Generation of Transgenic Mice that Conditionally Overexpress Tenascin-C.
Animals
Chromosome Walking
Cytokines
/ metabolism
Gene Expression Regulation, Developmental
Genome
Homozygote
Inflammation Mediators
/ metabolism
Integrases
/ genetics
Mice
Mice, Inbred C57BL
Mice, Transgenic
Myocardial Infarction
/ immunology
Neurodegenerative Diseases
/ genetics
Phenotype
Promoter Regions, Genetic
/ genetics
Tenascin
/ genetics
Ventricular Myosins
/ genetics
Atp8a2
Cre-Lox
Nkx2.5
alpha myosin heavy chain
heart development
matricellular protein
myocardial inafrction
Journal
Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960
Informations de publication
Date de publication:
2021
2021
Historique:
received:
23
10
2020
accepted:
10
02
2021
entrez:
25
3
2021
pubmed:
26
3
2021
medline:
29
6
2021
Statut:
epublish
Résumé
Tenascin-C (TNC) is an extracellular matrix glycoprotein that is expressed during embryogenesis. It is not expressed in normal adults, but is up-regulated under pathological conditions. Although TNC knockout mice do not show a distinct phenotype, analyses of disease models using TNC knockout mice combined with
Identifiants
pubmed: 33763067
doi: 10.3389/fimmu.2021.620541
pmc: PMC7982461
doi:
Substances chimiques
Cytokines
0
Inflammation Mediators
0
Tenascin
0
Cre recombinase
EC 2.7.7.-
Integrases
EC 2.7.7.-
Ventricular Myosins
EC 3.6.1.-
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
620541Informations de copyright
Copyright © 2021 Yonebayashi, Tajiri, Hara, Saito, Suzuki, Sakai, Kimura, Sato, Sekimoto, Fujita, Okamoto, Schwartz, Yoshida and Imanaka-Yoshida.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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