PKC "epsilon" and PKC "beta" are required for egf-mediated prevention of acetaldehyde-induced disruption of tight junction

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Seth, A

Sheth, P

Rao, R

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GASTROENTEROLOGY | 2005年 / 128卷 / 04期

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R57 [消化系及腹部疾病];

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页码：A490 / A490

页数：1

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[1] EGF activates Pkcβ1 and Pkcε by PLCγ and calcium-dependent mechanisms, and prevents acetaldehyde-induced disruption of tight junctions
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[3] L-glutamine-mediated prevention of acetaldehyde-induced disruption of tight junction involves C-Src, Metalloproteases (mmp) and ligand binding domain of Egf receptor (EGFR)
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[4] C-Src prevents acetaldehyde-induced disruption of tight junction, contrary to its requirement in the disruption of tight junction by hydrogen peroxide
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[5] ETHANOL-MEDIATED SENSITIZATION OF ACETALDEHYDE-INDUCED DISRUPTION OF INTESTINAL EPITHELIAL TIGHT JUNCTIONS
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[6] MAP kinase and PKC are independently involved in the mechanism of epidermal growth factor (EGF)-mediated prevention of oxidative stress-induced disruption of tight junctions
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[7] MAR interacts with occludin and mediates EGF-induced prevention of tight junction disruption by hydrogen peroxide
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[8] TLR4/PKC-mediated tight junction modulation: A clinical marker of chemotherapy-induced gut toxicity?
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[9] Role of phospholipase Cγ-induced activation of protein kinase C ε (PKCε) and PKCβI in epidermal growth factor-mediated protection of tight junctions from acetaldehyde in caco-2 cell monolayers
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[10] ATYPICAL PKCζ ACTIVITY AND RECRUITMENT TO PEDESTALS CONTRIBUTES TO AND PRECEDES TIGHT JUNCTION DISRUPTION INDUCED BY ENTEROPATHOGENIC ESCHERICHIA COLI (EPEC) INFECTION OF INTESTINAL EPITHELIAL CELLS
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