CD48

Chr 1

CD48 molecule

Also known as: BCM1, BLAST, BLAST1, MEM-102, SLAMF2, hCD48, mCD48

This gene encodes a member of the CD2 subfamily of immunoglobulin-like receptors which includes SLAM (signaling lymphocyte activation molecules) proteins. The encoded protein is found on the surface of lymphocytes and other immune cells, dendritic cells and endothelial cells, and participates in activation and differentiation pathways in these cells. The encoded protein does not have a transmembrane domain, however, but is held at the cell surface by a GPI anchor via a C-terminal domain which maybe cleaved to yield a soluble form of the receptor. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Dec 2011]

OMIMResearchGenerating clinical summary…
MultiplemechanismLOEUF 1.49
Clinical SummaryCD48
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
38 VUS of 55 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint?
1.49LOEUF
pLI 0.000
Z-score 0.48
OE 0.83 (0.491.49)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint?
0.04Z-score
OE missense 0.99 (0.861.15)
125 obs / 126.2 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios?
LoF OE?0.83 (0.491.49)
00.351.4
Missense OE?0.99 (0.861.15)
00.61.4
Synonymous OE?1.02
01.21.6
LoF obs/exp: 8 / 9.6Missense obs/exp: 125 / 126.2Syn Z: -0.14

This gene — mechanism propensity

DN
0.74top 25%
GOF
0.6736th %ile
LOF
0.2386th %ile

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

DNprediction above median
GOFprediction above median

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.

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312.

ClinVar Variant Classifications

55 submitted variants in ClinVar

Classification Summary

VUS38
Likely Benign5
Benign7
38
VUS
5
Likely Benign
7
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
0
0
0
Likely Pathogenic
0
0
0
0
0
VUS
0
38
0
0
38
Likely Benign
0
3
0
2
5
Benign
0
3
0
4
7
Total0440650

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

View in ClinVar →

11 pathogenic / likely-pathogenic (of 16) ClinVar copy-number / structural variants overlap CD48 — these span large chromosomal regions, not the gene specifically, and are excluded from the counts above. Explore in CNV tools →

Protein Context — Lollipop Plot

CD48 · protein map & ClinVar variants

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

Clinical Trials

Active and recruiting trials from ClinicalTrials.gov

No active trials found for this gene.

Search ClinicalTrials.gov →