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  1. Article ; Online: BECN1

    Sebti, Salwa / Zou, Zhongju / Shiloh, Michael U

    Autophagy

    2022  Volume 19, Issue 3, Page(s) 957–965

    Abstract: Macroautophagy/autophagy is necessary for lifespan extension in multiple model organisms and autophagy dysfunction impacts age-related phenotypes and diseases. Introduction of an F121A mutation into the essential autophagy protein BECN1 constitutively ... ...

    Abstract Macroautophagy/autophagy is necessary for lifespan extension in multiple model organisms and autophagy dysfunction impacts age-related phenotypes and diseases. Introduction of an F121A mutation into the essential autophagy protein BECN1 constitutively increases basal autophagy in young mice and reduces cardiac and renal age-related changes in longer lived
    MeSH term(s) Mice ; Animals ; Autophagy/physiology ; Aging/metabolism ; Mutation ; Phenotype ; Muscular Atrophy ; Beclin-1/metabolism
    Chemical Substances Becn1 protein, mouse ; Beclin-1
    Language English
    Publishing date 2022-08-21
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.1080/15548627.2022.2111852
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6741: Show issues Location:
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  2. Article ; Online: Infectious and Inflammatory Pathways to Cough.

    Naqvi, Kubra F / Mazzone, Stuart B / Shiloh, Michael U

    Annual review of physiology

    2022  Volume 85, Page(s) 71–91

    Abstract: Coughing is a dynamic physiological process resulting from input of vagal sensory neurons innervating the airways and perceived airway irritation. Although cough serves to protect and clear the airways, it can also be exploited by respiratory pathogens ... ...

    Abstract Coughing is a dynamic physiological process resulting from input of vagal sensory neurons innervating the airways and perceived airway irritation. Although cough serves to protect and clear the airways, it can also be exploited by respiratory pathogens to facilitate disease transmission. Microbial components or infection-induced inflammatory mediators can directly interact with sensory nerve receptors to induce a cough response. Analysis of cough-generated aerosols and transmission studies have further demonstrated how infectious disease is spread through coughing. This review summarizes the neurophysiology of cough, cough induction by respiratory pathogens and inflammation, and cough-mediated disease transmission.
    MeSH term(s) Humans ; Cough ; Respiratory System/innervation ; Vagus Nerve/physiology ; Sensory Receptor Cells ; Communicable Diseases
    Language English
    Publishing date 2022-09-28
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 207933-1
    ISSN 1545-1585 ; 0066-4278
    ISSN (online) 1545-1585
    ISSN 0066-4278
    DOI 10.1146/annurev-physiol-031422-092315
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.226: Show issues Location:
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  3. Article ; Online: Mechanisms of mycobacterial transmission: how does Mycobacterium tuberculosis enter and escape from the human host.

    Shiloh, Michael U

    Future microbiology

    2016  Volume 11, Page(s) 1503–1506

    Language English
    Publishing date 2016-12
    Publishing country England
    Document type Journal Article
    ISSN 1746-0921
    ISSN (online) 1746-0921
    DOI 10.2217/fmb-2016-0185
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Bioorthogonal Metabolic Labeling of the Virulence Factor Phenolic Glycolipid in Mycobacteria.

    Guzmán, Lindsay E / Cambier, C J / Cheng, Tan-Yun / Naqvi, Kubra F / Shiloh, Michael U / Moody, D Branch / Bertozzi, Carolyn R

    ACS chemical biology

    2024  Volume 19, Issue 3, Page(s) 707–717

    Abstract: Surface lipids on pathogenic mycobacteria modulate infection outcomes by regulating host immune responses. Phenolic glycolipid (PGL) is a host-modulating surface lipid that varies among ... ...

    Abstract Surface lipids on pathogenic mycobacteria modulate infection outcomes by regulating host immune responses. Phenolic glycolipid (PGL) is a host-modulating surface lipid that varies among clinical
    MeSH term(s) Animals ; Glycolipids/metabolism ; Virulence Factors/metabolism ; Zebrafish ; Mycobacterium tuberculosis/metabolism ; Mycobacterium marinum/metabolism
    Chemical Substances Glycolipids ; Virulence Factors
    Language English
    Publishing date 2024-03-05
    Publishing country United States
    Document type Journal Article
    ISSN 1554-8937
    ISSN (online) 1554-8937
    DOI 10.1021/acschembio.3c00724
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Pathogenicity and virulence of

    Rahlwes, Kathryn C / Dias, Beatriz R S / Campos, Priscila C / Alvarez-Arguedas, Samuel / Shiloh, Michael U

    Virulence

    2022  Volume 14, Issue 1, Page(s) 2150449

    Abstract: Mycobacterium ... ...

    Abstract Mycobacterium tuberculosis
    MeSH term(s) Humans ; Mycobacterium tuberculosis/metabolism ; Virulence ; Tuberculosis/microbiology ; Virulence Factors/metabolism ; Host-Pathogen Interactions
    Chemical Substances Virulence Factors
    Language English
    Publishing date 2022-11-24
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2657572-3
    ISSN 2150-5608 ; 2150-5594
    ISSN (online) 2150-5608
    ISSN 2150-5594
    DOI 10.1080/21505594.2022.2150449
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Bag it, tag it: ubiquitin ligases and host resistance to Mycobacterium tuberculosis.

    Campos, Priscila C / Cunha, Danielle T / Souza-Costa, Luiz P / Shiloh, Michael U / Franco, Luis H

    Trends in microbiology

    2022  Volume 30, Issue 10, Page(s) 973–985

    Abstract: Infection with Mycobacterium tuberculosis (Mtb), the etiological agent of tuberculosis (TB), remains a significant global epidemic. Host resistance to Mtb depends on both adaptive and innate immunity mechanisms, including development of antigen-specific ... ...

    Abstract Infection with Mycobacterium tuberculosis (Mtb), the etiological agent of tuberculosis (TB), remains a significant global epidemic. Host resistance to Mtb depends on both adaptive and innate immunity mechanisms, including development of antigen-specific CD4 and CD8 T cells, production of inflammatory cytokines, bacterial phagocytosis and destruction within phagolysosomes, host cell apoptosis, and autophagy. A key regulatory mechanism in innate immunity is the attachment of the small protein ubiquitin to protein and lipid targets by the enzymatic activity of ubiquitin ligases. Here, we summarize the latest advances on the role of ubiquitination and ubiquitin ligases in host immunity against Mtb, with a focus on innate immunity signaling, inflammation, and antimicrobial autophagy. Understanding how ubiquitin ligases mediate immunity to Mtb, and the specific substrates of distinct ubiquitin ligases in the context of Mtb infection, could facilitate development of new host-directed antimicrobials.
    MeSH term(s) Cytokines/metabolism ; Humans ; Immunity, Innate ; Ligases/metabolism ; Mycobacterium tuberculosis/metabolism ; Tuberculosis ; Ubiquitin/metabolism
    Chemical Substances Cytokines ; Ubiquitin ; Ligases (EC 6.-)
    Language English
    Publishing date 2022-04-29
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 1158963-2
    ISSN 1878-4380 ; 0966-842X
    ISSN (online) 1878-4380
    ISSN 0966-842X
    DOI 10.1016/j.tim.2022.03.010
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 3738: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  7. Article ; Online: CDKL5 regulates p62-mediated selective autophagy and confers protection against neurotropic viruses.

    Thinwa, Josephine W / Zou, Zhongju / Parks, Emily / Sebti, Salwa / Hui, Kelvin / Wei, Yongjie / Goodarzi, Mohammad / Singh, Vibha / Urquhart, Greg / Jewell, Jenna L / Pfeiffer, Julie K / Levine, Beth / Reese, Tiffany A / Shiloh, Michael U

    The Journal of clinical investigation

    2024  Volume 134, Issue 1

    Abstract: Virophagy, the selective autophagosomal engulfment and lysosomal degradation of viral components, is crucial for neuronal cell survival and antiviral immunity. However, the mechanisms leading to viral antigen recognition and capture by autophagic ... ...

    Abstract Virophagy, the selective autophagosomal engulfment and lysosomal degradation of viral components, is crucial for neuronal cell survival and antiviral immunity. However, the mechanisms leading to viral antigen recognition and capture by autophagic machinery remain poorly understood. Here, we identified cyclin-dependent kinase-like 5 (CDKL5), known to function in neurodevelopment, as an essential regulator of virophagy. Loss-of-function mutations in CDKL5 are associated with a severe neurodevelopmental encephalopathy. We found that deletion of CDKL5 or expression of a clinically relevant pathogenic mutant of CDKL5 reduced virophagy of Sindbis virus (SINV), a neurotropic RNA virus, and increased intracellular accumulation of SINV capsid protein aggregates and cellular cytotoxicity. Cdkl5-knockout mice displayed increased viral antigen accumulation and neuronal cell death after SINV infection and enhanced lethality after infection with several neurotropic viruses. Mechanistic studies demonstrated that CDKL5 directly binds the canonical selective autophagy receptor p62 and phosphorylates p62 at T269/S272 to promote its interaction with viral capsid aggregates. We found that CDKL5-mediated phosphorylation of p62 facilitated the formation of large p62 inclusion bodies that captured viral capsids to initiate capsid targeting to autophagic machinery. Overall, these findings identify a cell-autonomous innate immune mechanism for autophagy activation to clear intracellular toxic viral protein aggregates during infection.
    MeSH term(s) Mice ; Animals ; Protein Aggregates ; Viruses ; Autophagy/genetics ; Phosphorylation ; Mice, Knockout ; Capsid Proteins ; Antigens, Viral ; Protein Serine-Threonine Kinases/genetics
    Chemical Substances Protein Aggregates ; Capsid Proteins ; Antigens, Viral ; CDKL5 protein, mouse (EC 2.7.11.22) ; Protein Serine-Threonine Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2024-01-02
    Publishing country United States
    Document type Journal Article
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI168544
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ua VI Zs.184: Show issues Location:
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  8. Article ; Online: EBV-driven HIV-associated diffuse large B-cell lymphoma causing profound lactic acidosis.

    Prokesch, Bonnie C / Shiloh, Michael U

    Blood

    2014  Volume 124, Issue 6, Page(s) 842

    MeSH term(s) Acidosis, Lactic/etiology ; Adult ; Epstein-Barr Virus Infections/complications ; Epstein-Barr Virus Infections/pathology ; Humans ; Lymphoma, AIDS-Related/complications ; Lymphoma, AIDS-Related/pathology ; Lymphoma, Large B-Cell, Diffuse/complications ; Lymphoma, Large B-Cell, Diffuse/pathology ; Male
    Language English
    Publishing date 2014-08-27
    Publishing country United States
    Document type Case Reports ; Journal Article
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2014-04-567743
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uh III Zs.140: Show issues Location:
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    Zs.MO 364: Show issues

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  9. Article: Bag it, tag it: ubiquitin ligases and host resistance to Mycobacterium tuberculosis

    Campos, Priscila C. / Cunha, Danielle T. / Souza-Costa, Luiz P. / Shiloh, Michael U. / Franco, Luis H.

    Trends in microbiology. 2022,

    2022  

    Abstract: Infection with Mycobacterium tuberculosis (Mtb), the etiological agent of tuberculosis (TB), remains a significant global epidemic. Host resistance to Mtb depends on both adaptive and innate immunity mechanisms, including development of antigen-specific ... ...

    Abstract Infection with Mycobacterium tuberculosis (Mtb), the etiological agent of tuberculosis (TB), remains a significant global epidemic. Host resistance to Mtb depends on both adaptive and innate immunity mechanisms, including development of antigen-specific CD4 and CD8 T cells, production of inflammatory cytokines, bacterial phagocytosis and destruction within phagolysosomes, host cell apoptosis, and autophagy. A key regulatory mechanism in innate immunity is the attachment of the small protein ubiquitin to protein and lipid targets by the enzymatic activity of ubiquitin ligases. Here, we summarize the latest advances on the role of ubiquitination and ubiquitin ligases in host immunity against Mtb, with a focus on innate immunity signaling, inflammation, and antimicrobial autophagy. Understanding how ubiquitin ligases mediate immunity to Mtb, and the specific substrates of distinct ubiquitin ligases in the context of Mtb infection, could facilitate development of new host-directed antimicrobials.
    Keywords CD8-positive T-lymphocytes ; Mycobacterium tuberculosis ; anti-infective agents ; apoptosis ; autophagy ; cytokines ; enzyme activity ; etiological agents ; inflammation ; lipids ; microbiology ; phagocytosis ; phagosomes ; tuberculosis ; ubiquitin ; ubiquitin-protein ligase ; ubiquitination
    Language English
    Publishing place Elsevier Ltd
    Document type Article
    Note Pre-press version
    ZDB-ID 1158963-2
    ISSN 1878-4380 ; 0966-842X
    ISSN (online) 1878-4380
    ISSN 0966-842X
    DOI 10.1016/j.tim.2022.03.010
    Database NAL-Catalogue (AGRICOLA)

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    In stock of ZB MED Bonn / Germany

    Z 2005/714: Show issues

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  10. Article ; Online: Effect of carbon monoxide on Mycobacterium tuberculosis pathogenesis.

    Zacharia, Vineetha M / Shiloh, Michael U

    Medical gas research

    2012  Volume 2, Issue 1, Page(s) 30

    Abstract: The intracellular pathogen Mycobacterium tuberculosis (Mtb) is exposed to multiple host antimicrobial pathways, including toxic gases such as superoxide, nitric oxide and carbon monoxide (CO). To survive, mycobacteria evolved mechanisms to resist the ... ...

    Abstract The intracellular pathogen Mycobacterium tuberculosis (Mtb) is exposed to multiple host antimicrobial pathways, including toxic gases such as superoxide, nitric oxide and carbon monoxide (CO). To survive, mycobacteria evolved mechanisms to resist the toxic environment, and in this review we focus on a relatively new field, namely, the role of macrophage heme oxygenase and its enzymatic product CO in Mtb pathogenesis. In particular, we focus on (i) the induction of heme oxygenase during Mtb infection and its relevance to Mtb pathogenesis, (ii) the ability of mycobacteria to catabolize CO, (iii) the transcriptional reprogramming of Mtb by exposure to CO, (iv) the general antimicrobial properties of CO and (v) new genetic evidence characterizing the ability of Mtb to resist CO toxicity. Developing a complete molecular and genetic understanding of the pathogenesis of Mtb is essential to its eventual eradication.
    Language English
    Publishing date 2012-12-17
    Publishing country Australia
    Document type Journal Article
    ZDB-ID 2616230-1
    ISSN 2045-9912 ; 2045-9912
    ISSN (online) 2045-9912
    ISSN 2045-9912
    DOI 10.1186/2045-9912-2-30
    Database MEDical Literature Analysis and Retrieval System OnLINE

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