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  1. Article ; Online: Observational study investigating Tolerance Of Anticancer Systemic Therapy In the Elderly (TOASTIE)

    Sarah Taylor / Eleanor Smith / Christopher Mark Jones / Daniel Swinson / Mark A Baxter / Fiona Smith / R D Petty / Helen Dearden / Sally Martin / Michael Rowe / Kieran Zucker / Anna C Olsson-Brown / Clair Brunner / Anna Lewis / Lisa Rodgers / Anthea Cree

    BMJ Open, Vol 11, Iss

    a protocol

    2021  Volume 9

    Keywords Medicine ; R
    Language English
    Publishing date 2021-09-01T00:00:00Z
    Publisher BMJ Publishing Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: Quantitative analysis of lipid droplet fusion

    Samantha Murphy / Sally Martin / Robert G Parton

    PLoS ONE, Vol 5, Iss 12, p e

    inefficient steady state fusion but rapid stimulation by chemical fusogens.

    2010  Volume 15030

    Abstract: Lipid droplets (LDs) are dynamic cytoplasmic organelles containing neutral lipids and bounded by a phospholipid monolayer. Previous studies have suggested that LDs can undergo constitutive homotypic fusion, a process linked to the inhibitory effects of ... ...

    Abstract Lipid droplets (LDs) are dynamic cytoplasmic organelles containing neutral lipids and bounded by a phospholipid monolayer. Previous studies have suggested that LDs can undergo constitutive homotypic fusion, a process linked to the inhibitory effects of fatty acids on glucose transporter trafficking. Using strict quantitative criteria for LD fusion together with refined light microscopic methods and real-time analysis, we now show that LDs in diverse cell types show low constitutive fusogenic activity under normal growth conditions. To investigate the possible modulation of LD fusion, we screened for agents that can trigger fusion. A number of pharmacological agents caused homotypic fusion of lipid droplets in a variety of cell types. This provided a novel cell system to study rapid regulated fusion between homotypic phospholipid monolayers. LD fusion involved an initial step in which the two adjacent membranes became continuous (<10 s), followed by the slower merging (100 s) of the neutral lipid cores to produce a single spherical LD. These fusion events were accompanied by changes to the LD surface organization. Measurements of LDs undergoing homotypic fusion showed that fused LDs maintained their initial volume, with a corresponding decrease in surface area suggesting rapid removal of membrane from the fused LD. This study provides estimates for the level of constitutive LD fusion in cells and questions the role of LD fusion in vivo. In addition, it highlights the extent of LD restructuring which occurs when homotypic LD fusion is triggered in a variety of cell types.
    Keywords Medicine ; R ; Science ; Q
    Subject code 571
    Language English
    Publishing date 2010-12-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Inhibition of PIKfyve by YM-201636 dysregulates autophagy and leads to apoptosis-independent neuronal cell death.

    Sally Martin / Callista B Harper / Linda M May / Elizabeth J Coulson / Frederic A Meunier / Shona L Osborne

    PLoS ONE, Vol 8, Iss 3, p e

    2013  Volume 60152

    Abstract: The lipid phosphatidylinositol 3,5-bisphosphate (PtdIns(3,5)P 2), synthesised by PIKfyve, regulates a number of intracellular membrane trafficking pathways. Genetic alteration of the PIKfyve complex, leading to even a mild reduction in PtdIns(3,5)P 2, ... ...

    Abstract The lipid phosphatidylinositol 3,5-bisphosphate (PtdIns(3,5)P 2), synthesised by PIKfyve, regulates a number of intracellular membrane trafficking pathways. Genetic alteration of the PIKfyve complex, leading to even a mild reduction in PtdIns(3,5)P 2, results in marked neurodegeneration via an uncharacterised mechanism. In the present study we have shown that selectively inhibiting PIKfyve activity, using YM-201636, significantly reduces the survival of primary mouse hippocampal neurons in culture. YM-201636 treatment promoted vacuolation of endolysosomal membranes followed by apoptosis-independent cell death. Many vacuoles contained intravacuolar membranes and inclusions reminiscent of autolysosomes. Accordingly, YM-201636 treatment increased the level of the autophagosomal marker protein LC3-II, an effect that was potentiated by inhibition of lysosomal proteases, suggesting that alterations in autophagy could be a contributing factor to neuronal cell death.
    Keywords Medicine ; R ; Science ; Q
    Language English
    Publishing date 2013-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: High-throughput screening of Australian marine organism extracts for bioactive molecules affecting the cellular storage of neutral lipids.

    James Rae / Frank Fontaine / Angela A Salim / Harriet P Lo / Robert J Capon / Robert G Parton / Sally Martin

    PLoS ONE, Vol 6, Iss 8, p e

    2011  Volume 22868

    Abstract: Mammalian cells store excess fatty acids as neutral lipids in specialised organelles called lipid droplets (LDs). Using a simple cell-based assay and open-source software we established a high throughput screen for LD formation in A431 cells in order to ... ...

    Abstract Mammalian cells store excess fatty acids as neutral lipids in specialised organelles called lipid droplets (LDs). Using a simple cell-based assay and open-source software we established a high throughput screen for LD formation in A431 cells in order to identify small bioactive molecules affecting lipid storage. Screening an n-butanol extract library from Australian marine organisms we identified 114 extracts that produced either an increase or a decrease in LD formation in fatty acid-treated A431 cells with varying degrees of cytotoxicity. We selected for further analysis a non-cytotoxic extract derived from the genus Spongia (Heterofibria). Solvent partitioning, HPLC fractionation and spectroscopic analysis (NMR, MS) identified a family of related molecules within this extract with unique structural features, a subset of which reduced LD formation. We selected one of these molecules, heterofibrin A1, for more detailed cellular analysis. Inhibition of LD biogenesis by heterofibrin A1 was observed in both A431 cells and AML12 hepatocytes. The activity of heterofibrin A1 was dose dependent with 20 µM inhibiting LD formation and triglyceride accumulation by ∼50% in the presence of 50 µM oleic acid. Using a fluorescent fatty acid analogue we found that heterofibrin A1 significantly reduces the intracellular accumulation of fatty acids and results in the formation of distinct fatty acid metabolites in both cultured cells and in embryos of the zebrafish Danio rerio. In summary we have shown using readily accessible software and a relatively simple assay system that we can identify and isolate bioactive molecules from marine extracts, which affect the formation of LDs and the metabolism of fatty acids both in vitro and in vivo.
    Keywords Medicine ; R ; Science ; Q
    Subject code 571
    Language English
    Publishing date 2011-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: Flux of signalling endosomes undergoing axonal retrograde transport is encoded by presynaptic activity and TrkB

    Tong Wang / Sally Martin / Tam H. Nguyen / Callista B. Harper / Rachel S. Gormal / Ramon Martínez-Mármol / Shanker Karunanithi / Elizabeth J. Coulson / Nick R. Glass / Justin J. Cooper-White / Bruno van Swinderen / Frédéric A. Meunier

    Nature Communications, Vol 7, Iss 1, Pp 1-

    2016  Volume 16

    Abstract: Signalling endosomes are known to be essential for neuronal survival. Here the authors show that, in cultured hippocampal neurons and live Drosophilalarval motor neurons, neuronal activity increases the retrograde flux of signalling endosomes, and this ... ...

    Abstract Signalling endosomes are known to be essential for neuronal survival. Here the authors show that, in cultured hippocampal neurons and live Drosophilalarval motor neurons, neuronal activity increases the retrograde flux of signalling endosomes, and this coupling depends on TrkB activation.
    Keywords Science ; Q
    Language English
    Publishing date 2016-09-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article ; Online: Correction

    Tong Wang / Sally Martin / Tam H. Nguyen / Callista B. Harper / Rachel S. Gormal / Ramon Martínez-Mármol / Shanker Karunanithi / Elizabeth J. Coulson / Nick R. Glass / Justin J. Cooper-White / Bruno van Swinderen / Frédéric A. Meunier

    Nature Communications, Vol 7, Iss 1, Pp 1-

    Corrigendum: Flux of signalling endosomes undergoing axonal retrograde transport is encoded by presynaptic activity and TrkB

    2016  Volume 1

    Abstract: Nature Communications 7: Article number: 12976 doi: (2016); Published: 30 September 2016; Updated: 23 November 2016 In Fig. 3 of this Article, an image attribution was inadvertently omitted. The drawing of a Drosophila larva in Fig. 3a is reproduced from ...

    Abstract Nature Communications 7: Article number: 12976 doi: (2016); Published: 30 September 2016; Updated: 23 November 2016 In Fig. 3 of this Article, an image attribution was inadvertently omitted. The drawing of a Drosophila larva in Fig. 3a is reproduced from the website http://www.prokop.co.uk/Research/Drosi-Info/nerve-cords.
    Keywords Science ; Q
    Language English
    Publishing date 2016-11-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article ; Online: Increased Polyubiquitination and Proteasomal Degradation of a Munc18-1 Disease-Linked Mutant Causes Temperature-Sensitive Defect in Exocytosis

    Sally Martin / Andreas Papadopulos / Vanesa M. Tomatis / Emma Sierecki / Nancy T. Malintan / Rachel S. Gormal / Nichole Giles / Wayne A. Johnston / Kirill Alexandrov / Yann Gambin / Brett M. Collins / Frederic A. Meunier

    Cell Reports, Vol 9, Iss 1, Pp 206-

    2014  Volume 218

    Abstract: Summary: Munc18-1 is a critical component of the core machinery controlling neuroexocytosis. Recently, mutations in Munc18-1 leading to the development of early infantile epileptic encephalopathy have been discovered. However, which degradative pathway ... ...

    Abstract Summary: Munc18-1 is a critical component of the core machinery controlling neuroexocytosis. Recently, mutations in Munc18-1 leading to the development of early infantile epileptic encephalopathy have been discovered. However, which degradative pathway controls Munc18-1 levels and how it impacts on neuroexocytosis in this pathology is unknown. Using neurosecretory cells deficient in Munc18, we show that a disease-linked mutation, C180Y, renders the protein unstable at 37°C. Although the mutated protein retains its function as t-SNARE chaperone, neuroexocytosis is impaired, a defect that can be rescued at a lower permissive temperature. We reveal that Munc18-1 undergoes K48-linked polyubiquitination, which is highly increased by the mutation, leading to proteasomal, but not lysosomal, degradation. Our data demonstrate that functional Munc18-1 levels are controlled through polyubiquitination and proteasomal degradation. The C180Y disease-causing mutation greatly potentiates this degradative pathway, rendering Munc18-1 unable to facilitate neuroexocytosis, a phenotype that is reversed at a permissive temperature. : Mutations in Munc18-1, an essential component of the machinery controlling neurotransmission, are linked to the development of early infantile epileptic encephalopathy (EIEE). In this study, Martin et al. show that one of these mutations, C180Y, results in a thermolabile protein with a strong propensity to aggregate. The level of Munc18-1C180Y is regulated by K48-linked polyubiquitination and proteasomal degradation. The impaired exocytic function of Munc18-1C180Y is rescued by growth at a permissive temperature. An imbalance in exocytosis could therefore underpin EIEE.
    Keywords Biology (General) ; QH301-705.5
    Subject code 570
    Language English
    Publishing date 2014-10-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  8. Article ; Online: Caveolin-1 deficiency leads to increased susceptibility to cell death and fibrosis in white adipose tissue

    Sally Martin / Manuel A Fernandez-Rojo / Amanda C Stanley / Michele Bastiani / Satomi Okano / Susan J Nixon / Gethin Thomas / Jennifer L Stow / Robert G Parton

    PLoS ONE, Vol 7, Iss 9, p e

    characterization of a lipodystrophic model.

    2012  Volume 46242

    Abstract: Caveolin-1 (CAV1) is an important regulator of adipose tissue homeostasis. In the present study we examined the impact of CAV1 deficiency on the properties of mouse adipose tissue both in vivo and in explant cultures during conditions of metabolic stress. ...

    Abstract Caveolin-1 (CAV1) is an important regulator of adipose tissue homeostasis. In the present study we examined the impact of CAV1 deficiency on the properties of mouse adipose tissue both in vivo and in explant cultures during conditions of metabolic stress. In CAV1(-/-) mice fasting caused loss of adipose tissue mass despite a lack of hormone-sensitive lipase (HSL) phosphorylation. In addition, fasting resulted in increased macrophage infiltration, enhanced deposition of collagen, and a reduction in the level of the lipid droplet protein perilipin A (PLIN1a). Explant cultures of CAV1(-/-) adipose tissue also showed a loss of PLIN1a during culture, enhanced secretion of IL-6, increased release of lactate dehydrogenase, and demonstrated increased susceptibility to cell death upon collagenase treatment. Attenuated PKA-mediated signaling to HSL, loss of PLIN1a and increased secretion of IL-6 were also observed in adipose tissue explants of CAV1(+/+) mice with diet-induced obesity. Together these results suggest that while alterations in adipocyte lipid droplet biology support adipose tissue metabolism in the absence of PKA-mediated pro-lipolytic signaling in CAV1(-/-) mice, the tissue is intrinsically unstable resulting in increased susceptibility to cell death, which we suggest underlies the development of fibrosis and inflammation during periods of metabolic stress.
    Keywords Medicine ; R ; Science ; Q
    Language English
    Publishing date 2012-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article ; Online: Co-regulation of cell polarization and migration by caveolar proteins PTRF/Cavin-1 and caveolin-1.

    Michelle M Hill / Noor Huda Daud / Cho Sanda Aung / Dorothy Loo / Sally Martin / Samantha Murphy / Debra M Black / Rachael Barry / Fiona Simpson / Libin Liu / Paul F Pilch / John F Hancock / Marie-Odile Parat / Robert G Parton

    PLoS ONE, Vol 7, Iss 8, p e

    2012  Volume 43041

    Abstract: Caveolin-1 and caveolae are differentially polarized in migrating cells in various models, and caveolin-1 expression has been shown to quantitatively modulate cell migration. PTRF/cavin-1 is a cytoplasmic protein now established to be also necessary for ... ...

    Abstract Caveolin-1 and caveolae are differentially polarized in migrating cells in various models, and caveolin-1 expression has been shown to quantitatively modulate cell migration. PTRF/cavin-1 is a cytoplasmic protein now established to be also necessary for caveola formation. Here we tested the effect of PTRF expression on cell migration. Using fluorescence imaging, quantitative proteomics, and cell migration assays we show that PTRF/cavin-1 modulates cellular polarization, and the subcellular localization of Rac1 and caveolin-1 in migrating cells as well as PKCα caveola recruitment. PTRF/cavin-1 quantitatively reduced cell migration, and induced mesenchymal epithelial reversion. Similar to caveolin-1, the polarization of PTRF/cavin-1 was dependent on the migration mode. By selectively manipulating PTRF/cavin-1 and caveolin-1 expression (and therefore caveola formation) in multiple cell systems, we unveil caveola-independent functions for both proteins in cell migration.
    Keywords Medicine ; R ; Science ; Q
    Language English
    Publishing date 2012-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  10. Article ; Online: Caveolin-1 Is Necessary for Hepatic Oxidative Lipid Metabolism

    Manuel A. Fernández-Rojo / Milena Gongora / Rebecca L. Fitzsimmons / Nick Martel / Sheree D. Martin / Susan J. Nixon / Andrew J. Brooks / Maria P. Ikonomopoulou / Sally Martin / Harriet P. Lo / Stephen A. Myers / Christina Restall / Charles Ferguson / Paul F. Pilch / Sean L. McGee / Robin L. Anderson / Michael J. Waters / John F. Hancock / Sean M. Grimmond /
    George E.O. Muscat / Robert G. Parton

    Cell Reports, Vol 4, Iss 2, Pp 238-

    Evidence for Crosstalk between Caveolin-1 and Bile Acid Signaling

    2013  Volume 247

    Abstract: Caveolae and caveolin-1 (CAV1) have been linked to several cellular functions. However, a model explaining their roles in mammalian tissues in vivo is lacking. Unbiased expression profiling in several tissues and cell types identified lipid metabolism as ...

    Abstract Caveolae and caveolin-1 (CAV1) have been linked to several cellular functions. However, a model explaining their roles in mammalian tissues in vivo is lacking. Unbiased expression profiling in several tissues and cell types identified lipid metabolism as the main target affected by CAV1 deficiency. CAV1−/− mice exhibited impaired hepatic peroxisome proliferator-activated receptor α (PPARα)-dependent oxidative fatty acid metabolism and ketogenesis. Similar results were recapitulated in CAV1-deficient AML12 hepatocytes, suggesting at least a partial cell-autonomous role of hepatocyte CAV1 in metabolic adaptation to fasting. Finally, our experiments suggest that the hepatic phenotypes observed in CAV1−/− mice involve impaired PPARα ligand signaling and attenuated bile acid and FXRα signaling. These results demonstrate the significance of CAV1 in (1) hepatic lipid homeostasis and (2) nuclear hormone receptor (PPARα, FXRα, and SHP) and bile acid signaling.
    Keywords Biology (General) ; QH301-705.5
    Language English
    Publishing date 2013-07-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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