ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2010
The secreted form of a melanocyte membrane-bound glycoprotein (Pmel17/gp100) is released by ectodomain shedding.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed.
- VDAC1 negatively regulates melanogenesis through the CaLife science alliance · 2022Article
- sPmel17 Secreted by Ultraviolet B-Exposed Melanocytes Alters the Intercellular Adhesion of Keratinocytes.Oxidative medicine and cellular longevity · 2022Article
- Identification of critical amino acid residues in the regulatory N-terminal domain of PMEL.Scientific reports · 2021Article
- Article
- Functional Mammalian Amyloids and Amyloid-Like Proteins.Life (Basel, Switzerland) · 2020Review
- pH-controlled histone acetylation amplifies melanocyte differentiation downstream of MITF.EMBO reports · 2020Article
- Blood Biomarkers of Uveal Melanoma: Current Perspectives.Clinical ophthalmology (Auckland, N.Z.) · 2020Review
- Non-Synonymous variants in premelanosome protein (PMEL) cause ocular pigment dispersion and pigmentary glaucoma.Human molecular genetics · 2019Article
- Nonsense mutation in PMEL is associated with yellowish plumage colour phenotype in Japanese quail.Scientific reports · 2018Article
- SheddomeDB: the ectodomain shedding database for membrane-bound shed markers.BMC bioinformatics · 2017Review
- Melanosomal formation of PMEL core amyloid is driven by aromatic residues.Scientific reports · 2017Article
- Recent Advances in ADAM17 Research: A Promising Target for Cancer and Inflammation.Mediators of inflammation · 2017Review
- PMEL Amyloid Fibril Formation: The Bright Steps of Pigmentation.International journal of molecular sciences · 2016Review
- The Kringle-like Domain Facilitates Post-endoplasmic Reticulum Changes to Premelanosome Protein (PMEL) Oligomerization and Disulfide Bond Configuration and Promotes Amyloid Formation.The Journal of biological chemistry · 2016Article
- Broadening the repertoire of melanoma-associated T-cell epitopes.Cancer immunology, immunotherapy : CII · 2015Article
- Endogenous Antigen Presentation of MHC Class II Epitopes through Non-Autophagic Pathways.Frontiers in immunology · 2015Review
- Melanoma-associated leukoderma - immunology in black and white?Pigment cell & melanoma research · 2013Review
- The PKD domain distinguishes the trafficking and amyloidogenic properties of the pigment cell protein PMEL and its homologue GPNMB.Pigment cell & melanoma research · 2013Article
- PMEL: a pigment cell-specific model for functional amyloid formation.Pigment cell & melanoma research · 2013Review
- Critical residues in the PMEL/Pmel17 N-terminus direct the hierarchical assembly of melanosomal fibrils.Molecular biology of the cell · 2013Article
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3 authors.
Funding
Abstract
Ectodomain shedding is a proteolytic mechanism by which a transmembrane protein is converted into a secreted form. Pmel17/gp100 is a melanocyte-specific membrane-bound glycoprotein that has amyloid characteristics and forms fibrillar structures in melanosomes after a complex sequence of post-translational processing and trafficking events, including cleavage by a furin-like proprotein convertase (PC). A secreted form of Pmel17 (termed sPmel17) was also thought to be released due to cleavage by a PC. We used multidisciplinary approaches to demonstrate that sPmel17 is released by ectodomain shedding at the juxtamembrane and/or intramembrane motif and to show that this is independent of cleavage by a PC. We further show that sPmel17 consists of 2 fragments linked by disulfide bonds and that the shedding is inhibited at low temperature but not by metalloproteinase inhibitors. Moreover, treatment with a phorbol ester or a calmodulin inhibitor induces Pmel17 shedding. We also refine the reactivity of HMB50 and NKI/beteb, 2 monoclonal antibodies commonly used as melanoma-specific markers. The fact that those antibodies require physically separated domains of Pmel17 sheds interesting light on its 3-dimensional conformation. We conclude that sPmel17 is released by regulated proteolytic ectodomain shedding.-Hoashi, T., Tamaki, K., Hearing, V. J. The secreted form of a melanocyte membrane-bound glycoprotein (Pmel17/gp100) is released by ectodomain shedding.
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