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Titolo:
A role for MAP kinase in regulating ectodomain shedding of APLP2 in corneal epithelial cells
Autore:
Xu, KP; Zoukhri, D; Zieske, JD; Dartt, DA; Sergheraert, C; Loing, E; Yu, FSX;
Indirizzi:
Harvard Univ, Sch Med, Schepens Eye Res Inst, Boston, MA 02114 USA HarvardUniv Boston MA USA 02114 epens Eye Res Inst, Boston, MA 02114 USA Harvard Univ, Sch Med, Dept Ophthalmol, Boston, MA 02114 USA Harvard UnivBoston MA USA 02114 d, Dept Ophthalmol, Boston, MA 02114 USA Univ Lille 2, UMR 8525, Inst Biol, F-59021 Lille, France Univ Lille 2 Lille France F-59021 8525, Inst Biol, F-59021 Lille, France Inst Pasteur Lille, F-59021 Lille, France Inst Pasteur Lille Lille France F-59021 eur Lille, F-59021 Lille, France
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
fascicolo: 2, volume: 281, anno: 2001,
pagine: C603 - C614
SICI:
0363-6143(200108)281:2<C603:ARFMKI>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
AMYLOID PRECURSOR PROTEIN; CHONDROITIN SULFATE GLYCOSAMINOGLYCAN; ALPHA-SECRETASE CLEAVAGE; EPIDERMAL GROWTH-FACTOR; ALZHEIMERS-DISEASE; C-ALPHA; INHIBITOR DOMAIN; FACTOR RECEPTOR; NERVOUS-SYSTEM; PHORBOL ESTERS;
Keywords:
amyloid precursor-like protein 2; ectodomain shedding; epidermal growth factor; protein kinase C; mitogen-activated protein kinase;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
78
Recensione:
Indirizzi per estratti:
Indirizzo: Yu, FSX Harvard Univ, Sch Med, Schepens Eye Res Inst, 20 Staniford Sr, Boston, MA 02114 USA Harvard Univ 20 Staniford Sr Boston MA USA 02114 ton, MA 02114 USA
Citazione:
K.P. Xu et al., "A role for MAP kinase in regulating ectodomain shedding of APLP2 in corneal epithelial cells", AM J P-CELL, 281(2), 2001, pp. C603-C614

Abstract

We previously reported an increased secretion of amyloid precursor-like protein 2 (APLP2) in the healing corneal epithelium. The present study soughtto investigate signal transduction pathways involved in APLP2 shedding in vitro. APLP2 was constitutively shed and released into culture medium in SV40-immortalized human corneal epithelial cells as assessed by Western blotting, flow cytometry, and indirect immunofluorescence. Activation of proteinkinase C (PKC) by phorbol 12-myristate 13-acetate (PMA) caused significantincreases in APLP2 shedding. This was inhibited by staurosporine and a PKC-epsilon -specific, N-myristoylated peptide inhibitor. Epidermal growth factor (EGF) also induced APLP2 accumulation in culture medium. Basal APLP2 shedding as well as that induced by PMA and EGF was blocked by a mitogen-activated protein kinase (MAPK) kinase inhibitor, U-0126. Our results suggest that MAPK activity accounts for basal as well as PKC- and EGF-induced APLP2 shedding. In addition, PKC-epsilon may be involved in the induction of APLP2 shedding in corneal epithelial cells.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/04/20 alle ore 20:50:59