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  1. Article ; Online: Trophy hunting: A .moral imperative for bans

    Horowitz, Arie

    Science (New York, N.Y.)

    2019  Volume 366, Issue 6464, Page(s) 435

    MeSH term(s) Animals ; Biodiversity ; Lions ; Morals ; Sports
    Language English
    Publishing date 2019-10-24
    Publishing country United States
    Document type Letter ; Comment
    ZDB-ID 128410-1
    ISSN 1095-9203 ; 0036-8075
    ISSN (online) 1095-9203
    ISSN 0036-8075
    DOI 10.1126/science.aaz3315
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  2. Article ; Online: Comment on "Close loop peer review" by Michael Hill.

    Horowitz, Arie

    EMBO reports

    2019  Volume 20, Issue 8, Page(s) e48313

    Abstract: Comment on "Close loop peer review" by Michael Hill. ...

    Abstract Comment on "Close loop peer review" by Michael Hill.
    MeSH term(s) Peer Review
    Language English
    Publishing date 2019-06-21
    Publishing country England
    Document type Letter ; Comment
    ZDB-ID 2020896-0
    ISSN 1469-3178 ; 1469-221X
    ISSN (online) 1469-3178
    ISSN 1469-221X
    DOI 10.15252/embr.201948313
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  3. Book ; Online: Membrane Trafficking of Integral Cell Junction Proteins and its Functional Consequences

    Horowitz, Arie

    2021  

    Abstract: Though membrane trafficking of cell junction proteins has been studied extensively for more than two decades, the accumulated knowledge remains fragmentary. The goal of this review is to synthesize published studies on the membrane trafficking of the ... ...

    Abstract Though membrane trafficking of cell junction proteins has been studied extensively for more than two decades, the accumulated knowledge remains fragmentary. The goal of this review is to synthesize published studies on the membrane trafficking of the five major junction transmembrane proteins: claudins, occludin, and junction adhesion molecules (JAMs) in tight junctions; cadherins and nectins in adherens junctions; to identify underlying common mechanisms; to highlight their functional consequences on barrier function; and to identify knowledge gaps. Clathrin-mediated endocytosis appears to be the main, but not exclusive, mode of internalization. Caveolin-mediated endocytosis and macropinocytosis are employed less frequently. PDZ-domain binding is the predominant mode of interaction between junction protein cytoplasmic tails and scaffold proteins. It is shared by claudins, the largest family of junction integral proteins, by junction adhesion molecules A, B, and C, and by the three nectins. All eight proteins are destined to either recycling via Rab4/Rab11 GTPases or to degradation. The sorting mechanisms that underlie the specificity of their endocytic pathways and determine their fates are not fully known. New data is presented to introduce an emerging role of junction-associated scaffold proteins in claudin membrane trafficking.

    Comment: 34 pages; 6 figures
    Keywords Quantitative Biology - Subcellular Processes
    Subject code 571
    Publishing date 2021-01-13
    Publishing country us
    Document type Book ; Online
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  4. Article ; Online: Letter by Horowitz Regarding Article, "Protein Interactions at Endothelial Junctions and Signaling Mechanisms Regulating Endothelial Permeability".

    Horowitz, Arie

    Circulation research

    2017  Volume 120, Issue 5, Page(s) e27

    MeSH term(s) Adherens Junctions ; Permeability ; Signal Transduction
    Language English
    Publishing date 2017-03-02
    Publishing country United States
    Document type Letter ; 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.117.310613
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  5. Article ; Online: Paracellular permeability and tight junction regulation in gut health and disease.

    Horowitz, Arie / Chanez-Paredes, Sandra D / Haest, Xenia / Turner, Jerrold R

    Nature reviews. Gastroenterology & hepatology

    2023  Volume 20, Issue 7, Page(s) 417–432

    Abstract: Epithelial tight junctions define the paracellular permeability of the intestinal barrier. Molecules can cross the tight junctions via two distinct size-selective and charge-selective paracellular pathways: the pore pathway and the leak pathway. These ... ...

    Abstract Epithelial tight junctions define the paracellular permeability of the intestinal barrier. Molecules can cross the tight junctions via two distinct size-selective and charge-selective paracellular pathways: the pore pathway and the leak pathway. These can be distinguished by their selectivities and differential regulation by immune cells. However, permeability increases measured in most studies are secondary to epithelial damage, which allows non-selective flux via the unrestricted pathway. Restoration of increased unrestricted pathway permeability requires mucosal healing. By contrast, tight junction barrier loss can be reversed by targeted interventions. Specific approaches are needed to restore pore pathway or leak pathway permeability increases. Recent studies have used preclinical disease models to demonstrate the potential of pore pathway or leak pathway barrier restoration in disease. In this Review, we focus on the two paracellular flux pathways that are dependent on the tight junction. We discuss the latest evidence that highlights tight junction components, structures and regulatory mechanisms, their impact on gut health and disease, and opportunities for therapeutic intervention.
    MeSH term(s) Humans ; Tight Junctions/chemistry ; Tight Junctions/metabolism ; Mucous Membrane ; Permeability ; Intestinal Mucosa/metabolism
    Language English
    Publishing date 2023-04-25
    Publishing country England
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't
    ZDB-ID 2493722-8
    ISSN 1759-5053 ; 1759-5045
    ISSN (online) 1759-5053
    ISSN 1759-5045
    DOI 10.1038/s41575-023-00766-3
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  6. Article: Inference of Diagnostic Markers and Therapeutic Targets From CSF Proteomics for the Treatment of Hydrocephalus.

    Horowitz, Arie / Saugier-Veber, Pascale / Gilard, Vianney

    Frontiers in cellular neuroscience

    2020  Volume 14, Page(s) 576028

    Language English
    Publishing date 2020-10-21
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2452963-1
    ISSN 1662-5102
    ISSN 1662-5102
    DOI 10.3389/fncel.2020.576028
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  7. Article ; Online: Imaging of growth factor-augmented angiogenesis after myocardial infarction: glimmers of a spatiotemporal pattern?

    Horowitz, Arie

    Journal of molecular and cellular cardiology

    2010  Volume 48, Issue 6, Page(s) 1036–1038

    MeSH term(s) Animals ; Cytokines/metabolism ; Fibroblast Growth Factor 2/metabolism ; Humans ; Intercellular Signaling Peptides and Proteins/metabolism ; Myocardial Infarction/diagnosis ; Myocardial Infarction/metabolism ; Myocardium/pathology ; Neovascularization, Pathologic ; Time Factors ; Vascular Endothelial Growth Factor A/metabolism ; X-Ray Microtomography/methods
    Chemical Substances Cytokines ; Intercellular Signaling Peptides and Proteins ; Vascular Endothelial Growth Factor A ; Fibroblast Growth Factor 2 (103107-01-3)
    Language English
    Publishing date 2010-06
    Publishing country England
    Document type Editorial
    ZDB-ID 80157-4
    ISSN 1095-8584 ; 0022-2828
    ISSN (online) 1095-8584
    ISSN 0022-2828
    DOI 10.1016/j.yjmcc.2009.11.001
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  8. Article ; Online: The versatility of RhoA activities in neural differentiation.

    Horowitz, Arie / Yang, Junning / Cai, Jingli / Iacovitti, Lorraine

    Small GTPases

    2017  Volume 10, Issue 1, Page(s) 26–32

    Abstract: In this commentary we discuss a paper we published recently on the activities of the GTPase RhoA during neural differentiation of murine embryonic stem cells, and relate our findings to previous studies. We narrate how we found that RhoA impedes neural ... ...

    Abstract In this commentary we discuss a paper we published recently on the activities of the GTPase RhoA during neural differentiation of murine embryonic stem cells, and relate our findings to previous studies. We narrate how we found that RhoA impedes neural differentiation by inhibiting the production as well as the secretion of noggin, a soluble factor that antagonizes bone morphogenetic protein. We discuss how the questions we tried to address shaped the study, and how embryonic stem cells isolated from a genetically modified mouse model devoid of Syx, a RhoA-specific guanine exchange factor, were used to address them. We detail several signaling pathways downstream of RhoA that are hindered by the absence of Syx, and obstructed by retinoic acid, resulting in an increase of noggin production; we explain how the lower RhoA activity and, consequently, the sparser peri-junctional stress fibers in
    MeSH term(s) Animals ; Carrier Proteins/physiology ; Embryonic Stem Cells/cytology ; Embryonic Stem Cells/physiology ; Humans ; Neurogenesis ; Smad1 Protein/physiology ; rhoA GTP-Binding Protein/antagonists & inhibitors ; rhoA GTP-Binding Protein/physiology
    Chemical Substances Carrier Proteins ; Smad1 Protein ; noggin protein (148294-77-3) ; rhoA GTP-Binding Protein (EC 3.6.5.2)
    Language English
    Publishing date 2017-01-27
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2682247-7
    ISSN 2154-1256 ; 2154-1248
    ISSN (online) 2154-1256
    ISSN 2154-1248
    DOI 10.1080/21541248.2016.1273171
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  9. Article ; Online: Analysis of Retinoic Acid-induced Neural Differentiation of Mouse Embryonic Stem Cells in Two and Three-dimensional Embryoid Bodies.

    Yang, Junning / Wu, Chuanshen / Stefanescu, Ioana / Horowitz, Arie

    Journal of visualized experiments : JoVE

    2017  , Issue 122

    Abstract: Mouse embryonic stem cells (ESCs) isolated from the inner mass of the blastocyst (typically at day E3.5), can be used as in vitro model system for studying early embryonic development. In the absence of leukemia inhibitory factor (LIF), ESCs ... ...

    Abstract Mouse embryonic stem cells (ESCs) isolated from the inner mass of the blastocyst (typically at day E3.5), can be used as in vitro model system for studying early embryonic development. In the absence of leukemia inhibitory factor (LIF), ESCs differentiate by default into neural precursor cells. They can be amassed into a three dimensional (3D) spherical aggregate termed embryoid body (EB) due to its similarity to the early stage embryo. EBs can be seeded on fibronectin-coated coverslips, where they expand by growing two dimensional (2D) extensions, or implanted in 3D collagen matrices where they continue growing as spheroids, and differentiate into the three germ layers: endodermal, mesodermal, and ectodermal. The 3D collagen culture mimics the in vivo environment more closely than the 2D EBs. The 2D EB culture facilitates analysis by immunofluorescence and immunoblotting to track differentiation. We have developed a two-step neural differentiation protocol. In the first step, EBs are generated by the hanging-drop technique, and, simultaneously, are induced to differentiate by exposure to retinoic acid (RA). In the second step, neural differentiation proceeds in a 2D or 3D format in the absence of RA.
    MeSH term(s) Animals ; Cell Culture Techniques ; Collagen ; Ectoderm ; Embryoid Bodies/cytology ; Endoderm ; Mesoderm ; Mice ; Mice, Transgenic ; Mouse Embryonic Stem Cells/cytology ; Mouse Embryonic Stem Cells/drug effects ; Neural Stem Cells/cytology ; Neural Stem Cells/drug effects ; Neurogenesis/drug effects ; Tretinoin/pharmacology
    Chemical Substances Tretinoin (5688UTC01R) ; Collagen (9007-34-5)
    Language English
    Publishing date 2017-04-22
    Publishing country United States
    Document type Journal Article ; Video-Audio Media ; Research Support, N.I.H., Extramural
    ISSN 1940-087X
    ISSN (online) 1940-087X
    DOI 10.3791/55621
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  10. Article ; Online: Membrane traffic as a coordinator of cell migration and junction remodeling.

    Wu, Chuanshen / Horowitz, Arie

    Communicative & integrative biology

    2012  Volume 4, Issue 6, Page(s) 703–705

    Abstract: The change in the overall shape of developing organs is a consequence of the cumulative movement, reshaping, and proliferation of the individual mural cells that make up the walls of these organs. Recent observations suggest that the shape and the ... ...

    Abstract The change in the overall shape of developing organs is a consequence of the cumulative movement, reshaping, and proliferation of the individual mural cells that make up the walls of these organs. Recent observations suggest that the shape and the position of endothelial cells (ECs) in growing blood vessels are highly dynamic, implying that these cells remodel their junctions extensively and do not preserve their initial relative positions. In order to determine the mechanisms that confer the dynamic behavior of mural ECs, we tracked the trafficking of a cell junction protein complex that consists of the RhoA-specific guanine exchange factor (GEF) Syx, the scaffold protein Mupp1, and the phospholipid binding protein Amot.1 We found that RhoA co-trafficked with this complex on the same endocytic vesicles, and that its cellular activity pattern was determined by Rab13-dependent trafficking. The vesicles were targeted by a Rab13-associated protein complex to Tyr(1175)-phosphorylated VEGFR2 at the leading edge of ECs migrating under a VEGF gradient. These results indicate that the dynamic behavior of ECs in sprouting vessels is conferred by using the same protein complex for the regulation of both cell junctions and cell motility. Together with previous studies that demonstrated regulation of Rac signaling by Rab5-dependent trafficking,(2) it appears now that membrane traffic is tightly coupled to the regulation of Rho GTPases, and, consequently, to the regulation of the actin cytoskeleton, cell junctions, and cell migration.
    Language English
    Publishing date 2012-03-23
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2451097-X
    ISSN 1942-0889 ; 1942-0889
    ISSN (online) 1942-0889
    ISSN 1942-0889
    DOI 10.4161/cib.17140
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