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Fas Ag-FasL coupling leads to ERK1/2-mediated proliferation of gastric mucosal cells.

Fas Ag-FasL coupling leads to ERK1/2-mediated proliferation of gastric mucosal cells. Research Abstract Details 

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  • Fas Ag-FasL coupling leads to ERK1/2-mediated proliferation of gastric mucosal cells. Abstract Text:

    hanchen liHanchen Li,xun caiXun Cai,xueli fanXueli Fan,brian moquinBrian Moquin,calin stoicovCalin Stoicov,jeanmarie houghtonJeanmarie Houghton,hanchen liHanchen Li,xun caiXun Cai,xueli fanXueli Fan,brian moquinBrian Moquin,calin stoicovCalin Stoicov,jeanmarie houghtonJeanmarie Houghton,hanchen liHanchen Li,xun caiXun Cai,xueli fanXueli Fan,brian moquinBrian Moquin,calin stoicovCalin Stoicov,jeanmarie houghtonJeanmarie Houghton,

    When cells within the gastric mucosa progress from metaplasia to dysplasia to cancer, they acquire a Fas Ag apoptosis-resistant phenotype. It is unusual to completely abolish the pathway, suggesting other forms of Fas Ag signaling may be important or even necessary for gastric cancer to progress. Little is known about alternate signaling of the Fas Ag pathway in gastric mucosal cells. Using a cell culture model of rat gastric mucosal cells, we show that gastric mucosal cells utilize a type II signaling pathway for apoptosis. Under conditions of low receptor stimulation or under conditions where apoptosis is blocked downstream of the death-inducing signal complex, Fas Ag signaling proceeds toward proliferative signaling. Under conditions favoring proliferative signaling, cFLIP is recruited to the Fas-associated death domain-like interleukin-1beta-converting enzyme at the death-inducing signal complex and activates ERK1/2. ERK1/2 in turn activates NF-kappaB. ERK1/2 stimulates proliferation, whereas NF-kappaB activation results in upregulation of the antiapoptotic protein survivin, further promoting proliferation over apoptosis. These results suggest that factors that inhibit apoptosis confer a growth advantage to the cells beyond the survival advantage of avoiding apoptosis and in effect convert the Fas Ag signaling pathway from a tumor suppressor to a tumor promoter.

    Fas Ag-FasL coupling leads to ERK1/2-mediated proliferation of gastric mucosal cells. Publishing Authors By Initials

    h liH Li,x caiX Cai,x fanX Fan,b moquinB Moquin,c stoicovC Stoicov,j houghtonJ Houghton,h liH Li,x caiX Cai,x fanX Fan,b moquinB Moquin,c stoicovC Stoicov,j houghtonJ Houghton,h liH Li,x caiX Cai,x fanX Fan,b moquinB Moquin,c stoicovC Stoicov,j houghtonJ Houghton,

    For similar abstracts research abstracts see: abstracts research

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    Fas Ag-FasL coupling leads to ERK1/2-mediated proliferation of gastric mucosal cells. Journal Published:

    PUBLICATION TYPE: Journal Article

    Journal: American journal of physiology. Gastrointestinal a

    VOLUME: 294

    Page Numbers: G263-75

    Journal Abbreviation: Am. J. Physiol. Gastrointest.

    ISSN: 0193-1857

    DAY: 8

    MONTH: 11

    YEAR: 2007

    Fas Ag-FasL coupling leads to ERK1/2-mediated proliferation of gastric mucosal cells. Information

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    LANGUAGE: eng

    NlmUniqueID: 100901227

    Fas Ag-FasL coupling leads to ERK1/2-mediated proliferation of gastric mucosal cells. Keywords Mesh Terms:

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    Grant and Affiliation Information for Fas Ag-FasL coupling leads to ERK1/2-mediated proliferation of gastric mucosal cells.

    AFFILIATION: Dept. of Medicine, Univ. of Massachusetts Medical School, LRB 209, 364 Plantation St., Worcester MA 01605. jeanmarie.houghton@umassmed.edu).

    Country: United States

    United States Research PublicationUnited States Research Publication

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    MEDLINETA: Am J Physiol Gastrointest Live

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