Methods for the Administration of EDAR Pathway Modulators in Mice.
Details
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Version: Author's accepted manuscript
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UNIL restricted access
State: Public
Version: Author's accepted manuscript
License: Not specified
Serval ID
serval:BIB_7E7970A5AB18
Type
A part of a book
Publication sub-type
Chapter: chapter ou part
Collection
Publications
Institution
Title
Methods for the Administration of EDAR Pathway Modulators in Mice.
Title of the book
The TNF Superfamily
Publisher
Springer
ISSN
1940-6029 (Electronic)
ISSN-L
1064-3745
Publication state
Published
Issued date
2021
Peer-reviewed
Oui
Volume
2248
Series
Methods in molecular biology
Pages
167-183
Language
english
Abstract
Genetic deficiency of ectodysplasin A (EDA) causes X-linked hypohidrotic ectodermal dysplasia, a congenital condition characterized by the absence or abnormal formation of sweat glands, teeth, and several skin appendages. Stimulation of the EDA receptor (EDAR) with agonists in the form of recombinant EDA or anti-EDAR antibodies can compensate for the absence of Eda in a mouse model of Eda deficiency, provided that agonists are administered in a timely manner during fetal development. Here we provide detailed protocols for the administration of EDAR agonists or antagonists, or other proteins, by the intravenous, intraperitoneal, and intra-amniotic routes as well as protocols to collect blood, to visualize sweat gland function, and to prepare skulls in mice.
Keywords
Animals, Animals, Newborn, Disease Models, Animal, Drug Administration Routes, Ectodermal Dysplasia/drug therapy, Ectodermal Dysplasia/genetics, Ectodermal Dysplasia/metabolism, Edar Receptor/genetics, Edar Receptor/metabolism, Mice, Phenotype, Recombinant Proteins/administration & dosage, Signal Transduction/drug effects, Treatment Outcome, Amniotic fluid, EDAR signaling, Ectodermal dysplasia, Protein replacement therapy, Route of administration
Pubmed
Web of science
Create date
23/11/2020 15:57
Last modification date
12/04/2024 8:45