Evidence map›Paper›PMID 28869973›Full record

ArticleNature2017

Palmitoylation-dependent activation of MC1R prevents melanomagenesis.

Shuyang Chen, Bo Zhu, Chengqian Yin, Wei Liu, Changpeng Han, Baoen Chen, Tongzheng Liu, Xin Li, Xiang Chen, Chunying Li and 7 more

Open access · greenAbstract read
In one paragraph

Article in Nature, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 144 papers.

0numbers the graph read from it
0cells of the map it votes in
144citing papers in PubMed
8.7field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

144 citing papers in PubMed, 236 citations in OpenAlex.

  1. Unique Features of Melanoma Risk and Diagnosis in Red-Haired Populations.International journal of molecular sciences · 2026
    Review
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  9. Crosstalk between protein lipidation and ubiquitination in tumor biology.Apoptosis : an international journal on programmed cell death · 2026
    Review
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84 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 10 institutions in 3 countries.

Shuyang ChenDepartment of Pharmacology and Experimental Therapeutics, Boston University School of Medicine, Boston, Massachusetts 02118, USA.
Bo ZhuDepartment of Pharmacology and Experimental Therapeutics, Boston University School of Medicine, Boston, Massachusetts 02118, USA.
Chengqian YinDepartment of Pharmacology and Experimental Therapeutics, Boston University School of Medicine, Boston, Massachusetts 02118, USA.
Wei LiuDepartment of Pharmacology and Experimental Therapeutics, Boston University School of Medicine, Boston, Massachusetts 02118, USA.
Changpeng HanDepartment of Pharmacology and Experimental Therapeutics, Boston University School of Medicine, Boston, Massachusetts 02118, USA.
Baoen ChenCutaneous Biology Research Center, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA.
Tongzheng LiuJinan University Institute of Tumor Pharmacology, Guangzhou, Guangdong 510632, China.
Xin LiDepartment of Pharmacology and Experimental Therapeutics, Boston University School of Medicine, Boston, Massachusetts 02118, USA.
Xiang ChenHunan Key Laboratory of Skin Cancer and Psoriasis/Department of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China.
Chunying LiDepartment of Dermatology, Xijing Hospital, The Fourth Military Medical University, Xi'an, Shaanxi 710000, China.
Limin HuTianjin State Key Laboratory of Modern Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, 300193, China.
Jun ZhouState Key Laboratory of Medicinal Chemical Biology, College of Life Sciences, Nankai University, Tianjin 300071, China.
Zhi-Xiang XuDivision of Hematology and Oncology, Department of Medicine, Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA.
Xiumei GaoTianjin State Key Laboratory of Modern Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, 300193, China.
Xu WuCutaneous Biology Research Center, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA.
Colin R GodingLudwig Institute for Cancer Research, University of Oxford, Headington, Oxford OX3 7DQ, UK.
Rutao CuiDepartment of Pharmacology and Experimental Therapeutics, Boston University School of Medicine, Boston, Massachusetts 02118, USA.
Boston University · USTianjin University of Traditional Chinese Medicine · CNAir Force Medical University · CNCentral South University · CNHarvard University · USJinan University · CNMassachusetts General Hospital · USNankai University · CNUniversity of Alabama at Birmingham · USUniversity of Oxford · GB

Funding

Tumor Assessment CoreP01CA128814 · NCI · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI SMITH, JEFFREY W · 2009 to 2020
$19.1M
Chemical approach to study autopalmitoylation of transcription factorsR01DK107651 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI LUO, XUELIAN, WU, XU · 2016 to 2020
$1.9M
Metabolic regulation of cellular junction proteinsR01CA181537 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI WU, XU · 2014 to 2018
$1.8M
The role of pheomelanin in cutaneous melanomaR01CA137098 · NCI · TUFTS MEDICAL CENTER · PI CUI, RUTAO · 2009 to 2014
$1.6M
Molecular connections among UV exposure, red hair, nevi and melanomaR01CA193913 · NCI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI CUI, RUTAO · 2016 to 2019
$1.5M
Why red-haired individuals are so prone to developing melanomaR01CA196896 · NCI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI CUI, RUTAO · 2015 to 2017
$1.1M
NCI NIH HHS P01 CA128814NCI NIH HHS R01 CA137098NCI NIH HHS R01 CA181537NCI NIH HHS R01 CA193913NCI NIH HHS R01 CA196896NIDDK NIH HHS R01 DK107651
6 · The paper itself

Abstract

The melanocortin-1 receptor (MC1R), a G-protein-coupled receptor, has a crucial role in human and mouse pigmentation. Activation of MC1R in melanocytes by α-melanocyte-stimulating hormone (α-MSH) stimulates cAMP signalling and melanin production and enhances DNA repair after ultraviolet irradiation. Individuals carrying MC1R variants, especially those associated with red hair colour, fair skin and poor tanning ability (denoted as RHC variants), are associated with higher risk of melanoma. However, how MC1R activity is modulated by ultraviolet irradiation, why individuals with red hair are more prone to developing melanoma, and whether the activity of RHC variants might be restored for therapeutic benefit are unknown. Here we demonstrate a potential MC1R-targeted intervention strategy in mice to rescue loss-of-function MC1R in MC1R RHC variants for therapeutic benefit by activating MC1R protein palmitoylation. MC1R palmitoylation, primarily mediated by the protein-acyl transferase ZDHHC13, is essential for activating MC1R signalling, which triggers increased pigmentation, ultraviolet-B-induced G1-like cell cycle arrest and control of senescence and melanomagenesis in vitro and in vivo. Using C57BL/6J-Mc1r

Indexed as

LipoylationPigmentationAcyltransferasesAnimalsCell Transformation, NeoplasticFemaleHumansMaleMelanocytesMelanomaMiceMice, Inbred C57BLMice, TransgenicMutationReceptor, Melanocortin, Type 1AcyltransferasesReceptor, Melanocortin, Type 1ZDHHC13 protein, humanZdhhc13 protein, mouse

Identifiers

PMID28869973
PMCPMC5902815
OpenAlexW2751331717

What OpenQuestion holds

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Read underepoch 390

Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.