MC1R

Chr 16AR

melanocortin 1 receptor

Also known as: CMM5, MSH-R, SHEP2

This intronless gene encodes the receptor protein for melanocyte-stimulating hormone (MSH). The encoded protein, a seven pass transmembrane G protein coupled receptor, controls melanogenesis. Two types of melanin exist: red pheomelanin and black eumelanin. Gene mutations that lead to a loss in function are associated with increased pheomelanin production, which leads to lighter skin and hair color. Eumelanin is photoprotective but pheomelanin may contribute to UV-induced skin damage by generating free radicals upon UV radiation. Binding of MSH to its receptor activates the receptor and stimulates eumelanin synthesis. This receptor is a major determining factor in sun sensitivity and is a genetic risk factor for melanoma and non-melanoma skin cancer. Over 30 variant alleles have been identified which correlate with skin and hair color, providing evidence that this gene is an important component in determining normal human pigment variation. [provided by RefSeq, Jul 2008]

Primary Disease Associations & Inheritance

[Analgesia from kappa-opioid receptor agonist, female-specific]MIM #613098
[Skin/hair/eye pigmentation 2, blond hair/fair skin]MIM #266300
AR
[Skin/hair/eye pigmentation 2, red hair/fair skin]MIM #266300
AR
{Albinism, oculocutaneous, type II, modifier of}MIM #203200
AR
{Melanoma, cutaneous malignant, 5}MIM #613099
{UV-induced skin damage}MIM #266300
AR
0
Active trials
8
Pathogenic / LP
500
ClinVar variants
6
Pubs (1 yr)
Missense Z
LOEUF
Clinical SummaryMC1R
📋
ClinVar Variants
8 Pathogenic / Likely Pathogenic· 323 VUS of 500 total submissions
📖
GeneReview available — MC1R
Authoritative clinical overview · Recommended first read
Open GeneReview ↗
Some data sources returned errors (2)

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Population Genetics & Constraint

Constraint data not available from gnomAD.

DN
0.7326th %ile
GOF
0.84top 5%
LOF
0.2776th %ile

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

GOFprediction above median
DNprediction 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

500 submitted variants in ClinVar

Classification Summary

Pathogenic7
Likely Pathogenic1
VUS323
Likely Benign153
Benign3
Conflicting13
7
Pathogenic
1
Likely Pathogenic
323
VUS
153
Likely Benign
3
Benign
13
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
7
0
7
Likely Pathogenic
0
0
1
0
1
VUS
14
276
27
6
323
Likely Benign
0
2
1
150
153
Benign
0
0
2
1
3
Conflicting
13
Total1427838157500

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

View in ClinVar →

Protein Context — Lollipop Plot

MC1R · 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 →
Clinical Literature
Landmark / reviewRecent case evidence
Key Publications
Landmark & review papers · by relevance
PubMed
Top 5 results · since 2015Search PubMed ↗