Tgfbi/Bigh3 silencing activates ERK in mouse retina.


Autoria(s): Allaman-Pillet, N.; Oberson, A.; Bustamante, M.; Tasinato, A.; Hummler, E.; Schorderet, D.F.
Data(s)

2015

Resumo

BIGH3 is a secreted protein, part of the extracellular matrix where it interacts with collagen and integrins on the cell surface. BIGH3 can play opposing roles in cancer, acting as either tumor suppressor or promoter, and its mutations lead to different forms of corneal dystrophy. Although many studies have been carried out, little is known about the physiological role of BIGH3. Using the cre-loxP system, we generated a mouse model with disruption of the Bigh3 genomic locus. Bigh3 silencing did not result in any apparent phenotype modifications, the mice remained viable and fertile. We were able to determine the presence of BIGH3 in the retinal pigment epithelium (RPE). In the absence of BIGH3, a transient decrease in the apoptotic process involved in retina maturation was observed, leading to a transient increase in the INL thickness at P15. This phenomenon was accompanied by an increased activity of the pro-survival ERK pathway.

Identificador

https://serval.unil.ch/notice/serval:BIB_D266D06B98BD

info:pmid:26387839

https://serval.unil.ch/resource/serval:BIB_D266D06B98BD.P001/REF

http://nbn-resolving.org/urn/resolver.pl?urn=urn:nbn:ch:serval-BIB_D266D06B98BD3

urn:nbn:ch:serval-BIB_D266D06B98BD3

Idioma(s)

eng

Fonte

Experimental Eye Research140159-170

Tipo

info:eu-repo/semantics/article

article

Formato

application/pdf

Direitos

info:eu-repo/semantics/openAccess

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