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  1. Article ; Online: No need for juvenile language in Nature.

    Moss, Stephen E

    Nature

    2018  Volume 562, Issue 7727, Page(s) 344

    MeSH term(s) Language ; Periodicals as Topic/standards ; Wit and Humor as Topic
    Language English
    Publishing date 2018-11-28
    Publishing country England
    Document type Letter
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/d41586-018-07061-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  2. Article ; Online: Correction: LRG1 as a novel therapeutic target in eye disease.

    De Rossi, Giulia / Da Vitoria Lobo, Marlene E / Greenwood, John / Moss, Stephen E

    Eye (London, England)

    2022  Volume 37, Issue 7, Page(s) 1517

    Language English
    Publishing date 2022-02-23
    Publishing country England
    Document type Published Erratum
    ZDB-ID 91001-6
    ISSN 1476-5454 ; 0950-222X
    ISSN (online) 1476-5454
    ISSN 0950-222X
    DOI 10.1038/s41433-022-01988-6
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  3. Article ; Online: Publisher Correction: Angiopathic activity of LRG1 is induced by the IL-6/STAT3 pathway.

    Dritsoula, Athina / Dowsett, Laura / Pilotti, Camilla / O'Connor, Marie N / Moss, Stephen E / Greenwood, John

    Scientific reports

    2022  Volume 12, Issue 1, Page(s) 5347

    Language English
    Publishing date 2022-03-29
    Publishing country England
    Document type Published Erratum
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-022-09460-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Book: The annexins

    Moss, Stephen E.

    (Portland Press research monograph ; 2)

    1992  

    Author's details ed. by Stephen E. Moss
    Series title Portland Press research monograph ; 2
    Collection
    Keywords Annexins
    Language English
    Size XI, 173 S. :Ill., graph. Darst.
    Publisher Portland Pr
    Publishing place London u.a.
    Publishing country Great Britain
    Document type Book
    HBZ-ID HT004979851
    ISBN 1-85578-008-9 ; 978-1-85578-008-8
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    1993 A 2746 order for loan Magazin

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  5. Article ; Online: LRG1: an emerging player in disease pathogenesis.

    Camilli, Carlotta / Hoeh, Alexandra E / De Rossi, Giulia / Moss, Stephen E / Greenwood, John

    Journal of biomedical science

    2022  Volume 29, Issue 1, Page(s) 6

    Abstract: The secreted glycoprotein leucine-rich α-2 glycoprotein 1 (LRG1) was first described as a key player in pathogenic ocular neovascularization almost a decade ago. Since then, an increasing number of publications have reported the involvement of LRG1 in ... ...

    Abstract The secreted glycoprotein leucine-rich α-2 glycoprotein 1 (LRG1) was first described as a key player in pathogenic ocular neovascularization almost a decade ago. Since then, an increasing number of publications have reported the involvement of LRG1 in multiple human conditions including cancer, diabetes, cardiovascular disease, neurological disease, and inflammatory disorders. The purpose of this review is to provide, for the first time, a comprehensive overview of the LRG1 literature considering its role in health and disease. Although LRG1 is constitutively expressed by hepatocytes and neutrophils, Lrg1
    MeSH term(s) Animals ; Glycoproteins/genetics ; Mice ; Neovascularization, Pathologic ; Neutrophils ; Prognosis ; Signal Transduction
    Chemical Substances Glycoproteins ; LRG1 protein, mouse
    Language English
    Publishing date 2022-01-21
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 1193378-1
    ISSN 1423-0127 ; 1021-7770
    ISSN (online) 1423-0127
    ISSN 1021-7770
    DOI 10.1186/s12929-022-00790-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: LRG1 as a novel therapeutic target in eye disease.

    De Rossi, Giulia / Da Vitoria Lobo, Marlene E / Greenwood, John / Moss, Stephen E

    Eye (London, England)

    2022  Volume 36, Issue 2, Page(s) 328–340

    Abstract: Retinal and choroidal diseases are major causes of blindness and visual impairment in the developed world and on the rise due to an ageing population and diabetes epidemic. Standard of care is centred around blockade of vascular endothelial growth factor ...

    Abstract Retinal and choroidal diseases are major causes of blindness and visual impairment in the developed world and on the rise due to an ageing population and diabetes epidemic. Standard of care is centred around blockade of vascular endothelial growth factor (VEGF), but despite having halved the number of patients losing sight, a high rate of patient non-response and loss of efficacy over time are key challenges. Dysregulation of vascular homoeostasis, coupled with fibrosis and inflammation, are major culprits driving sight-threatening eye diseases. Improving our knowledge of these pathological processes should inform the development of new drugs to address the current clinical challenges for patients. Leucine-rich α-2 glycoprotein 1 (LRG1) is an emerging key player in vascular dysfunction, inflammation and fibrosis. Under physiological conditions, LRG1 is constitutively expressed by the liver and granulocytes, but little is known about its normal biological function. In pathological scenarios, such as diabetic retinopathy (DR) and neovascular age-related macular degeneration (nvAMD), its expression is ectopically upregulated and it acquires a much better understood pathogenic role. Context-dependent modulation of the transforming growth-factor β (TGFβ) pathway is one of the main activities of LRG1, but additional roles have recently been emerging. This review aims to highlight the clinical and pre-clinical evidence for the pathogenic contribution of LRG1 to vascular retinopathies, as well as extrapolate from other diseases, functions which may be relevant to eye disease. Finally, we will provide a current update on the development of anti-LRG1 therapies for the treatment of nvAMD.
    MeSH term(s) Diabetic Retinopathy/drug therapy ; Diabetic Retinopathy/metabolism ; Fibrosis ; Glycoproteins/metabolism ; Humans ; Inflammation ; Vascular Endothelial Growth Factor A
    Chemical Substances Glycoproteins ; LRG1 protein, human ; Vascular Endothelial Growth Factor A
    Language English
    Publishing date 2022-01-05
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 91001-6
    ISSN 1476-5454 ; 0950-222X
    ISSN (online) 1476-5454
    ISSN 0950-222X
    DOI 10.1038/s41433-021-01807-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Angiopathic activity of LRG1 is induced by the IL-6/STAT3 pathway.

    Dritsoula, Athina / Dowsett, Laura / Pilotti, Camilla / O'Connor, Marie N / Moss, Stephen E / Greenwood, John

    Scientific reports

    2022  Volume 12, Issue 1, Page(s) 4867

    Abstract: Leucine-rich α-2-glycoprotein 1 (LRG1) is a secreted glycoprotein that under physiological conditions is produced predominantly by the liver. In disease, its local induction promotes pathogenic neovascularisation while its inhibition leads to reduced ... ...

    Abstract Leucine-rich α-2-glycoprotein 1 (LRG1) is a secreted glycoprotein that under physiological conditions is produced predominantly by the liver. In disease, its local induction promotes pathogenic neovascularisation while its inhibition leads to reduced dysfunctional angiogenesis. Here we examine the role of interleukin-6 (IL-6) in defective angiogenesis mediated by LRG1. IL-6 treatment induced LRG1 expression in endothelial cells and ex vivo angiogenesis cultures and promoted vascular growth with reduced mural cell coverage. In Lrg1
    MeSH term(s) COVID-19 ; Endothelial Cells/metabolism ; Glycoproteins/metabolism ; Humans ; Interleukin-6/metabolism ; Neovascularization, Pathologic/metabolism ; STAT3 Transcription Factor/metabolism
    Chemical Substances Glycoproteins ; IL6 protein, human ; Interleukin-6 ; LRG1 protein, human ; STAT3 Transcription Factor ; STAT3 protein, human
    Language English
    Publishing date 2022-03-22
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-022-08516-2
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  8. Article ; Online: Aging-related defects in macrophage function are driven by MYC and USF1 transcriptional programs.

    Moss, Charlotte E / Johnston, Simon A / Kimble, Joshua V / Clements, Martha / Codd, Veryan / Hamby, Stephen / Goodall, Alison H / Deshmukh, Sumeet / Sudbery, Ian / Coca, Daniel / Wilson, Heather L / Kiss-Toth, Endre

    Cell reports

    2024  Volume 43, Issue 4, Page(s) 114073

    Abstract: Macrophages are central innate immune cells whose function declines with age. The molecular mechanisms underlying age-related changes remain poorly understood, particularly in human macrophages. We report a substantial reduction in phagocytosis, ... ...

    Abstract Macrophages are central innate immune cells whose function declines with age. The molecular mechanisms underlying age-related changes remain poorly understood, particularly in human macrophages. We report a substantial reduction in phagocytosis, migration, and chemotaxis in human monocyte-derived macrophages (MDMs) from older (>50 years old) compared with younger (18-30 years old) donors, alongside downregulation of transcription factors MYC and USF1. In MDMs from young donors, knockdown of MYC or USF1 decreases phagocytosis and chemotaxis and alters the expression of associated genes, alongside adhesion and extracellular matrix remodeling. A concordant dysregulation of MYC and USF1 target genes is also seen in MDMs from older donors. Furthermore, older age and loss of either MYC or USF1 in MDMs leads to an increased cell size, altered morphology, and reduced actin content. Together, these results define MYC and USF1 as key drivers of MDM age-related functional decline and identify downstream targets to improve macrophage function in aging.
    MeSH term(s) Humans ; Macrophages/metabolism ; Aging ; Proto-Oncogene Proteins c-myc/metabolism ; Proto-Oncogene Proteins c-myc/genetics ; Adult ; Upstream Stimulatory Factors/metabolism ; Upstream Stimulatory Factors/genetics ; Middle Aged ; Adolescent ; Phagocytosis/genetics ; Young Adult ; Transcription, Genetic ; Aged ; Chemotaxis/genetics
    Chemical Substances Proto-Oncogene Proteins c-myc ; Upstream Stimulatory Factors ; USF1 protein, human ; MYC protein, human
    Language English
    Publishing date 2024-04-04
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2024.114073
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  9. Article ; Online: Functional Evaluation of AMD-Associated Risk Variants of Complement Factor B.

    Pilotti, Camilla / Greenwood, John / Moss, Stephen E

    Investigative ophthalmology & visual science

    2020  Volume 61, Issue 5, Page(s) 19

    Abstract: Purpose: The 32W and 32Q variants of complement factor B (CFB) are associated with reduced risk of developing neovascular age-related macular degeneration (AMD) compared with the common 32R allele. The objective of this study was to determine if the ... ...

    Abstract Purpose: The 32W and 32Q variants of complement factor B (CFB) are associated with reduced risk of developing neovascular age-related macular degeneration (AMD) compared with the common 32R allele. The objective of this study was to determine if the most protective R32Q variant affects the neovascular process in a manner consistent with the reported reduced disease association.
    Methods: The 32R, 32W, and 32Q human CFB variants were expressed in human embryonic kidney 293T cells and purified from culture supernatant. The ex vivo mouse fetal metatarsal explant model was used to investigate the effect of these three human CFB variants on angiogenesis. Metatarsal bones were isolated from mouse embryos and cultured in the presence of the three CFB variants, and angiogenesis was measured following immunostaining of fixed samples. ELISAs were used to quantify C3 and VEGF protein levels in metatarsal culture and quantitative PCR to measure Cfb, C3, and Vegf expression.
    Results: We show here that the three CFB variants have different biological activities in the mouse metatarsal assay, with CFBR32 exhibiting significantly greater angiogenic activity than CFBQ32 or CFBW32, which were broadly similar. We also observed differences in macrophage phenotype with these two variants that may contribute to their activities in this experimental model.
    Conclusions: We have demonstrated that the biological activities of CFBR32, CFBW32, and CFBQ32 are consistent with their AMD risk association, and we provide functional evidence of roles for these variants in angiogenesis that may be relevant to the pathogenesis of the neovascular form of AMD.
    MeSH term(s) Animals ; Choroidal Neovascularization ; Complement Activation ; Complement C3/genetics ; Complement C3/metabolism ; Complement Factor B/genetics ; Complement Factor B/metabolism ; Disease Models, Animal ; Genetic Variation ; Macrophages/metabolism ; Macular Degeneration/genetics ; Mice ; Polymorphism, Genetic ; RNA, Messenger/metabolism ; Recombinant Proteins ; Vascular Endothelial Growth Factor A/genetics ; Vascular Endothelial Growth Factor A/metabolism
    Chemical Substances Complement C3 ; RNA, Messenger ; Recombinant Proteins ; Vascular Endothelial Growth Factor A ; Complement Factor B (EC 3.4.21.47)
    Language English
    Publishing date 2020-05-14
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 391794-0
    ISSN 1552-5783 ; 0146-0404
    ISSN (online) 1552-5783
    ISSN 0146-0404
    DOI 10.1167/iovs.61.5.19
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  10. Article: Analyzing the mechanisms that facilitate the subtype-specific assembly of

    Choi, Catherine / Smalley, Joshua L / Lemons, Abigail H S / Ren, Qiu / Bope, Christopher E / Dengler, Jake S / Davies, Paul A / Moss, Stephen J

    Frontiers in molecular neuroscience

    2022  Volume 15, Page(s) 1017404

    Abstract: Impaired inhibitory signaling underlies the pathophysiology of many neuropsychiatric and neurodevelopmental disorders including autism spectrum disorders and epilepsy. Neuronal inhibition is regulated by synaptic and ... ...

    Abstract Impaired inhibitory signaling underlies the pathophysiology of many neuropsychiatric and neurodevelopmental disorders including autism spectrum disorders and epilepsy. Neuronal inhibition is regulated by synaptic and extrasynaptic
    Language English
    Publishing date 2022-10-03
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2452967-9
    ISSN 1662-5099
    ISSN 1662-5099
    DOI 10.3389/fnmol.2022.1017404
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