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超越红发与晒伤:揭示MC1R信号传导及紫外线诱导DNA损伤修复的分子机制

Beyond Red Hair and Sunburns: Uncovering the Molecular Mechanisms of MC1R Signaling and Repair of UV-Induced DNA Damage.

作者信息

Cassidy Pamela B, Abdel-Malek Zalfa A, Leachman Sancy A

机构信息

Department of Dermatology, Oregon Health & Science University, Portland, Oregon, USA.

Department of Dermatology, University of Cincinnati, Cincinnati, Ohio, USA.

出版信息

J Invest Dermatol. 2015 Dec;135(12):2918-2921. doi: 10.1038/jid.2015.349.

DOI:10.1038/jid.2015.349
PMID:26569585
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4648680/
Abstract

Scientists at the University of Kentucky are unraveling the details of DNA-damage repair in the melanocyte, with an eye towards finding druggable targets for melanoma prevention. Jarret et al., (2015, this issue) report in this issue three new assays that can yield mechanistic information about nucleotide excision repair (NER) stimulated by cAMP-dependent signaling downstream of the melanocortin-1 receptor (MC1R).

摘要

肯塔基大学的科学家们正在深入研究黑素细胞中DNA损伤修复的细节,旨在寻找可用于预防黑色素瘤的药物靶点。贾勒特等人(2015年,本期)在本期报告了三种新的检测方法,这些方法能够提供有关由黑皮质素-1受体(MC1R)下游的cAMP依赖性信号传导所刺激的核苷酸切除修复(NER)的机制信息。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e390/4648680/5283c76237bf/nihms720458f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e390/4648680/5283c76237bf/nihms720458f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e390/4648680/5283c76237bf/nihms720458f1.jpg

相似文献

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Beyond Red Hair and Sunburns: Uncovering the Molecular Mechanisms of MC1R Signaling and Repair of UV-Induced DNA Damage.超越红发与晒伤:揭示MC1R信号传导及紫外线诱导DNA损伤修复的分子机制
J Invest Dermatol. 2015 Dec;135(12):2918-2921. doi: 10.1038/jid.2015.349.
2
Defining the Contribution of MC1R Physiological Ligands to ATR Phosphorylation at Ser435, a Predictor of DNA Repair in Melanocytes.确定黑素细胞中DNA修复预测指标——丝氨酸435处ATR磷酸化的MC1R生理配体的作用。
J Invest Dermatol. 2015 Dec;135(12):3086-3095. doi: 10.1038/jid.2015.280. Epub 2015 Jul 13.
3
Melanocortins and the melanocortin 1 receptor, moving translationally towards melanoma prevention.促黑素细胞激素和促黑素细胞激素1受体,在预防黑色素瘤方面取得进展。
Arch Biochem Biophys. 2014 Dec 1;563:4-12. doi: 10.1016/j.abb.2014.07.002. Epub 2014 Jul 11.
4
Divergence of cAMP signalling pathways mediating augmented nucleotide excision repair and pigment induction in melanocytes.cAMP 信号通路在介导黑色素细胞中增强的核苷酸切除修复和色素诱导中的分歧。
Exp Dermatol. 2017 Jul;26(7):577-584. doi: 10.1111/exd.13291. Epub 2017 Apr 21.
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The melanocortin 1 receptor and the UV response of human melanocytes--a shift in paradigm.黑皮质素1受体与人类黑素细胞的紫外线反应——范式转变
Photochem Photobiol. 2008 Mar-Apr;84(2):501-8. doi: 10.1111/j.1751-1097.2008.00294.x. Epub 2008 Feb 11.
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cAMP-independent non-pigmentary actions of variant melanocortin 1 receptor: AKT-mediated activation of protective responses to oxidative DNA damage.变异型黑素皮质素 1 受体的 cAMP 非依赖性非色素作用:AKT 介导的对氧化 DNA 损伤的保护反应的激活。
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J Biol Chem. 2008 May 2;283(18):12564-70. doi: 10.1074/jbc.M800480200. Epub 2008 Feb 21.
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Melanin content and MC1R function independently affect UVR-induced DNA damage in cultured human melanocytes.黑色素含量和MC1R功能独立影响培养的人黑素细胞中紫外线辐射诱导的DNA损伤。
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Polo-like kinases and UV-induced skin carcinogenesis: What we know and what's next.波罗样激酶与紫外线诱导的皮肤癌发生:我们所知与后续研究方向
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Cutaneous melanoma.皮肤黑色素瘤

本文引用的文献

1
Defining the Contribution of MC1R Physiological Ligands to ATR Phosphorylation at Ser435, a Predictor of DNA Repair in Melanocytes.确定黑素细胞中DNA修复预测指标——丝氨酸435处ATR磷酸化的MC1R生理配体的作用。
J Invest Dermatol. 2015 Dec;135(12):3086-3095. doi: 10.1038/jid.2015.280. Epub 2015 Jul 13.
2
Melanocortins and the melanocortin 1 receptor, moving translationally towards melanoma prevention.促黑素细胞激素和促黑素细胞激素1受体,在预防黑色素瘤方面取得进展。
Arch Biochem Biophys. 2014 Dec 1;563:4-12. doi: 10.1016/j.abb.2014.07.002. Epub 2014 Jul 11.
3
RETRACTED: PKA-mediated phosphorylation of ATR promotes recruitment of XPA to UV-induced DNA damage.
Nat Rev Dis Primers. 2025 Apr 3;11(1):23. doi: 10.1038/s41572-025-00603-8.
4
Racial Differences in Cancer Susceptibility and Survival: More Than the Color of the Skin?癌症易感性和生存率的种族差异:仅仅是肤色的问题吗?
Trends Cancer. 2017 Mar;3(3):181-197. doi: 10.1016/j.trecan.2017.02.002. Epub 2017 Mar 6.
5
ATR Mutations Promote the Growth of Melanoma Tumors by Modulating the Immune Microenvironment.ATR突变通过调节免疫微环境促进黑色素瘤肿瘤生长。
Cell Rep. 2017 Mar 7;18(10):2331-2342. doi: 10.1016/j.celrep.2017.02.040.
6
Germline MC1R status influences somatic mutation burden in melanoma.胚系 MC1R 状态影响黑色素瘤的体细胞突变负担。
Nat Commun. 2016 Jul 12;7:12064. doi: 10.1038/ncomms12064.
撤回:蛋白激酶A介导的ATR磷酸化促进XPA募集至紫外线诱导的DNA损伤处。
Mol Cell. 2014 Jun 19;54(6):999-1011. doi: 10.1016/j.molcel.2014.05.030.
4
MC1R variants increased the risk of sporadic cutaneous melanoma in darker-pigmented Caucasians: a pooled-analysis from the M-SKIP project.MC1R基因变异增加了肤色较深的白种人患散发性皮肤黑色素瘤的风险:来自M-SKIP项目的汇总分析。
Int J Cancer. 2015 Feb 1;136(3):618-31. doi: 10.1002/ijc.29018. Epub 2014 Jun 18.
5
A rapid assay for measuring nucleotide excision repair by oligonucleotide retrieval.一种通过寡核苷酸回收来测量核苷酸切除修复的快速检测方法。
Sci Rep. 2014 May 8;4:4894. doi: 10.1038/srep04894.
6
Significance of the melanocortin 1 receptor in the DNA damage response of human melanocytes to ultraviolet radiation.黑皮质素1受体在人黑素细胞对紫外线辐射的DNA损伤反应中的意义。
Pigment Cell Melanoma Res. 2014 Jul;27(4):601-10. doi: 10.1111/pcmr.12252. Epub 2014 May 12.
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Targeted molecular therapy in melanoma.黑色素瘤的靶向分子治疗
Semin Cutan Med Surg. 2010 Sep;29(3):196-201. doi: 10.1016/j.sder.2010.06.005.
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Melanocortin 1 receptor genotype: an important determinant of the damage response of melanocytes to ultraviolet radiation.黑皮质素 1 受体基因型:影响黑素细胞对紫外线辐射损伤反应的重要因素。
FASEB J. 2010 Oct;24(10):3850-60. doi: 10.1096/fj.10-158485. Epub 2010 Jun 2.
9
alpha-MSH tripeptide analogs activate the melanocortin 1 receptor and reduce UV-induced DNA damage in human melanocytes.α-促黑素三肽类似物可激活黑皮质素1受体并减少紫外线诱导的人黑素细胞DNA损伤。
Pigment Cell Melanoma Res. 2009 Oct;22(5):635-44. doi: 10.1111/j.1755-148X.2009.00598.x. Epub 2009 Jun 23.
10
Agouti protein, mahogunin, and attractin in pheomelanogenesis and melanoblast-like alteration of melanocytes: a cAMP-independent pathway.刺鼠蛋白、大褐蛋白和吸引素在黑素细胞的褐黑素生成及黑素母细胞样改变中的作用:一条不依赖环磷酸腺苷的信号通路
Pigment Cell Melanoma Res. 2009 Oct;22(5):623-34. doi: 10.1111/j.1755-148X.2009.00582.x. Epub 2009 May 26.