC:

AN:

15284

Ashkenazi Jewish (ASJ)

AF:

0.000288

AC:

AN:

3472

East Asian (EAS)

AF:

0.00

AC:

AN:

5192

South Asian (SAS)

AF:

0.00

AC:

AN:

4826

European-Finnish (FIN)

AF:

0.00

AC:

AN:

10622

Middle Eastern (MID)

AF:

0.00

AC:

AN:

316

European-Non Finnish (NFE)

AF:

0.00

AC:

AN:

68040

Other (OTH)

AF:

0.00

AC:

AN:

2092

⚠️ The allele balance in gnomAD version 4 Genomes is significantly skewed from the expected value of 0.5. (p-value = 0), which strongly suggests a high chance of mosaicism in these individuals.

Allele Balance Distribution

Red line indicates average allele balance

Average allele balance: 0.275

Heterozygous variant carriers

0.00

0.20

0.40

0.60

0.80

0.95

Allele balance

Alfa

AF:

0.00

Hom.:

Bravo

AF:

0.0000151

ClinVar

Significance: Pathogenic/Likely pathogenic

Submissions summary: Pathogenic:13

Revision: criteria provided, multiple submitters, no conflicts

LINK: link

Submissions by phenotype

not provided

Pathogenic:4

Jun 10, 2025

GeneDx

Significance:Likely pathogenic

Review Status:criteria provided, single submitter

Collection Method:clinical testing

Reported in individuals with sub-clinical cardiomyopathy (PMID: 25228707, 25543971); Not observed at significant frequency in large population cohorts (gnomAD); Functional analysis of the Drosophila myosin heavy chain ortholog and molecular modeling of human beta-cardiac myosin suggest that charge reversal of E497 disrupts a salt bridge with R712, which may decrease ATPase activity and actin sliding velocity (PMID: 26446785); In silico analysis supports that this missense variant has a deleterious effect on protein structure/function; This variant is associated with the following publications: (PMID: 18555187, 21958740, 24510615, 25543971, 25351510, 27247418, 27532257, 23549607, 26246073, 24793961, 16267253, 25558701, 28193612, 32894683, 33605878, 34542152, 29121657, 31447099, 25228707, 37652022, 29300372, 26446785, 34556856, 21310275, 33764162, 35470680, 25611685, 33495597, 38186735, 38757491) -

Oct 08, 2014

Stanford Center for Inherited Cardiovascular Disease, Stanford University

Significance:Likely pathogenic

Review Status:no assertion criteria provided

Collection Method:clinical testing

Note this variant was found in clinical genetic testing performed by one or more labs who may also submit to ClinVar. Thus any internal case data may overlap with the internal case data of other labs. The interpretation reviewed below is that of the Stanford Center for Inherited Cardiovascular Disease. p.Glu497Asp (c.1419G>T) in MYH7. The results have been re-reviewed multiple times, most recently on August 27th, 2014. Additional data further supporting pathogenicity was available. Given the strong case data, the segregation data, and the absence in the general population we consider this variant likely disease causing. To the best of our knowledge this variant has been seen in at least 9, but possibly 14 unrelated families with HCM (not including this patient's family). There may be overlap between some of the published cases and cases in our center and in the genetic testing labs databases. We have seen this variant in three families with HCM in our center. The variant was reported in two members of one family with HCM studied by the Seidman group (Arad et al 2005).The proband in this family had apical hypertrophy while the other family member with this variant had massive concentric hypertrophy, syncope, and an ICD, along with comorbid coronary artery disease. For one of the family’s in our center, there is moderate co-segregation data to support the pathogenicity of this variant in that four individuals with HCM either tested positive for this variant or can be inferred to carry it based on pedigree analysis. However, we do not have confirmation of either phenotype or genotype on anyone in this family. The testing was reportedly done as part of a research endeavor. Of note, this case may overlap with the one reported by the Seidman group (Arad et al 2005). We also have segregation data in another family with both the proband and his affected mother having the variant. Per their ClinVar submission(SCV000059378), LMM has seen this variant in 5 probands with HCM. In one of those families another affected individual also had the variant. They classify this as likely pathogenic. Ackerman's group observed the variant in two unrelated patients with HCM in their Mayo cohort who underwent analysis in their local lab (Bos et al 2014). A polar, neutral Glutamate is substituted with a polar, neutral Asparagine therefore this variant change does not affect the net charge. The Glutamate at codon 497 is completely conserved across species as are the neighboring amino acids. In silico analysis with Polyphen-2 predicts this variant to be probably damaging. Per the LMM ClinVar submission, the variant was predicted to be pathogenic using a computational tool, which was validated by our laboratory using a set of cardiomyopathy variants with well-established clinical significance. This tool's pathogenic prediction is estimated to be correct 94% of the time (Jordan 2011). Mutation Taster predicts this variant to be disease-causing. Other variants in nearby codons have been reported in association with cardiomyopathy including p.Met493Leu, p.Met493Lys, p.Glu299Lys, p.Glu500Ala, p.Tyr501His, and p.Tyr501Cys. In total the variant has not been seen in ~6,800 published controls and individuals from publicly available population datasets. There is no variation at codon 497 listed in the NHLBI Exome Sequencing Project dataset, which currently includes variant calls on ~6,500 Caucasian and African American individuals (as of 10/8/13). There is also no variation at this codon listed in dbSNP or 1000 genomes (as of 10/8/13). The variant was not observed in the following published control samples: Arad et al. did not find this variant in 100 presumed normal control individuals. Unfortunately we don’t have control data from any of the testing laboratories. Bos et al did not observe the variant in 200 ostensibly healthy controls." -

Mar 24, 2021

Mayo Clinic Laboratories, Mayo Clinic

Significance:Likely pathogenic

Review Status:criteria provided, single submitter

Collection Method:clinical testing

PS4, PM2_supporting, PM1, PP3 -

Feb 10, 2021

Revvity Omics, Revvity

Significance:Likely pathogenic

Review Status:criteria provided, single submitter

Collection Method:clinical testing

- -

Hypertrophic cardiomyopathy

Pathogenic:3

Jul 29, 2024

All of Us Research Program, National Institutes of Health

Significance:Likely pathogenic

Review Status:criteria provided, single submitter

Collection Method:clinical testing

This missense variant replaces glutamic acid with aspartic acid at codon 497 in the myosin head/motor domain of the MYH7 protein. Computational prediction suggests that this variant may have a deleterious impact on protein structure and function (internally defined REVEL score threshold >= 0.7, PMID: 27666373). This variant is found within a highly conserved region of the myosin head domain. Missense variants in this region have been shown to be significantly overrepresented in individuals with hypertrophic cardiomyopathy (PMID: 27532257). To our knowledge, functional studies have not been reported for this variant. This variant has been reported in over ten individuals affected with hypertrophic cardiomyopathy (PMID: 16267253, 21958740, 23549607, 24793961, 25351510, 25558701, 25611685, 27247418, 27532257, 29121657, 32894683, 33495597, 33764162, 34556856, 35470680). It has been shown that this variant segregates with disease in two affected individuals in one family (PMID: 16267253). This variant has been identified in 2/251488 chromosomes in the general population by the Genome Aggregation Database (gnomAD). Based on the available evidence, this variant is classified as Likely Pathogenic. -

Apr 05, 2019

Laboratory for Molecular Medicine, Mass General Brigham Personalized Medicine

Significance:Likely pathogenic

Review Status:criteria provided, single submitter

Collection Method:clinical testing

The p.Glu497Asp variant in MYH7 has been reported in >=6 individuals with HCM and segregated with disease in 3 affected relatives from 2 families (Arad 2005, Ho 2013, Kapplinger 2014, Homburger 2016, LMM data). This variant has also been reported by other clinical laboratories in in ClinVar (Variation ID 14124) and has been identified in 2/9850 Ashkenazi Jewish chromosomes by the Genome Aggregation Database (gnomAD, http://gnomad.broadinstitute.org/; dbSNP rs267606911). Please note that for diseases with clinical variability or reduced penetrance, pathogenic variants may be present at a low frequency in the general population. Glutamic acid (Glu) at position 497 is highly conserved in mammals and across evolutionarily distant species and the change to aspartic acid (Asp) was predicted to be pathogenic using a computational tool clinically validated by our laboratory. This tool's pathogenic prediction is estimated to be correct 94% of the time (Jordan 2011). Of note, the p.Glu497Asp variant lies in the head region of the protein. Missense variants in this region have been reported and statistically indicated to be more likely to cause disease (Walsh 2016). In summary, although additional studies are required to fully establish its clinical significance, the p.Glu497Asp variant is likely pathogenic. The ACMG/AMP Criteria applied (Richards 2015): PS4_Moderate, PP1_Supporting, PP3, PM1. -

Jan 19, 2025

Labcorp Genetics (formerly Invitae), Labcorp

Significance:Pathogenic

Review Status:criteria provided, single submitter

Collection Method:clinical testing

This sequence change replaces glutamic acid, which is acidic and polar, with aspartic acid, which is acidic and polar, at codon 497 of the MYH7 protein (p.Glu497Asp). This variant is present in population databases (rs267606911, gnomAD 0.02%). This missense change has been observed in individuals with hypertrophic cardiomyopathy (PMID: 16267253, 23549607, 24510615). ClinVar contains an entry for this variant (Variation ID: 14124). Invitae Evidence Modeling of protein sequence and biophysical properties (such as structural, functional, and spatial information, amino acid conservation, physicochemical variation, residue mobility, and thermodynamic stability) indicates that this missense variant is expected to disrupt MYH7 protein function with a positive predictive value of 95%. Experimental studies have shown that this missense change affects MYH7 function (PMID: 21310275, 26446785). For these reasons, this variant has been classified as Pathogenic. -

Cardiomyopathy

Pathogenic:2

Feb 18, 2025

Color Diagnostics, LLC DBA Color Health

Significance:Likely pathogenic

Review Status:criteria provided, single submitter

Collection Method:clinical testing

This missense variant replaces glutamic acid with aspartic acid at codon 497 of the MYH7 protein. Computational prediction suggests that this variant may have a deleterious impact on protein structure and function. This variant is found within a highly conserved region of the myosin head domain. Missense variants in this region have been shown to be significantly overrepresented in individuals with affected with hypertrophic cardiomyopathy (PMID: 27532257). To our knowledge, functional studies have not been reported for this variant. This variant has been reported in more than ten individuals affected with hypertrophic cardiomyopathy (PMID: 16267253, 21958740, 23549607, 24793961, 25351510, 25558701, 25611685, 27247418, 27532257, 29121657, 32894683, 33495597, 33764162, 34542152, 34556856, 35470680, 38186735, 38757491). It has been shown that this variant segregates with disease in two affected individuals in one family (PMID: 16267253). This variant has been identified in 2/251488 chromosomes in the general population by the Genome Aggregation Database (gnomAD). Based on the available evidence, this variant is classified as Likely Pathogenic. -

Feb 01, 2023

CHEO Genetics Diagnostic Laboratory, Children's Hospital of Eastern Ontario

Significance:Likely pathogenic

Review Status:criteria provided, single submitter

Collection Method:clinical testing

- -

Dilated cardiomyopathy 1S;C1842160:Myosin storage myopathy;C1850709:Myopathy, myosin storage, autosomal recessive;C3495498:Hypertrophic cardiomyopathy 1;C4552004:MYH7-related skeletal myopathy

Pathogenic:1

Feb 21, 2024

Fulgent Genetics, Fulgent Genetics

Significance:Likely pathogenic

Review Status:criteria provided, single submitter

Collection Method:clinical testing

- -

Dilated cardiomyopathy 1S

Pathogenic:1

Jan 01, 2022

Provincial Medical Genetics Program of British Columbia, University of British Columbia

Significance:Likely pathogenic

Review Status:criteria provided, single submitter

Collection Method:clinical testing

- -

Cardiovascular phenotype

Pathogenic:1

May 03, 2022

Ambry Genetics

Significance:Pathogenic

Review Status:criteria provided, single submitter

Collection Method:clinical testing

The p.E497D pathogenic mutation (also known as c.1491G>T), located in coding exon 13 of the MYH7 gene, results from a G to T substitution at nucleotide position 1491. The glutamic acid at codon 497 is replaced by aspartic acid, an amino acid with highly similar properties. This alteration is located in the myosin head domain, which contains a statistically significant clustering of pathogenic missense variants (Homburger JR et al. Proc Natl Acad Sci U S A, 2016 06;113:6701-6; Walsh R et al. Genet Med, 2017 02;19:192-203; Ambry internal data). This alteration has been identified in numerous unrelated patients with hypertrophic cardiomyopathy and has been reported to co-segregate with disease in one small family (Arad M et al. Circulation. 2005;112(18):2805-11; Maron BJ et al. Am J Cardiol. 2011;108(12):1783-7; Arad M et al. Isr Med Assoc J. 2014;16(11):707-13; Kapplinger JD et al. J Cardiovasc Transl Res. 2014;7:347-61; Walsh R et al. Genet. Med. 2017;19:192-203; Mattivi CL et al. Circ Genom Precis Med. 2020 10;13(5):453-459; Puckelwartz MJ et a. J Am Heart Assoc. 2021 04;10(7):e019944; Ambry internal data). Functional studies of the orthologous residue in a transgenic Drosophila model, coupled with molecular modeling of human beta-cardiac myosin, demonstrated that E497 is involved in charge-dependent interactions between the relay helix and the converter domain. Disruption of this interaction by either charge reversal or introduction of a sterically smaller amino acid obviate this interaction, resulting in reduced ATPase activity and actin sliding velocity (Kronert WA et al. J. Biol. Chem., 2015 Dec;290:29270-80). In addition, this alteration is predicted to be deleterious by in silico analysis. Based on the supporting evidence, this alteration is interpreted as a disease-causing mutation. -

Hypertrophic cardiomyopathy 1

Pathogenic:1

Nov 01, 2005

OMIM

Significance:Pathogenic

Review Status:no assertion criteria provided

Collection Method:literature only

- -

Computational scores

Source: dbNSFP v4.3

Name

Calibrated prediction

Score

Prediction

AlphaMissense

Pathogenic

1.0

CardioboostCm

Pathogenic

1.0

BayesDel_addAF

Pathogenic

0.44

BayesDel_noAF

Pathogenic

0.39

CADD

Uncertain

(source)

DANN

Uncertain

1.0

DEOGEN2

Pathogenic

0.95

Eigen

Uncertain

0.40

Eigen_PC

Uncertain

0.31

FATHMM_MKL

Uncertain

0.93

LIST_S2

Uncertain

0.96

M_CAP

Pathogenic

0.98

MetaRNN

Pathogenic

0.98

MetaSVM

Pathogenic

0.98

MutationAssessor

Pathogenic

3.4

PhyloP100

2.7

PrimateAI

Pathogenic

0.88

PROVEAN

Uncertain

-2.6

REVEL

Pathogenic

0.88

Sift

Uncertain

0.0010

Sift4G

Pathogenic

0.0010

Polyphen

0.51

Vest4

0.95

MutPred

0.83

Gain of catalytic residue at H492 (P = 0.0343);

MVP

0.92

MPC

2.0

ClinPred

0.98

GERP RS

3.6

Varity_R

0.84

gMVP

1.0

Mutation Taster

=0/100

disease causing (ClinVar)

(source)

Splicing

Name

Calibrated prediction

Score

Prediction

SpliceAI score (max)

0.0

Details are displayed if max score is > 0.2

Find out detailed SpliceAI scores and Pangolin per-transcript scores at spliceailookup.broadinstitute.org

Publications

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Variant summary

Frequency

Consequence

Scores

Clinical Significance

Conservation

Publications

ACMG classification

Transcripts

RefSeq

Ensembl

Frequencies

Age Distribution

ClinVar

Submissions by phenotype

Computational scores

Splicing

Publications

Other links and lift over