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  • 1
    Language: English
    In: Cell Communication and Signaling, March 13, 2012, Vol.10, p.7
    Description: Macroautophagy (commonly abbreviated as autophagy) is an evolutionary conserved lysosome-directed vesicular trafficking pathway in eukaryotic cells that mediates the lysosomal degradation of intracellular components. The cytoplasmic cargo is initially enclosed by a specific double membrane vesicle, termed the autophagosome. By this means, autophagy either helps to remove damaged organelles, long-lived proteins and protein aggregates, or serves as a recycling mechanism for molecular building blocks. Autophagy was once invented by unicellular organisms to compensate the fluctuating external supply of nutrients. In higher eukaryotes, it is strongly enhanced under various stress conditions, such as nutrient and growth factor deprivation or DNA damage. The serine/threonine kinase Atg1 was the first identified autophagy-related gene (ATG) product in yeast. The corresponding nematode homolog UNC-51, however, has additional neuronal functions. Vertebrate genomes finally encode five closely related kinases, of which UNC-51-like kinase 1 (Ulk1) and Ulk2 are both involved in the regulation of autophagy and further neuron-specific vesicular trafficking processes. This review will mainly focus on the vertebrate Ulk1/2-Atg13-FIP200 protein complex, its function in autophagy initiation, its evolutionary descent from the yeast Atg1-Atg13-Atg17 complex, as well as the additional non-autophagic functions of its components. Since the rapid nutrient- and stress-dependent cellular responses are mainly mediated by serine/threonine phosphorylation, it will summarize our current knowledge about the relevant upstream signaling pathways and the altering phosphorylation status within this complex during autophagy induction.
    Keywords: Autophagy (Cytology) -- Research ; Protein Kinases -- Physiological Aspects ; Protein Kinases -- Research ; Phosphorylation -- Research
    ISSN: 1478-811X
    Source: Cengage Learning, Inc.
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  • 2
    Language: English
    In: Current Biology, 11 January 2011, Vol.21(1), pp.96-96
    Keywords: Biology
    ISSN: 0960-9822
    E-ISSN: 1879-0445
    Source: ScienceDirect Journals (Elsevier)
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  • 3
    Language: English
    In: Current Biology, Nov 9, 2010, Vol.20(21), p.R940-R942
    Description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.cub.2010.09.066 Byline: Christoph Peter (1), Sebastian Wesselborg (1), Kirsten Lauber (2) Abstract: Extracellular nucleotides have been reported to act as a 'find-me' signal in the context of phagocyte recruitment by apoptotically dying cells. A new study now examines the mechanisms of nucleotide release during apoptosis and describes the hemichannel-forming protein pannexin 1 as a crucial player in this scenario. Author Affiliation: (1) Dept. of Internal Medicine I, Eberhard-Karls-University of Tuebingen, Otfried-Mueller-Str. 10, D-72076 Tuebingen, Germany (2) Dept. of Radiation Oncology, Ludwig-Maximilians-University of Munich, Marchioninistr. 15, D-81377 Munich, Germany
    Keywords: Cytological Research ; Apoptosis
    ISSN: 0960-9822
    Source: Cengage Learning, Inc.
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  • 4
    Language: English
    In: Cellular and Molecular Life Sciences, 2015, Vol.72(24), pp.4721-4757
    Description: Autophagy represents an intracellular degradation process which is involved in both cellular homeostasis and disease settings. In the last two decades, the molecular machinery governing this process has been characterized in detail. To date, several key factors regulating this intracellular degradation process have been identified. The so-called autophagy-related (ATG) genes and proteins are central to this process. However, several additional molecules contribute to the outcome of an autophagic response. Several review articles describing the molecular process of autophagy have been published in the recent past. In this review article we would like to add the most recent findings to this knowledge, and to give an overview of the network character of the autophagy signaling machinery.
    Keywords: Autophagy ; ATG ; ULK ; PtdIns3K ; LC3
    ISSN: 1420-682X
    E-ISSN: 1420-9071
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  • 5
    Language: English
    In: Current Biology, 09 November 2010, Vol.20(21), pp.R940-R942
    Description: Extracellular nucleotides have been reported to act as a ‘find-me’ signal in the context of phagocyte recruitment by apoptotically dying cells. A new study now examines the mechanisms of nucleotide release during apoptosis and describes the hemichannel-forming protein pannexin 1 as a crucial player in this scenario.
    Keywords: Biology
    ISSN: 0960-9822
    E-ISSN: 1879-0445
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  • 6
    Language: English
    In: Cell Communication and Signaling, March 13, 2012, Vol.10, p.7
    Description: Macroautophagy (commonly abbreviated as autophagy) is an evolutionary conserved lysosome-directed vesicular trafficking pathway in eukaryotic cells that mediates the lysosomal degradation of intracellular components. The cytoplasmic cargo is initially enclosed by a specific double membrane vesicle, termed the autophagosome. By this means, autophagy either helps to remove damaged organelles, long-lived proteins and protein aggregates, or serves as a recycling mechanism for molecular building blocks. Autophagy was once invented by unicellular organisms to compensate the fluctuating external supply of nutrients. In higher eukaryotes, it is strongly enhanced under various stress conditions, such as nutrient and growth factor deprivation or DNA damage. The serine/threonine kinase Atg1 was the first identified autophagy-related gene (ATG) product in yeast. The corresponding nematode homolog UNC-51, however, has additional neuronal functions. Vertebrate genomes finally encode five closely related kinases, of which UNC-51-like kinase 1 (Ulk1) and Ulk2 are both involved in the regulation of autophagy and further neuron-specific vesicular trafficking processes. This review will mainly focus on the vertebrate Ulk1/2-Atg13-FIP200 protein complex, its function in autophagy initiation, its evolutionary descent from the yeast Atg1-Atg13-Atg17 complex, as well as the additional non-autophagic functions of its components. Since the rapid nutrient- and stress-dependent cellular responses are mainly mediated by serine/threonine phosphorylation, it will summarize our current knowledge about the relevant upstream signaling pathways and the altering phosphorylation status within this complex during autophagy induction.
    Keywords: Autophagy (Cytology) -- Research ; Protein Kinases -- Physiological Aspects ; Protein Kinases -- Research ; Phosphorylation -- Research
    ISSN: 1478-811X
    Source: Cengage Learning, Inc.
    Library Location Call Number Volume/Issue/Year Availability
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  • 7
    Language: English
    In: The Journal of organic chemistry, 20 December 2013, Vol.78(24), pp.12409-25
    Description: Four tetrahydroxanthone dimers (1-4) and four biogenetically related monomers (5-8), including the new derivatives 4-6, were isolated from the endophyte Phomopsis longicolla. The absolute configurations of 2-4 were established for the first time by TDDFT electronic circular dichroism calculations, and that of phomoxanthone A (1) was revised by X-ray crystallography. Phomoxanthone A (1) showed the strongest pro-apoptotic activity when tested against a panel of human cancer cell lines, including cisplatin-resistant cells, whereas it was up to 100-fold less active against healthy blood cells. It was also the most potent activator of murine T lymphocytes, NK cells, and macrophages, suggesting an activation of the immune system in parallel to its pro-apoptotic activity. This dual effect in combating cancer cells could help in fighting resistance during chemotherapy. Preliminary structure-activity studies of isolated compounds and derivatives obtained by semisynthesis (9a-11) hinted at the location of the biaryl axis and the presence of acetyl groups as important structural elements for the biological activity of the studied tetrahydroxanthones.
    Keywords: Antineoplastic Agents -- Pharmacology ; Apoptosis -- Drug Effects ; Ascomycota -- Chemistry ; Xanthones -- Pharmacology
    ISSN: 00223263
    E-ISSN: 1520-6904
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  • 8
    Language: English
    In: Gut, 23 February 2011, Vol.60(2), p.156
    Description: The cytokine tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) has shown promising anticancer activity in early clinical settings by selectively inducing apoptosis in different tumour types. However, some tumour entities such as hepatocellular carcinoma (HCC) display an inherent resistance to TRAIL. A huge effort has been made to unravel strategies for a clinically applicable sensitisation of resistant cancer cells to TRAIL. Reversible epigenetic alterations such as DNA methylation play a major role in development, maintenance and resistance phenomena of tumour cells. Currently, several clinical trials are exploiting the potential of epigenetic drugs, such as 5-azacytidine (5-aza-CR) or 5-aza-2′-deoxycytidine (5-aza-dC) to break primary or secondary resistance phenomena of cancer cells. Therefore, 5-aza-CR and 5-aza-dC were investigated in the context of TRAIL resistance.
    Keywords: Apoptosis ; Cancer ; Hepatobiliary Cancer ; Hepatocellular Carcinoma ; Liver
    ISSN: 0017-5749
    ISSN: 00175749
    E-ISSN: 1468-3288
    E-ISSN: 14683288
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  • 9
    Language: English
    In: Organic letters, 03 January 2014, Vol.16(1), pp.266-9
    Description: A novel macrolide, callyspongiolide, whose structure was determined by comprehensive analysis of the NMR and HRMS spectra, was isolated from the marine sponge Callyspongia sp. collected in Indonesia. The compound features a carbamate-substituted 14-membered macrocyclic lactone ring with a conjugated structurally unprecedented diene-ynic side chain terminating at a brominated benzene ring. Callyspongiolide showed strong cytotoxicity against human Jurkat J16 T and Ramos B lymphocytes.
    Keywords: B-Lymphocytes -- Drug Effects ; Callyspongia -- Chemistry ; Macrolides -- Pharmacology
    ISSN: 15237060
    E-ISSN: 1523-7052
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  • 10
    Language: English
    In: PLoS ONE, 01 January 2017, Vol.12(5), p.e0177450
    Description: Excessive neutrophil activation accompanied by delayed apoptotic cell death in inflammatory conditions causes progressive damage of cells and tissues, leading to life-threatening multiple organ dysfunction syndrome. Previous work suggested that circulating serum factors during inflammation are critically involved in the suppression of neutrophil cell death although the identity of these antiapoptotic mediators remained elusive. In this study, we identified the acute phase protein α-1 Antitrypsin (AAT) as a potent suppressor of staurosporine (STS)-induced apoptosis in human neutrophils through a mechanism implicating caspases-independent pathways. We show here that serum levels of AAT, potentially in part released by stimulated neutrophils, are markedly elevated in major trauma patients suffering from systemic inflammatory response syndrome (SIRS). Notably, AAT depletion from serum increased sensitivity of human neutrophils for STS-induced cell death. In fact, AAT was demonstrated to confer intrinsic apoptosis resistance by preventing PKC/Akt inactivation and subsequent proteasomal degradation of antiapoptotic Mcl-1 protein in response to STS treatment. Neither MAP kinase ERK1/2 nor caspases were found to be involved in AAT-triggered antiapoptotic pathways in neutrophils. In summary, these results establish a novel pivotal role of circulating AAT in mediating survival by antagonizing the proapoptotic action of the PKC inhibitor STS and should be considered for AAT augmentation therapies in future.
    Keywords: Sciences (General)
    E-ISSN: 1932-6203
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