NM_000435.3:c.1725G>T

Variant summary

Our verdict is Likely benign.
-1 Likely Benign
-7
-6
-1
0
+5
+6
+9
+10
B
LB
VUS
LP
P
The variant received -1 classification points (ACMG Germline Pathogenicity v2019). PM2BP4_ModerateBP7

The NM_000435.3(NOTCH3):c.1725G>T (p.Thr575Thr) variant causes a synonymous change involving the alteration of a non-conserved nucleotide. The variant allele was found at a cumulative frequency of 0.00000137 (AC=2) in the gnomAD database across 1,461,768 control chromosomes (no homozygotes observed). The grpmax filtering allele frequency (95% CI) is 0.0000003. In-silico predictor (BayesDel (noAF)) classifies this variant as likely benign. Splicing prediction tools (SpliceAI) predict no significant impact on normal splicing. No clinical diagnostic laboratories have submitted clinical-significance assessments for this variant to ClinVar.

Frequency

Genomes: not found (cov: 33)
Exomes 𝑓: 0.0000014 ( 0 hom. )

Consequence

NOTCH3
NM_000435.3 synonymous

Scores

3

Clinical Significance

Not reported in ClinVar

Conservation

PhyloP100: -6.82

Publications

10 publications found
Variant links:
Genes affected
NOTCH3 (HGNC:7883): (notch receptor 3) This gene encodes the third discovered human homologue of the Drosophilia melanogaster type I membrane protein notch. In Drosophilia, notch interaction with its cell-bound ligands (delta, serrate) establishes an intercellular signalling pathway that plays a key role in neural development. Homologues of the notch-ligands have also been identified in human, but precise interactions between these ligands and the human notch homologues remains to be determined. Mutations in NOTCH3 have been identified as the underlying cause of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). [provided by RefSeq, Jul 2008]
NOTCH3 Gene-Disease associations (from GenCC):
  • cerebral arteriopathy, autosomal dominant, with subcortical infarcts and leukoencephalopathy, type 1
    Inheritance: AD, AR Classification: DEFINITIVE, STRONG, MODERATE, SUPPORTIVE Submitted by: Genomics England PanelApp, ClinGen, Labcorp Genetics (formerly Invitae), Laboratory for Molecular Medicine, Orphanet, Ambry Genetics
  • lateral meningocele syndrome
    Inheritance: AD Classification: STRONG, SUPPORTIVE Submitted by: Labcorp Genetics (formerly Invitae), Orphanet
  • infantile myofibromatosis
    Inheritance: AD Classification: SUPPORTIVE Submitted by: Orphanet
  • myofibromatosis, infantile, 2
    Inheritance: AD Classification: LIMITED Submitted by: G2P
  • inherited thrombocytopenia
    Inheritance: AR Classification: LIMITED Submitted by: ClinGen
  • pulmonary arterial hypertension
    Inheritance: AD Classification: NO_KNOWN Submitted by: ClinGen

Genome browser will be placed here

new If you want to explore the variant's impact on the transcript NM_000435.3, 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: Likely_benign. The variant received -1 points.

PM2Absent/extremely low in population databases
Very rare in gnomAD for AD/XL gene (popmax AF < threshold/10) — PM2; GnomAD popmax AF = 0.0000003 — very rare for AD+AR gene (threshold 0.0001) — PM2 moderate.
BP4Computational evidence suggests no impact
Computational evidence supports benign — no pathogenic computational or splicing signal (BP4); Splicing verdict: benign (Strong).; Germline computational verdict: benign (Moderate).
BP7Synonymous variant, no splicing impact
Synonymous variant at non-conserved position with no predicted splicing impact (BP7); Synonymous at non-conserved position, no splicing concern — benign (BP7).

Variant Effect in Transcripts

Automated classification analysis was done for transcript: NM_000435.3. You can select a different transcript below to see updated classification assignments.

RefSeq Transcripts

NOTCH3 NM_000435.3
MANE Select
HGVSc / HGVSpc.1725G>Tp.Thr575Thr
Exon rankExon 11 of 33
synonymous
Prot: NP_000426.2UniProt: Q9UM47

Ensembl Transcripts

NOTCH3 ENST00000263388.7
TSL:1MANE Select
HGVSc / HGVSpc.1725G>Tp.Thr575Thr
Exon rankExon 11 of 33
synonymous
Prot: ENSP00000263388.1UniProt: Q9UM47
NOTCH3 ENST00000931534.1
HGVSc / HGVSpc.1725G>Tp.Thr575Thr
Exon rankExon 11 of 34
synonymous
Prot: ENSP00000601593.1UniProt: A0ACI8TLY8
NOTCH3 ENST00000931532.1
HGVSc / HGVSpc.1704G>Tp.Thr568Thr
Exon rankExon 11 of 32
synonymous
Prot: ENSP00000601591.1UniProt: A0ACI8TLB6

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 3 sources
GnomAD3 genomes
Cov:33
GnomAD4 exome
AF: 0.00000137
AC:2
Hom:0
AN:1461768
Cov:33
GnomAD4 genome
Cov:33
Showing 3 sources

ClinVar

Not reported in ClinVar

Computational Scores

AlphaGenome AVI
Benign0.0013
BayesDel_noAF
Benign-0.46
CADD
Benign0.35
DANN
Benign0.75
GPN-Star LLR
N/A-3.1
GPN-Star score
N/A3.1
PhyloP100
Benign-6.8
Showing 7 of 7 scores

Splicing Scores

Pangolin (max)
Benign0.0
SpliceAI score (max)
Benign0.0
Details are displayed if max score is > 0.2
Showing 2 of 2 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.

No MaveDB functional evidence found for this variant.

Publications

Other links and lift over

For research and educational, non-commercial use only. Not for clinical or diagnostic use. GeneBe does not provide medical advice. Data use for AI modeling is prohibited: if used, the cost is $0.001 per byte of downloaded uncompressed data.