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Verfasst von:Shatirishvili, Marine [VerfasserIn]   i
 Burk, Alexandra Serena [VerfasserIn]   i
 Breuhahn, Kai [VerfasserIn]   i
 Tanaka, Motomu [VerfasserIn]   i
Titel:Epidermal-specific deletion of CD44 reveals a function in keratinocytes in response to mechanical stress
Verf.angabe:M Shatirishvili, AS Burk, CM Franz, G Pace, T Kastilan, K Breuhahn, E Hinterseer, A Dierich, L Bakiri, EF Wagner, H Ponta, TN Hartmann, M Tanaka and V Orian-Rousseau
E-Jahr:2016
Jahr:10 November 2016
Umfang:12 S.
Fussnoten:Gesehen am 06.05.2020
Titel Quelle:Enthalten in: Cell death & disease
Ort Quelle:London [u.a.] : Nature Publishing Group, 2010
Jahr Quelle:2016
Band/Heft Quelle:7(2016,11) Artikel-Nummer e2461, 12 Seiten
ISSN Quelle:2041-4889
Abstract:CD44, a large family of transmembrane glycoproteins, plays decisive roles in physiological and pathological conditions. CD44 isoforms are involved in several signaling pathways essential for life such as growth factor-induced signaling by EGF, HGF or VEGF. CD44 is also the main hyaluronan (HA) receptor and as such is involved in HA-dependent processes. To allow a genetic dissection of CD44 functions in homeostasis and disease, we generated a Cd44 floxed allele allowing tissue- and time-specific inactivation of all CD44 isoforms in vivo. As a proof of principle, we inactivated Cd44 in the skin epidermis using the K14Cre allele. Although the skin of such Cd44Δker mutants appeared morphologically normal, epidermal stiffness was reduced, wound healing delayed and TPA induced epidermal thickening decreased. These phenotypes might be caused by cell autonomous defects in differentiation and HA production as well as impaired adhesion and migration on HA by Cd44Δker keratinocytes. These findings support the usefulness of the conditional Cd44 allele in unraveling essential physiological and pathological functions of CD44 isoforms.
DOI:doi:10.1038/cddis.2016.342
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext ; Verlag: https://doi.org/10.1038/cddis.2016.342
 Volltext: https://www.nature.com/articles/cddis2016342
 DOI: https://doi.org/10.1038/cddis.2016.342
Datenträger:Online-Ressource
Sprache:eng
K10plus-PPN:1697278124
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