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Identification of SLURP-1 as an epidermal neuromodulator explains the clinical phenotype of Mal de Meleda

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Identification of SLURP-1 as an epidermal neuromodulator explains the clinical phenotype of Mal de Meleda. / Chimienti, Fabrice; Hogg, Ronald C; Plantard, Laure; Lehmann, Caroline; Brakch, Noureddine; Fischer, Judith; Huber, Marcel; Bertrand, Daniel; Hohl, Daniel.

I: Human Molecular Genetics, Bind 12, Nr. 22, 15.11.2003, s. 3017-24.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Chimienti, F, Hogg, RC, Plantard, L, Lehmann, C, Brakch, N, Fischer, J, Huber, M, Bertrand, D & Hohl, D 2003, 'Identification of SLURP-1 as an epidermal neuromodulator explains the clinical phenotype of Mal de Meleda', Human Molecular Genetics, bind 12, nr. 22, s. 3017-24. https://doi.org/10.1093/hmg/ddg320

APA

Chimienti, F., Hogg, R. C., Plantard, L., Lehmann, C., Brakch, N., Fischer, J., Huber, M., Bertrand, D., & Hohl, D. (2003). Identification of SLURP-1 as an epidermal neuromodulator explains the clinical phenotype of Mal de Meleda. Human Molecular Genetics, 12(22), 3017-24. https://doi.org/10.1093/hmg/ddg320

Vancouver

Chimienti F, Hogg RC, Plantard L, Lehmann C, Brakch N, Fischer J o.a. Identification of SLURP-1 as an epidermal neuromodulator explains the clinical phenotype of Mal de Meleda. Human Molecular Genetics. 2003 nov 15;12(22):3017-24. https://doi.org/10.1093/hmg/ddg320

Author

Chimienti, Fabrice ; Hogg, Ronald C ; Plantard, Laure ; Lehmann, Caroline ; Brakch, Noureddine ; Fischer, Judith ; Huber, Marcel ; Bertrand, Daniel ; Hohl, Daniel. / Identification of SLURP-1 as an epidermal neuromodulator explains the clinical phenotype of Mal de Meleda. I: Human Molecular Genetics. 2003 ; Bind 12, Nr. 22. s. 3017-24.

Bibtex

@article{4b51ce07eee74287a9c0eb969edde361,
title = "Identification of SLURP-1 as an epidermal neuromodulator explains the clinical phenotype of Mal de Meleda",
abstract = "Mal de Meleda is an autosomal recessive inflammatory and keratotic palmoplantar skin disorder due to mutations in the ARS B gene, encoding for SLURP-1 (secreted mammalian Ly-6/uPAR-related protein 1). SLURP-1 belongs to the Ly-6/uPAR superfamily of receptor and secreted proteins, which participate in signal transduction, immune cell activation or cellular adhesion. The high degree of structural similarity between SLURP-1 and the three fingers motif of snake neurotoxins and Lynx1 suggests that this protein interacts with the neuronal acetylcholine receptors. We found that SLURP-1 potentiates the human alpha 7 nicotinic acetylcholine receptors that are present in keratinocytes. These results identify SLURP-1 as a secreted epidermal neuromodulator which is likely to be essential for both epidermal homeostasis and inhibition of TNF-alpha release by macrophages during wound healing. This explains both the hyperproliferative as well as the inflammatory clinical phenotype of Mal de Meleda.",
keywords = "Acetylcholine, Amino Acid Sequence, Animals, Antigens, Ly, Cell Line, Cell Nucleus, Clone Cells, DNA, Complementary, Dose-Response Relationship, Drug, Epidermis, Female, Genes, Recessive, Humans, Keratoderma, Palmoplantar, Microinjections, Models, Molecular, Moths, Mutation, Neurotransmitter Agents, Oocytes, Patch-Clamp Techniques, Peptides, Phenotype, Protein Structure, Tertiary, Receptors, Cholinergic, Recombinant Proteins, Urokinase-Type Plasminogen Activator, Xenopus laevis",
author = "Fabrice Chimienti and Hogg, {Ronald C} and Laure Plantard and Caroline Lehmann and Noureddine Brakch and Judith Fischer and Marcel Huber and Daniel Bertrand and Daniel Hohl",
year = "2003",
month = nov,
day = "15",
doi = "10.1093/hmg/ddg320",
language = "English",
volume = "12",
pages = "3017--24",
journal = "Human Molecular Genetics",
issn = "0964-6906",
publisher = "Oxford University Press",
number = "22",

}

RIS

TY - JOUR

T1 - Identification of SLURP-1 as an epidermal neuromodulator explains the clinical phenotype of Mal de Meleda

AU - Chimienti, Fabrice

AU - Hogg, Ronald C

AU - Plantard, Laure

AU - Lehmann, Caroline

AU - Brakch, Noureddine

AU - Fischer, Judith

AU - Huber, Marcel

AU - Bertrand, Daniel

AU - Hohl, Daniel

PY - 2003/11/15

Y1 - 2003/11/15

N2 - Mal de Meleda is an autosomal recessive inflammatory and keratotic palmoplantar skin disorder due to mutations in the ARS B gene, encoding for SLURP-1 (secreted mammalian Ly-6/uPAR-related protein 1). SLURP-1 belongs to the Ly-6/uPAR superfamily of receptor and secreted proteins, which participate in signal transduction, immune cell activation or cellular adhesion. The high degree of structural similarity between SLURP-1 and the three fingers motif of snake neurotoxins and Lynx1 suggests that this protein interacts with the neuronal acetylcholine receptors. We found that SLURP-1 potentiates the human alpha 7 nicotinic acetylcholine receptors that are present in keratinocytes. These results identify SLURP-1 as a secreted epidermal neuromodulator which is likely to be essential for both epidermal homeostasis and inhibition of TNF-alpha release by macrophages during wound healing. This explains both the hyperproliferative as well as the inflammatory clinical phenotype of Mal de Meleda.

AB - Mal de Meleda is an autosomal recessive inflammatory and keratotic palmoplantar skin disorder due to mutations in the ARS B gene, encoding for SLURP-1 (secreted mammalian Ly-6/uPAR-related protein 1). SLURP-1 belongs to the Ly-6/uPAR superfamily of receptor and secreted proteins, which participate in signal transduction, immune cell activation or cellular adhesion. The high degree of structural similarity between SLURP-1 and the three fingers motif of snake neurotoxins and Lynx1 suggests that this protein interacts with the neuronal acetylcholine receptors. We found that SLURP-1 potentiates the human alpha 7 nicotinic acetylcholine receptors that are present in keratinocytes. These results identify SLURP-1 as a secreted epidermal neuromodulator which is likely to be essential for both epidermal homeostasis and inhibition of TNF-alpha release by macrophages during wound healing. This explains both the hyperproliferative as well as the inflammatory clinical phenotype of Mal de Meleda.

KW - Acetylcholine

KW - Amino Acid Sequence

KW - Animals

KW - Antigens, Ly

KW - Cell Line

KW - Cell Nucleus

KW - Clone Cells

KW - DNA, Complementary

KW - Dose-Response Relationship, Drug

KW - Epidermis

KW - Female

KW - Genes, Recessive

KW - Humans

KW - Keratoderma, Palmoplantar

KW - Microinjections

KW - Models, Molecular

KW - Moths

KW - Mutation

KW - Neurotransmitter Agents

KW - Oocytes

KW - Patch-Clamp Techniques

KW - Peptides

KW - Phenotype

KW - Protein Structure, Tertiary

KW - Receptors, Cholinergic

KW - Recombinant Proteins

KW - Urokinase-Type Plasminogen Activator

KW - Xenopus laevis

U2 - 10.1093/hmg/ddg320

DO - 10.1093/hmg/ddg320

M3 - Journal article

C2 - 14506129

VL - 12

SP - 3017

EP - 3024

JO - Human Molecular Genetics

JF - Human Molecular Genetics

SN - 0964-6906

IS - 22

ER -

ID: 45161578