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  1. Article ; Online: A Call for Standardization in Cell Therapy Studies: Commentary on an article by Iain R. Murray, BMedSci(Hons), MRCS, MFSEM, PhD, et al.: "International Expert Consensus on a Cell Therapy Communication Tool: DOSES".

    Rodeo, Scott A

    The Journal of bone and joint surgery. American volume

    2019  Volume 101, Issue 10, Page(s) e47

    MeSH term(s) Arthroplasty, Replacement, Hip ; Cell- and Tissue-Based Therapy ; Consensus ; Prosthesis Design ; Reference Standards
    Language English
    Publishing date 2019-07-08
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 220625-0
    ISSN 1535-1386 ; 0021-9355
    ISSN (online) 1535-1386
    ISSN 0021-9355
    DOI 10.2106/JBJS.19.00189
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  2. Book: Lysine based post-translational modification of proteins

    Scott, Iain

    (Essays in biochemistry ; 52)

    2012  

    Title variant Lysine-based post-translational modification of proteins
    Author's details ed. by Iain Scott
    Series title Essays in biochemistry ; 52
    Collection
    Language English
    Size XXVI, 182 S. : Ill., graph. Darst.
    Publisher Portland Press
    Publishing place London
    Publishing country Great Britain
    Document type Book
    HBZ-ID HT017337437
    ISBN 978-1-85578-185-6 ; 1-85578-185-9
    Database Catalogue ZB MED Medicine, Health

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    Zs A 12 -52- not available for loan Zeitschriften-Lesesaal

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  3. Article ; Online: Differential bioenergetics in adult rodent cardiomyocytes isolated from the right versus left ventricle.

    Nguyen, Quyen L / Rao, Krithika / Sembrat, John C / St Croix, Claudette / Kaufman, Brett A / Scott, Iain / Goetzman, Eric / Shiva, Sruti

    Journal of molecular and cellular cardiology

    2024  Volume 190, Page(s) 79–81

    Language English
    Publishing date 2024-04-11
    Publishing country England
    Document type Letter
    ZDB-ID 80157-4
    ISSN 1095-8584 ; 0022-2828
    ISSN (online) 1095-8584
    ISSN 0022-2828
    DOI 10.1016/j.yjmcc.2024.04.003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Rethinking Protein Acetylation in Pressure Overload-Induced Heart Failure.

    Scott, Iain / Sack, Michael N

    Circulation research

    2020  Volume 127, Issue 8, Page(s) 1109–1111

    MeSH term(s) Acetylation ; Heart ; Heart Failure/etiology ; Heart Failure/metabolism ; Humans ; Mitochondria/metabolism ; Proteome/metabolism
    Chemical Substances Proteome
    Language English
    Publishing date 2020-09-24
    Publishing country United States
    Document type Editorial ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural ; Comment
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/CIRCRESAHA.120.317910
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: GCN5L1-mediated acetylation prevents Rictor degradation in cardiac cells after hypoxic stress.

    Bugga, Paramesha / Manning, Janet R / Mushala, Bellina A S / Stoner, Michael W / Sembrat, John / Scott, Iain

    Cellular signalling

    2024  Volume 116, Page(s) 111065

    Abstract: Cardiomyocyte apoptosis and cardiac fibrosis are the leading causes of mortality in patients with ischemic heart disease. As such, these processes represent potential therapeutic targets to treat heart failure resulting from ischemic insult. We ... ...

    Abstract Cardiomyocyte apoptosis and cardiac fibrosis are the leading causes of mortality in patients with ischemic heart disease. As such, these processes represent potential therapeutic targets to treat heart failure resulting from ischemic insult. We previously demonstrated that the mitochondrial acetyltransferase protein GCN5L1 regulates cardiomyocyte cytoprotective signaling in ischemia-reperfusion injury in vivo and hypoxia-reoxygenation injury in vitro. The current study investigated the mechanism underlying GCN5L1-mediated regulation of the Akt/mTORC2 cardioprotective signaling pathway. Rictor protein levels in cardiac tissues from human ischemic heart disease patients were significantly decreased relative to non-ischemic controls. Rictor protein levels were similarly decreased in cardiac AC16 cells following hypoxic stress, while mRNA levels remained unchanged. The reduction in Rictor protein levels after hypoxia was enhanced by the knockdown of GCN5L1, and was blocked by GCN5L1 overexpression. These findings correlated with changes in Rictor lysine acetylation, which were mediated by GCN5L1 acetyltransferase activity. Rictor degradation was regulated by proteasomal activity, which was antagonized by increased Rictor acetylation. Finally, we found that GCN5L1 knockdown restricted cytoprotective Akt signaling, in conjunction with decreased mTOR abundance and activity. In summary, these studies suggest that GCN5L1 promotes cardioprotective Akt/mTORC2 signaling by maintaining Rictor protein levels through enhanced lysine acetylation.
    MeSH term(s) Humans ; Acetylation ; Acetyltransferases/genetics ; Acetyltransferases/metabolism ; Hypoxia/metabolism ; Lysine/metabolism ; Mechanistic Target of Rapamycin Complex 2/metabolism ; Mitochondrial Proteins/metabolism ; Myocardial Ischemia/metabolism ; Myocytes, Cardiac/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Rapamycin-Insensitive Companion of mTOR Protein/genetics ; Transcription Factors/metabolism
    Chemical Substances Acetyltransferases (EC 2.3.1.-) ; Lysine (K3Z4F929H6) ; Mechanistic Target of Rapamycin Complex 2 (EC 2.7.11.1) ; Mitochondrial Proteins ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Rapamycin-Insensitive Companion of mTOR Protein ; Transcription Factors ; BLOC1S1 protein, human
    Language English
    Publishing date 2024-01-26
    Publishing country England
    Document type Journal Article
    ZDB-ID 1002702-6
    ISSN 1873-3913 ; 0898-6568
    ISSN (online) 1873-3913
    ISSN 0898-6568
    DOI 10.1016/j.cellsig.2024.111065
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: β3 Receptor Signaling in Pregnant Human Myometrium Suggests a Role for β3 Agonists as Tocolytics.

    Buxton, Iain L O / Asif, Hazik / Barnett, Scott D

    Biomolecules

    2023  Volume 13, Issue 6

    Abstract: Preterm labor leading to preterm birth is the leading cause of infant morbidity and mortality. At the present time, nothing can reliably halt labor once it begins. The knowledge that agonists of the β2 adrenergic receptor relax airway smooth muscle and ... ...

    Abstract Preterm labor leading to preterm birth is the leading cause of infant morbidity and mortality. At the present time, nothing can reliably halt labor once it begins. The knowledge that agonists of the β2 adrenergic receptor relax airway smooth muscle and are effective in the treatment of asthma led to the notion that β2 mimetics would prevent preterm birth by relaxing uterine smooth muscle. The activation of cAMP-dependent protein kinase by β2 receptors is unable to provide meaningful tocolysis. The failure of β2 agonists such as ritodrine and terbutaline to prevent preterm birth suggests that the regulation of uterine smooth muscle is disparate from that of airway. Other smooth muscle quiescent-mediating molecules, such as nitric oxide, relax vascular smooth muscle in a cGMP-protein kinase G-dependent manner; however, nitric oxide activation of protein kinase G fails to explain the relaxation of the myometrium to nitric oxide. Moreover, nitric oxide-mediated relaxation is blunted in preterm labor, and thus, for this reason and because of the fall in maternal blood pressure, nitric oxide cannot be employed as a tocolytic. The β3 adrenergic receptor-mediated relaxation of the human myometrium is claimed to be cAMP-dependent protein kinase-dependent. This is scientifically displeasing given the failure of β2 agonists as tocolytics and suggests a non-canonical signaling role for β3AR in myometrium. The addition of the β3 agonist mirabegron to pregnant human myometrial strips in the tissue bath relaxes oxytocin-induced contractions. Mirabegron stimulates nitric oxide production in myometrial microvascular endothelial cells, and the relaxation of uterine tissue in vitro is partially blocked by the addition of the endothelial nitric oxide synthase blocker Nω-Nitro-L-arginine. Recent data suggest that both endothelial and smooth muscle cells respond to β3 stimulation and contribute to relaxation through disparate signaling pathways. The repurposing of approved medications such as mirabegron (Mybetriq™) tested in human myometrium as uterine tocolytics can advance the prevention of preterm birth.
    MeSH term(s) Infant, Newborn ; Pregnancy ; Female ; Humans ; Myometrium/metabolism ; Tocolytic Agents/pharmacology ; Tocolytic Agents/metabolism ; Tocolytic Agents/therapeutic use ; Premature Birth/prevention & control ; Nitric Oxide/metabolism ; Endothelial Cells/metabolism ; Obstetric Labor, Premature/drug therapy ; Obstetric Labor, Premature/prevention & control ; Obstetric Labor, Premature/metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Receptors, Adrenergic/metabolism
    Chemical Substances Tocolytic Agents ; mirabegron (MVR3JL3B2V) ; Nitric Oxide (31C4KY9ESH) ; Cyclic AMP-Dependent Protein Kinases (EC 2.7.11.11) ; Receptors, Adrenergic
    Language English
    Publishing date 2023-06-17
    Publishing country Switzerland
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural
    ZDB-ID 2701262-1
    ISSN 2218-273X ; 2218-273X
    ISSN (online) 2218-273X
    ISSN 2218-273X
    DOI 10.3390/biom13061005
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Multitargeted anti-infective drugs: resilience to resistance in the antimicrobial resistance era.

    Suckling, Colin J / Hunter, Iain S / Scott, Fraser J

    Future drug discovery

    2022  Volume 4, Issue 1, Page(s) FDD73

    Abstract: The standard drug discovery paradigm of single molecule - single biological target - single biological effect is perhaps particularly unsuitable for anti-infective drug discovery. This is due to the rapid evolution of resistance likely to be observed ... ...

    Abstract The standard drug discovery paradigm of single molecule - single biological target - single biological effect is perhaps particularly unsuitable for anti-infective drug discovery. This is due to the rapid evolution of resistance likely to be observed with single target drugs. Multitargeted anti-infective drugs are likely to be superior due to their lower susceptibility to target-related resistance mechanisms. Strathclyde minor groove binders are a class of compounds which have been developed by adopting the multitargeted anti-infective drugs paradigm, and their effectiveness against a wide range of pathogenic organisms is discussed. The renaming of this class to Strathclyde nucleic acid binders is also presented due to their likely targets including both DNA and RNA.
    Language English
    Publishing date 2022-05-05
    Publishing country England
    Document type Journal Article ; Review
    ISSN 2631-3316
    ISSN (online) 2631-3316
    DOI 10.4155/fdd-2022-0001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: GCN5L1-mediated acetylation prevents Rictor degradation in cardiac cells after hypoxic stress.

    Bugga, Paramesha / Manning, Janet R / Mushala, Bellina A S / Stoner, Michael W / Sembrat, John / Scott, Iain

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Cardiomyocyte apoptosis and cardiac fibrosis are the leading causes of mortality in patients with ischemic heart disease. As such, these processes represent potential therapeutic targets to treat heart failure resulting from ischemic insult. We ... ...

    Abstract Cardiomyocyte apoptosis and cardiac fibrosis are the leading causes of mortality in patients with ischemic heart disease. As such, these processes represent potential therapeutic targets to treat heart failure resulting from ischemic insult. We previously demonstrated that the mitochondrial acetyltransferase protein GCN5L1 regulates cardiomyocyte cytoprotective signaling in ischemia-reperfusion injury
    Language English
    Publishing date 2023-10-26
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.10.26.564170
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article: Validation of GCN5L1/BLOC1S1/BLOS1 Antibodies Using Knockout Cells and Tissue.

    Bugga, Paramesha / Stoner, Michael W / Manning, Janet R / Mushala, Bellina A S / Thapa, Dharendra / Scott, Iain

    bioRxiv : the preprint server for biology

    2023  

    Abstract: GCN5L1, also known as BLOC1S1 and BLOS1, is a small intracellular protein involved in a number of key biological processes. Over the last decade, GCN5L1 has been implicated in the regulation of protein lysine acetylation, energy metabolism, endo- ... ...

    Abstract GCN5L1, also known as BLOC1S1 and BLOS1, is a small intracellular protein involved in a number of key biological processes. Over the last decade, GCN5L1 has been implicated in the regulation of protein lysine acetylation, energy metabolism, endo-lysosomal function, and cellular immune pathways. An increasing number of published papers have used commercially-available reagents to interrogate GCN5L1 function. However, in many cases these reagents have not been rigorously validated, leading to potentially misleading results. In this report we tested several commercially-available antibodies for GCN5L1, and found that two-thirds of those available did not unambiguously detect the protein by western blot in cultured mouse cells or
    Language English
    Publishing date 2023-07-21
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.07.21.550091
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Adropin: a hepatokine modulator of vascular function and cardiac fuel metabolism.

    Mushala, Bellina A S / Scott, Iain

    American journal of physiology. Heart and circulatory physiology

    2020  Volume 320, Issue 1, Page(s) H238–H244

    Abstract: Adropin is a nutritionally regulated peptide hormone, secreted primarily by the liver, which modulates metabolic homeostasis in a number of tissues. Growing evidence suggests that adropin is an important regulatory component in a number of cardiovascular ...

    Abstract Adropin is a nutritionally regulated peptide hormone, secreted primarily by the liver, which modulates metabolic homeostasis in a number of tissues. Growing evidence suggests that adropin is an important regulatory component in a number of cardiovascular pathologies, and may be central to the control of cardiac fuel metabolism and vascular function. In this mini-review, we examine the known facets of adropin biology, discuss open questions in the field, and speculate on the therapeutic potential of targeting adropin-related signaling pathways in cardiovascular diseases.
    MeSH term(s) Animals ; Blood Vessels/drug effects ; Blood Vessels/metabolism ; Blood Vessels/physiopathology ; Cardiovascular Agents/therapeutic use ; Cardiovascular Diseases/drug therapy ; Cardiovascular Diseases/metabolism ; Cardiovascular Diseases/physiopathology ; Energy Metabolism/drug effects ; Humans ; Intercellular Signaling Peptides and Proteins/metabolism ; Intercellular Signaling Peptides and Proteins/therapeutic use ; Myocardium/metabolism ; Signal Transduction
    Chemical Substances Cardiovascular Agents ; Enho protein, human ; Intercellular Signaling Peptides and Proteins
    Language English
    Publishing date 2020-11-20
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 603838-4
    ISSN 1522-1539 ; 0363-6135
    ISSN (online) 1522-1539
    ISSN 0363-6135
    DOI 10.1152/ajpheart.00449.2020
    Database MEDical Literature Analysis and Retrieval System OnLINE

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