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S100A8/9 induces ce...
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Ghavami, SaeidDepartment of Biochemistry and Medical Genetics, Manitoba Institute of Cell Biology, Cancer Care Manitoba, Winnipeg, Manitoba, Canada
(författare)
S100A8/9 induces cell death via a novel, RAGE-independent pathway that involves selective release of Smac/DIABLO and Omi/HtrA2
- Artikel/kapitelEngelska2008
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Elsevier,2008
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LIBRIS-ID:oai:DiVA.org:liu-86930
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https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-86930URI
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https://doi.org/10.1016/j.bbamcr.2007.10.015DOI
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Språk:engelska
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Sammanfattning på:engelska
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AbbreviationsΔΨm, mitochondrial membrane potential; AIF, apoptosis-inducing factor; BH3, Bcl2 homology 3; BNIP3, Bcl2/adenovirus E1B 19 kD-interacting protein 3; DD, death domain; DED, death effector domain; DISC, death inducing signaling complex; Drp, dynamin-related protein; DTPA, diethylene triamine pentaacetate; Endo G, endonuclease G; FADD, Fas-Associated Death Domain; FADD-DN, dominant-negative FADD mutant; HtrA2, high-temperature requirement A2; IAPs, inhibitors of apoptosis; IM, inner membrane; JC-1, 5,5′,6,6′-tetrachloro-1,1′,3,3′-tetraethylbenzimidazolylcarbocyanine iodide; MTT, 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide; RAGE, receptor for advanced glycation endproducts; ROS, reactive oxygen species; Smac/DIABLO, second mitochondrial activator of caspases/direct inhibitor of apoptosis binding protein of low PI; XIAP, X-linked inhibitor of apoptosis
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A complex of two S100 EF-hand calcium-binding proteins S100A8/A9 induces apoptosis in various cells, especially tumor cells. Using several cell lines, we have shown that S100A8/A9-induced cell death is not mediated by the receptor for advanced glycation endproducts (RAGE), a receptor previously demonstrated to engage S100 proteins. Investigation of cell lines either deficient in, or over-expressing components of the death signaling machinery provided insight into the S100A8/A9-mediated cell death pathway. Treatment of cells with S100A8/A9 caused a rapid decrease in the mitochondrial membrane potential (ΔΨm) and activated Bak, but did not cause release of apoptosis-inducing factor (AIF), endonuclease G (Endo G) or cytochrome c. However, both Smac/DIABLO and Omi/HtrA2 were selectively released into the cytoplasm concomitantly with a decrease in Drp1 expression, which inhibits mitochondrial fission machinery. S100A8/A9 treatment also resulted in decreased expression of the anti-apoptotic proteins Bcl2 and Bcl-XL, whereas expression of the pro-apoptotic proteins Bax, Bad and BNIP3 was not altered. Over-expression of Bcl2 partially reversed the cytotoxicity of S100A8/A9. Together, these data indicate that S100A8/A9-induced cell death involves Bak, selective release of Smac/DIABLO and Omi/HtrA2 from mitochondria, and modulation of the balance between pro- and anti-apoptotic proteins.
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Kerkhoff, ClausInstitute of Experimental Dermatology, Münster, Germany
(författare)
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Chazin, Walter J.Department of Biochemistry Vanderbilt University, Nashville, USA; Department of Chemistry, Vanderbilt University, Nashville, USA; Center for Structural Biology, Vanderbilt University, Nashville, TN 37232-8725, USA
(författare)
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Kadhoka, KamranManitoba Institute of Cell Biology, Canada; Department of Biochemistry and Medical Genetics, University of Manitoba, Winnipeg, Canada
(författare)
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Xiao, WenyanManitoba Institute of Cell Biology, Canada
(författare)
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Zusea, AnneManitoba Institute of Cell Biology, Canada; Department of Biochemistry and Medical Genetics, University of Manitoba, Winnipeg, Canada
(författare)
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Hashemi, MohammadDepartment of Clinical Biochemistry, School of Medicine, Zahedan University of Medical Science, Zahedan, Iran
(författare)
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Eshraghi, MehdiManitoba Institute of Cell Biology, Canada b Department of Biochemistry and Medical Genetics, University of Manitoba, Winnipeg, Canada
(författare)
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Schulze-Osthoff, KlausInstitute of Molecular Medicine, University of Düsseldorf, Düsseldorf, Germany
(författare)
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Klonisch, ThomasDepartment of Human Anatomy and Cell Sciences, and Manitoba Institute of Child Health, Winnipeg, Canada
(författare)
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Los, Marek JanManitoba Institute of Cell Biology, Canada; Department of Biochemistry and Medical Genetics, University of Manitoba, Winnipeg, Canada; BioApplications Enterprises, Winnipeg, MB, Canada(Swepub:liu)marlo14
(författare)
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Department of Biochemistry and Medical Genetics, Manitoba Institute of Cell Biology, Cancer Care Manitoba, Winnipeg, Manitoba, CanadaInstitute of Experimental Dermatology, Münster, Germany
(creator_code:org_t)
Sammanhörande titlar
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Ingår i:Biochimica et Biophysica Acta. Molecular Cell Research: Elsevier1783:2, s. 297-3110167-48891879-2596
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Ghavami, Saeid
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