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  • Chemistry  (1)
  • Heart ischemia  (1)
  • IN-VIVO  (1)
  • 1
    Abstract: Cancer cells showing low apoptotic effects following oxidative stress-induced DNA damage are mainly affected by growth arrest. Thus, recent studies focus on improving anti-cancer therapies by increasing apoptosis sensitivity. We aimed at identifying a universal molecule as potential target to enhance oxidative stress-based anti-cancer therapy through a switch from cell cycle arrest to apoptosis. A cDNA microarray was performed with hydrogen peroxide-treated oesophageal squamous epithelial cancer cells TE7. This cell line showed checkpoint activation via p21(WAF1) , but low apoptotic response following DNA damage. The potential target molecule was chosen depended on the following demands: it should regulate DNA damage response, cell cycle and apoptosis. As the transcription factor ATF2 is implicated in all these processes, we focused on this protein. We investigated checkpoint activation via ATF2. Indeed, ATF2 knockdown revealed ATF2-triggered p21(WAF1) protein expression, suggesting p21(WAF1) transactivation through ATF2. Using chromatin immunoprecipitation (ChIP), we identified a hitherto unknown ATF2-binding sequence in the p21(WAF1) promoter. p-ATF2 was found to interact with p-c-Jun, creating the AP-1 complex. Moreover, ATF2 knockdown led to c-Jun downregulation. This suggests ATF2-driven induction of c-Jun expression, thereby enhancing ATF2 transcriptional activity via c-Jun-ATF2 heterodimerization. Notably, downregulation of ATF2 caused a switch from cell cycle arrest to reinforced apoptosis, presumably via p21(WAF1) downregulation, confirming the importance of ATF2 in the establishment of cell cycle arrest. 1-Chloro-2,4-dinitrobenzene also led to ATF2-dependent G2/M arrest, suggesting that this is a general feature induced by oxidative stress. As ATF2 knockdown also increased apoptosis, we propose ATF2 as a target for combined oxidative stress-based anti-cancer therapies.
    Type of Publication: Journal article published
    PubMed ID: 23800081
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  • 2
    ISSN: 0044-2313
    Keywords: Chemistry ; Inorganic Chemistry
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology
    Description / Table of Contents: LCAO MO Calculations on Donor-Acceptor Complexes. II. Formation of Donor-Acceptor Complexes of Cyclic Anhydrides with Lewis AcidsComplex formation between succinic or maleic anhydride with SbCl5, AlCl3, AlBr3 has been investigated by means of IR and PMR spectroscopy. In molar ratios of donor to acceptor 1:1 and 1:2 complex formation is uncomplete. A cleavage of anhydride bond system is not observed. Only one oxygen atom of anhydride is complexed with Lewis acid. From CNDO/2 calculation it is suggested that an unsymmetrical complex structure is most stable.
    Notes: Die Komplexbildung zwischen Bernsteinsäure- sowie Maleinsäureanhydrid mit SbCl5, AlCl3 und AlBr3 wird IR- und 1H-NMR-spektroskopisch untersucht. Für molare Donator-Akzeptor-Mischungen von 1:1 und 1:2 bleibt die Komplexbildung unvollständig. Eine Spaltung des Anhydrid-Bindungssystems wird nicht beobachtet. Nur ein Sauerstoffatom des Anhydridmoleküls wird von der Lewissäure koordiniert. Nach CNDO/2 Berechnungen ist eine unsymmetrische Komplexstruktur am stabilsten.
    Additional Material: 1 Ill.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1912
    Keywords: Dog heart ; Beta-adrenoceptors ; Adenylate cyclase ; Heart ischemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We evaluated the effects of ischemic injury on the myocardial adenylate cyclase system, 5 h after ligation of the left anterior descending coronary in 5 anesthetized dogs. Crude cardiac membrane preparations were isolated from control and ischemic areas of ventricular myocardium and tested for: 1. L-(125I)iodocyanopindolol binding, in the absence and presence of ±-isoprenaline and GTP, and 2. adenylate cyclase activity. The density of beta-adrenoceptors increased by 35% in membranes from ischemic areas while the proportion of receptors in a high affinity state for ±-isoprenaline decreased from 43% to 20%. Adenylate cyclase activities in the basal state and under stimulation with NaF, forskolin, Gpp(NH)p, ±-isoprenaline and VIP were all markedly and similarly reduced, being only about 30% of comparable activities in membranes from control areas. The ±-isoprenaline subsensitivity of cardiac adenylate cyclase can, thus, be attributed to a defective enzymatic system and not to a reduction in the number of beta-adrenoceptors implying that the internal components of the system were more sensitive to acute ischemia than the outward oriented hormone receptors. It is tempting to ascribe this uncoupling to a functional depletion in the guanine nucleotide-binding regulatory protein Ns that might reflect a loss of high energy phosphate stores including GTP.
    Type of Medium: Electronic Resource
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