NM_000527.5:c.2389G>A

Variant summary

Our verdict is Pathogenic.
+14 Pathogenic
-7
-6
-1
0
+5
+6
+9
+10
B
LB
VUS
LP
P
The variant received 14 classification points (ACMG Germline Pathogenicity v2019). PS3PM1PM5PP3_ModeratePP5_Strong

The NM_000527.5(LDLR):c.2389G>A (p.Val797Met) variant causes a missense, splice region change involving the alteration of a non-conserved nucleotide. The variant allele was found at a cumulative frequency of 0.00000434 (AC=7) in the gnomAD database across 1,613,688 control chromosomes (no homozygotes observed). The grpmax filtering allele frequency (95% CI) is 0.000207. Variant has been reported in ClinVar as Pathogenic/Likely Pathogenic (★★). ClinVar reports functional evidence for this variant: "SCV005427660: "In vitro functional studies have shown that this variant causes a reduction in LDLR internalization and expression at the cellular membrane (PMID:34497632)."" and additional evidence is available in ClinVar. A different missense at the same amino acid position has been reported as Pathogenic/Likely Pathogenic in ClinVar: p.V797L: Pathogenic/Likely_pathogenic (ClinVar VariationId 252298, 2 stars) Other variants at the same amino acid position have been reported in ClinVar (not pathogenic): p.V797= (synonymous): Conflicting_classifications_of_pathogenicity (ClinVar VariationId 891738); p.V797= (synonymous): Likely_benign (ClinVar VariationId 1094170, 1 star) This exact variant is curated in the UniProt human variants database as Uncertain Significance.

Frequency

Genomes: 𝑓 0.000013 ( 0 hom., cov: 31)
Exomes 𝑓: 0.0000034 ( 0 hom. )

Consequence

LDLR
NM_000527.5 missense, splice_region

Scores

2
5
7
Splicing: ADA: 0.9997
2

Clinical Significance

Pathogenic/Likely pathogenic criteria provided, multiple submitters, no conflicts P:23U:3

Conservation

PhyloP100: 2.41

Publications

32 publications found
Variant links:
Genes affected
LDLR (HGNC:6547): (low density lipoprotein receptor) The low density lipoprotein receptor (LDLR) gene family consists of cell surface proteins involved in receptor-mediated endocytosis of specific ligands. The encoded protein is normally bound at the cell membrane, where it binds low density lipoprotein/cholesterol and is taken into the cell. Lysosomes release the cholesterol, which is made available for repression of microsomal enzyme 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase, the rate-limiting step in cholesterol synthesis. At the same time, a reciprocal stimulation of cholesterol ester synthesis takes place. Mutations in this gene cause the autosomal dominant disorder, familial hypercholesterolemia. Alternate splicing results in multiple transcript variants.[provided by RefSeq, May 2022]
LDLR Gene-Disease associations (from GenCC):
  • hypercholesterolemia, familial, 1
    Inheritance: SD, AD Classification: DEFINITIVE, STRONG Submitted by: ClinGen, Genomics England PanelApp, Laboratory for Molecular Medicine, Labcorp Genetics (formerly Invitae), Natera
  • homozygous familial hypercholesterolemia
    Inheritance: AR Classification: SUPPORTIVE Submitted by: Orphanet

Genome browser will be placed here

new If you want to explore the variant's impact on the transcript NM_000527.5, check out the Mutation Effect Viewer. This is especially useful for frameshift variants or if you want to visualize the effect of exon loss / intron retention.

Classification according to ACMG Germline Pathogenicity v2019

Classification was made for transcript:

Our verdict: Pathogenic. The variant received 14 points.

PS3Functional studies show damaging effect
Well-established functional study supports damaging effect (PS3); SCV005427660: "In vitro functional studies have shown that this variant causes a reduction in LDLR internalization and expression at the cellular membrane (PMID: 34497632)."; SCV006101202: "Well-established in vitro or in vivo functional studies supportive of a damaging effect on the gene or gene product."; SCV000589577: Functional splice studies of a different variant at this same nucleotide position (c.2389 G>T, p.V797L) demonstrate skipping of exon 16, further supporting the functional importance of this nucleotide position (PMID: 28169869);; SCV002047264: In addition, this variant is located at an exon-intron junction and an RT-PCR study suggests the variant may affect LDLR mRNA splicing (PMID: 9763532 (1998)).; SCV000904109: "In vitro functional studies have shown that this variant causes a reduction in LDLR internalization and expression at the cellular membrane (PMID: 34497632)."; SCV000731742: This variant has been shown to cause altered splicing leading to absent protein (Mak 1998).
PM1Mutational hot spot or critical domain
Missense neighbourhood hotspot (≥2 P/LP within ±8 AA, OR ≥ 5 vs. background) — PM1; In-domain: 0 pathogenic, 0 benign rare missense variants.; ±8 AA neighbourhood: 6 pathogenic, 3 benign (OR vs. background: 9.3).
PM5Novel missense at known pathogenic residue
Different pathogenic missense at same AA residue in ClinVar (PM5); ClinVar contains a germline Pathogenic/Likely Pathogenic entry at the same amino acid position with a different amino acid change: p.V797L: Pathogenic/Likely_pathogenic (ClinVar VariationId 252298, 2 stars); Other variants at the same amino acid residue (not pathogenic): p.V797= (synonymous): Conflicting_classifications_of_pathogenicity (ClinVar VariationId 891738); p.V797= (synonymous): Likely_benign (ClinVar VariationId 1094170, 1 star)
PP3Computational evidence supports damaging effect
Splicing predictors (SpliceAI/dbscSNV) support splicing impact — moderate computational evidence (PP3); Splicing verdict: pathogenic (Moderate).; Germline computational verdict: not pathogenic.
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 (23/26 total P/LP).

Variant Effect in Transcripts

Automated classification analysis was done for transcript: NM_000527.5. You can select a different transcript below to see updated classification assignments.

RefSeq Transcripts

LDLR NM_000527.5
MANE Select
HGVSc / HGVSpc.2389G>Ap.Val797Met
Exon rankExon 16 of 18
missensesplice_region
Prot: NP_000518.1UniProt: P01130-1
LDLR NM_001195798.2
HGVSc / HGVSpc.2389G>Ap.Val797Met
Exon rankExon 16 of 18
missensesplice_region
Prot: NP_001182727.1UniProt: P01130-5
LDLR NM_001195799.2
HGVSc / HGVSpc.2266G>Ap.Val756Met
Exon rankExon 15 of 17
missensesplice_region
Prot: NP_001182728.1UniProt: P01130-4

Ensembl Transcripts

LDLR ENST00000558518.6
TSL:1MANE Select
HGVSc / HGVSpc.2389G>Ap.Val797Met
Exon rankExon 16 of 18
missensesplice_region
Prot: ENSP00000454071.1UniProt: P01130-1
LDLR ENST00000252444.10
TSL:1
HGVSc / HGVSpc.2647G>Ap.Val883Met
Exon rankExon 16 of 18
missensesplice_region
Prot: ENSP00000252444.6UniProt: J3KMZ9
LDLR ENST00000558013.5
TSL:1
HGVSc / HGVSpc.2389G>Ap.Val797Met
Exon rankExon 16 of 18
missensesplice_region
Prot: ENSP00000453346.1UniProt: P01130-5

Frequencies

Allele frequencies (AF), counts (AC/AN), homozygotes and coverage

Common (AF > 0.05 / Hom > 5)
Rare (AF ≤ 0.0001 / Hom ≤ 1)
Global population databases 6 sources
GnomAD3 genomes
AF: 0.0000132
AC:2
Hom:0
AN:152078
Cov:31
GnomAD2 exomes
AF: 0.00000796
AC:2
AN:251360
GnomAD4 exome
AF: 0.00000342
AC:5
Hom:0
AN:1461610
Cov:32
GnomAD4 genome
AF: 0.0000132
AC:2
Hom:0
AN:152078
Cov:31
TOPMed (Bravo)
AF: 0.00000378
ALFA (dbGaP/dbSNP Allele Frequency Aggregator)
AF: 0.00
AC:0
Hom:0
AN:54058
Local & regional cohorts 1 source
ChinaMAP Phase 1
AF: 0.0000985
Showing 7 sources

Case/control cohorts

CohortCasesControls
AFACANAFACAN
Epi25
(Epilepsy)
0.00 041958 0.0000150 166888
SCHEMA
(Schizophrenia)
0.0000195 2102690 0.0000273 5183358
Showing 2 cohortsAllele count / allele number. AF is computed from the counts for ASC (not provided by the source).

ClinVar

ClinVar submissions
Significance:Pathogenic/Likely pathogenic
Revision:criteria provided, multiple submitters, no conflicts
View on ClinVar
Pathogenic
VUS
Benign
Condition
12
3
-
Hypercholesterolemia, familial, 1 (15)
5
-
-
Familial hypercholesterolemia (5)
3
-
-
not provided (3)
1
-
-
Cardiovascular phenotype (1)
1
-
-
Dyslipidemia (1)
1
-
-
Homozygous familial hypercholesterolemia (1)

Computational Scores

AlphaGenome AVI
Pathogenic24
AlphaMissense
Benign0.17
BayesDel_addAF
Pathogenic0.17D
BayesDel_noAF
Uncertain0.050
CADD
Uncertain24
DANN
Benign0.97
Eigen
Benign0.010
Eigen_PC
Benign0.033
FATHMM_MKL
Uncertain0.94D
FuncVEP CTI
Benign0.17
GPN-Star LLR
N/A-5.0
GPN-Star score
N/A4.7
LIST_S2
Benign0.31T
M_CAP
Pathogenic0.75D
MetaRNN
Benign0.38T
Mutation Taster
N/A5/95disease causing (ClinVar)
PhyloP100
Benign2.4
popEVE
Benign-3.0
PROVEAN
Benign0.24N
RBP_binding_hub_radar
N/A0.0
RBP_regulation_power_radar
N/A1.8
Sift
Uncertain0.0060D
Sift4G
Uncertain0.014D
Varity_R
N/A0.088
VESM-3B
Benign-5.8
Showing 25 of 25 scores

Splicing Scores

dbscSNV1_ADA
Pathogenic1.0
dbscSNV1_RF
Pathogenic0.93
DS_DL_spliceai
Uncertain0.32
Position offset: 0
Pangolin (max)
Uncertain0.31
Pangolin loss
Uncertain0.31
Position offset: 0
SpliceAI score (max)
Uncertain0.32
Details are displayed if max score is > 0.2
Showing 6 of 6 scores

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

MaxEntScan Visualizer can be used to analyze the impact of this mutation on the neighboring sequence.

MaveDB functional evidence

MaveDB is a public repository of laboratory assays that test the effect of thousands of variants at once — treat this as supporting research data and interpret it with great caution; it is not a clinical classification.

2 no calibration
Protein level
LDLR missense variant effects on LDL uptake.
The functional landscape of coding variation in the familial hypercholesterolemia gene LDLR.
Gene
LDLR
Assay type
Flow cytometry assay
Mechanism
Gain or loss of function
Model system
Immortalized human cells
Score
1.06 · p.Val797Met (assay numbering)
No calibration data
This score is at approximately the 87th percentile of all variants tested in this assay.
This score has not been calibrated against ACMG evidence — shown for context only, not as clinical evidence.
Protein level
LDLR missense variant effects on LDLR cell-surface abundance.
The functional landscape of coding variation in the familial hypercholesterolemia gene LDLR.
Gene
LDLR
Assay type
Flow cytometry assay
Mechanism
Gain or loss of function
Model system
Immortalized human cells
Score
1.06 · p.Val797Met (assay numbering)
No calibration data
This score is at approximately the 86th percentile of all variants tested in this assay.
This score has not been calibrated against ACMG evidence — shown for context only, not as clinical evidence.

Publications

Other links and lift over

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