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Keywords {🔍}

cell, pik, hiec, cells, survival, fig, article, google, scholar, isoform, pubmed, akt, complexes, cas, activation, signaling, isoforms, cultures, anoikis, expression, fak, src, control, sipβ, roles, pαpβ, pαpγ, regulation, activity, sipγ, cancer, apoptosis, engagement, human, selective, suppression, specific, inhibition, intestinal, kinase, significant, differences, sipα, andor, suspension, treated, analyses, epithelial, subunit, expressed,

Topics {✒️}

acetyl asp-glu-val-asp 7-amido-4-methylcoumarin integrin β1/fak/src-mediated signaling β1 integrin/fak/src-mediated signaling integrin β1/fak/src-mediated regulation β1 integrin/fak/src-mediated suppression integrin β1/fak/src-mediated suppression β1 integrin/fak/pi3-k-dependent β1 integrin/fak-mediated signaling integrin/fak/src-mediated signaling β1 integrin/fak/src signaling integrin β1/fak/src signaling β1 integrin/fak/src-signaling integrin-regulated fak-src signaling fak/src-mediated signaling cassettes integrin/fak/src-mediated regulation β1 integrin/fak-dependent extensive caspase-dependent apoptosis integrin/fak/src signaling platelet-derived growth factor �integrin-mediated cell death” isoform-specific pi3k signalling article download pdf egfr-mediated sustained activation additional proline-rich motif semi-quantitative rt-pcr analyses fak/src signaling cassettes sirna-mediated expression silencing differentiation state-specific uncoupling marie-josée demers & pierre serine-threonine kinase activity src-mediated phosphorylation substrate ac-devd-amc targeting pi3k signalling integrin signalling gmcsf-stimulated human neutrophils differentiation state-distinct regulation related subjects intestinal epithelial cells n-terminal sh2 domain �detachment-induced apoptosis-anoikis” de biologie cellulaire isel-positive cells counterstained human intestinal cells p4c10 blocking antibody caspase-activated dnase phosphatidylinositol 3-kinase alpha altogether pi3-k-independent [16–18 5 mm tris–hcl differentiation state-selective roles focal adhesion kinase

Questions {❓}

• Chen J (2008) Is Src the key to understanding metastasis and developing new treatments for colon cancer?
• Jia S, Roberts TM, Zhao JJ (2009) Should individual PI3 kinase isoforms be targeted in cancer?
• Ulukaya E, Acilan C, Yilmaz Y (2011) Apoptosis: why and how does it occur in biology?

Schema {🗺️}

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         headline:Integrin/Fak/Src-mediated regulation of cell survival and anoikis in human intestinal epithelial crypt cells: selective engagement and roles of PI3-K isoform complexes
         description:In human intestinal epithelial crypt (HIEC) cells, the PI3-K/Akt-1 pathway is crucial for the promotion of cell survival and suppression of anoikis. Class I PI3-K consists of a complex formed by a catalytic (C) and regulatory (R) subunit. Three R (p85α, β, and p55γ) and four C (p110α, β, γ and δ) isoforms are known. Herein, we analyzed the expression of PI3-K isoforms in HIEC cells and determined their roles in cell survival, as well as in the β1 integrin/Fak/Src-mediated suppression of anoikis. We report that: (1) the predominant PI3-K complexes expressed by HIEC cells are p110α/p85β and p110α/p55γ; (2) the inhibition and/or siRNA-mediated expression silencing of p110α, but not that of p110β, γ or δ, results in Akt-1 down-activation and consequent apoptosis; (3) the expression silencing of p85β or p55γ, but not that of p85α, likewise induces Akt-1 down-activation and apoptosis; however, the impact of a loss of p55γ on both Akt-1 activation and cell survival is significantly greater than that from the loss of p85β; and (4) both the p110α/p85β and p110α/p55γ complexes are engaged by β1 integrin/Fak/Src signaling; however, the engagement of p110α/p85β is primarily Src-dependent, whereas that of p110α/p55γ is primarily Fak-dependent (but Src-independent). Hence, HIEC cells selectively express PI3-K isoform complexes, translating into distinct roles in Akt-1 activation and cell survival, as well as in a selective engagement by Fak and/or Src within the context of β1 integrin/Fak/Src-mediated suppression of anoikis.
         datePublished:2012-03-09T00:00:00Z
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      headline:Integrin/Fak/Src-mediated regulation of cell survival and anoikis in human intestinal epithelial crypt cells: selective engagement and roles of PI3-K isoform complexes
      description:In human intestinal epithelial crypt (HIEC) cells, the PI3-K/Akt-1 pathway is crucial for the promotion of cell survival and suppression of anoikis. Class I PI3-K consists of a complex formed by a catalytic (C) and regulatory (R) subunit. Three R (p85α, β, and p55γ) and four C (p110α, β, γ and δ) isoforms are known. Herein, we analyzed the expression of PI3-K isoforms in HIEC cells and determined their roles in cell survival, as well as in the β1 integrin/Fak/Src-mediated suppression of anoikis. We report that: (1) the predominant PI3-K complexes expressed by HIEC cells are p110α/p85β and p110α/p55γ; (2) the inhibition and/or siRNA-mediated expression silencing of p110α, but not that of p110β, γ or δ, results in Akt-1 down-activation and consequent apoptosis; (3) the expression silencing of p85β or p55γ, but not that of p85α, likewise induces Akt-1 down-activation and apoptosis; however, the impact of a loss of p55γ on both Akt-1 activation and cell survival is significantly greater than that from the loss of p85β; and (4) both the p110α/p85β and p110α/p55γ complexes are engaged by β1 integrin/Fak/Src signaling; however, the engagement of p110α/p85β is primarily Src-dependent, whereas that of p110α/p55γ is primarily Fak-dependent (but Src-independent). Hence, HIEC cells selectively express PI3-K isoform complexes, translating into distinct roles in Akt-1 activation and cell survival, as well as in a selective engagement by Fak and/or Src within the context of β1 integrin/Fak/Src-mediated suppression of anoikis.
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         Fak
         HIEC
         PI3-K
         Src
         Survival
         Cancer Research
         Cell Biology
         Oncology
         Biochemistry
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      name:Département d’anatomie et de Biologie Cellulaire, Faculté de Médecine et des Sciences de la Santé, Université de Sherbrooke, Sherbrooke, Canada

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