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Lawson Tait 《BMJ (Clinical research ed.)》1888,2(1460):1416-1417
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Bcl-2 family member Bfl-1/A1 sequesters truncated bid to inhibit is collaboration with pro-apoptotic Bak or Bax 总被引:11,自引:0,他引:11
Werner AB de Vries E Tait SW Bontjer I Borst J 《The Journal of biological chemistry》2002,277(25):22781-22788
Following caspase-8 mediated cleavage, a carboxyl-terminal fragment of the BH3 domain-only Bcl-2 family member Bid transmits the apoptotic signal from death receptors to mitochondria. In a screen for possible regulators of Bid, we defined Bfl-1/A1 as a potent Bid interacting protein. Bfl-1 is an anti-apoptotic Bcl-2 family member, whose preferential expression in hematopoietic cells and endothelium is controlled by inflammatory stimuli. Its mechanism of action is unknown. We find that Bfl-1 associates with both full-length Bid and truncated (t)Bid, via the Bid BH3 domain. Cellular expression of Bfl-1 confers protection against CD95- and Trail receptor-induced cytochrome c release. In vitro assays, using purified mitochondria and recombinant proteins, demonstrate that Bfl-1 binds full-length Bid, but does not interfere with its processing by caspase-8, or with its mitochondrial association. Confocal microscopy supports that Bfl-1, which at least in part constitutively localizes to mitochondria, does not impede tBid translocation. However, Bfl-1 remains tightly and selectively bound to tBid and blocks collaboration between tBid and Bax or Bak in the plane of the mitochondrial membrane, thereby preventing mitochondrial apoptotic activation. Lack of demonstrable interaction between Bfl-1 and Bak or Bax in the mitochondrial membrane suggests that Bfl-1 generally prevents the formation of a pro-apoptotic complex by sequestering BH3 domain-only proteins. 相似文献
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MJ Allen K Tait M Mühling K Weynberg C Bradley U Trivedi K Gharbi J Nissimov K Mavromatis CN Jensen G Grogan ST Ali 《Journal of bacteriology》2012,194(17):4753-4754
Stenotrophomonas maltophilia PML168 was isolated from Wembury Beach on the English Coast from a rock pool following growth and selection on agar plates. Here we present the permanent draft genome sequence, which has allowed prediction of function for several genes encoding enzymes relevant to industrial biotechnology, including a novel flavoprotein monooxygenase. 相似文献
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Anna L. Koessinger Catherine Cloix Dominik Koessinger Dieter Henrik Heiland Florian J. Bock Karen Strathdee Kevin Kinch Laura Martínez-Escard Nikki R. Paul Colin Nixon Gaurav Malviya Mark R. Jackson Kirsteen J. Campbell Katrina Stevenson Sandeep Davis Yassmin Elmasry Asma Ahmed Jim OPrey Gabriel Ichim Oliver Schnell William Stewart Karen Blyth Kevin M. Ryan Anthony J. Chalmers Jim C. Norman Stephen W. G. Tait 《Cell death and differentiation》2022,29(10):2089
Glioblastoma (GBM) is the most prevalent malignant primary brain tumour in adults. GBM typically has a poor prognosis, mainly due to a lack of effective treatment options leading to tumour persistence or recurrence. We investigated the therapeutic potential of targeting anti-apoptotic BCL-2 proteins in GBM. Levels of anti-apoptotic BCL-xL and MCL-1 were consistently increased in GBM compared with non-malignant cells and tissue. Moreover, we found that relative to their differentiated counterparts, patient-derived GBM stem-like cells also displayed higher expression of anti-apoptotic BCL-2 family members. High anti-apoptotic BCL-xL and MCL-1 expression correlated with heightened susceptibility of GBM to BCL-2 family protein-targeting BH3-mimetics. This is indicative of increased apoptotic priming. Indeed, GBM displayed an obligate requirement for MCL-1 expression in both tumour development and maintenance. Investigating this apoptotic sensitivity, we found that sequential inhibition of BCL-xL and MCL-1 led to robust anti-tumour responses in vivo, in the absence of overt toxicity. These data demonstrate that BCL-xL and MCL-1 pro-survival function is a fundamental prerequisite for GBM survival that can be therapeutically exploited by BH3-mimetics.Subject terms: Cancer genetics, Cell biology 相似文献
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The economic importance of bovine theilerioses has prompted several new approaches to understanding the diseases in the hope of developing more efficient methods of control. Most Theileria species that infect cattle cause a lymphoproli ferative disease. Sporozoites, injected into the host bloodstream by the tick vectors, rapidly invade host lymphocytes and stimulate rapid division of infected cells. As these rupture, merozoites are released which invade red blood cells ready to infect feeding ticks again. The process by which Theileria parasites can control host lymphocytes, and induce them to divide in synchrony with the parasites themselves, is poorly understood but seems to be the key to pathogenesis. In this article, Michael Dyer and Andrew Tait discuss the possible mechanisms of cellular control in the light of recent work revealing sequences homologous to oncogenes in the DNA of T. annulata. 相似文献
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