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  1. Article ; Online: Cellular stress promotes NOD1/2-dependent inflammation via the endogenous metabolite sphingosine-1-phosphate.

    Pei, Gang / Zyla, Joanna / He, Lichun / Moura-Alves, Pedro / Steinle, Heidrun / Saikali, Philippe / Lozza, Laura / Nieuwenhuizen, Natalie / Weiner, January / Mollenkopf, Hans-Joachim / Ellwanger, Kornelia / Arnold, Christine / Duan, Mojie / Dagil, Yulia / Pashenkov, Mikhail / Boneca, Ivo Gomperts / Kufer, Thomas A / Dorhoi, Anca / Kaufmann, Stefan He

    The EMBO journal

    2021  Volume 40, Issue 13, Page(s) e106272

    Abstract: ... receptors NOD1/2, which sense bacterial peptidoglycans, as general stress sensors detecting perturbations ... Cellular stress has been associated with inflammation, yet precise underlying mechanisms remain ... elusive. In this study, various unrelated stress inducers were employed to screen for sensors linking ...

    Abstract Cellular stress has been associated with inflammation, yet precise underlying mechanisms remain elusive. In this study, various unrelated stress inducers were employed to screen for sensors linking altered cellular homeostasis and inflammation. We identified the intracellular pattern recognition receptors NOD1/2, which sense bacterial peptidoglycans, as general stress sensors detecting perturbations of cellular homeostasis. NOD1/2 activation upon such perturbations required generation of the endogenous metabolite sphingosine-1-phosphate (S1P). Unlike peptidoglycan sensing via the leucine-rich repeats domain, cytosolic S1P directly bound to the nucleotide binding domains of NOD1/2, triggering NF-κB activation and inflammatory responses. In sum, we unveiled a hitherto unknown role of NOD1/2 in surveillance of cellular homeostasis through sensing of the cytosolic metabolite S1P. We propose S1P, an endogenous metabolite, as a novel NOD1/2 activator and NOD1/2 as molecular hubs integrating bacterial and metabolic cues.
    MeSH term(s) Animals ; Cell Line ; Cell Line, Tumor ; Female ; HEK293 Cells ; HeLa Cells ; Humans ; Inflammation/metabolism ; Lysophospholipids/metabolism ; Mice ; NF-kappa B/metabolism ; Nod1 Signaling Adaptor Protein/metabolism ; Nod2 Signaling Adaptor Protein/metabolism ; Peptidoglycan/metabolism ; Signal Transduction/physiology ; Sphingosine/analogs & derivatives ; Sphingosine/metabolism ; THP-1 Cells
    Chemical Substances Lysophospholipids ; NF-kappa B ; NOD1 protein, human ; NOD2 protein, human ; Nod1 Signaling Adaptor Protein ; Nod2 Signaling Adaptor Protein ; Peptidoglycan ; sphingosine 1-phosphate (26993-30-6) ; Sphingosine (NGZ37HRE42)
    Language English
    Publishing date 2021-05-04
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 586044-1
    ISSN 1460-2075 ; 0261-4189
    ISSN (online) 1460-2075
    ISSN 0261-4189
    DOI 10.15252/embj.2020106272
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1808: Show issues Location:
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  2. Article ; Online: Activation of the Endoplasmic Reticulum Stress Response Impacts the NOD1 Signaling Pathway.

    Mendez, Jonathan M / Kolora, Lakshmi Divya / Lemon, James S / Dupree, Steven L / Keestra-Gounder, A Marijke

    Infection and immunity

    2019  Volume 87, Issue 8

    Abstract: ... and the closely related PRR NOD2 have been linked to inflammation by responding ... to the endoplasmic reticulum (ER) stress-induced unfolded protein response (UPR). Here we show that differential ER stress ... Nucleotide-binding oligomerization domain 1 (NOD1) is an intracellular pattern recognition receptor ...

    Abstract Nucleotide-binding oligomerization domain 1 (NOD1) is an intracellular pattern recognition receptor (PRR) responsible for sensing bacterial peptidoglycan fragments. Stimulation of NOD1 leads to a robust innate immune response via activation of the major transcription factor NF-κB. In addition to peptidoglycan sensing, NOD1 and the closely related PRR NOD2 have been linked to inflammation by responding to the endoplasmic reticulum (ER) stress-induced unfolded protein response (UPR). Here we show that differential ER stress induction renders cells more susceptible to
    MeSH term(s) Animals ; Endoplasmic Reticulum Stress/physiology ; HeLa Cells ; Humans ; Inositol 1,4,5-Trisphosphate Receptors/physiology ; Mice ; NF-kappa B/physiology ; Nod1 Signaling Adaptor Protein/physiology ; RAW 264.7 Cells ; Signal Transduction/physiology ; Unfolded Protein Response ; eIF-2 Kinase/physiology
    Chemical Substances Inositol 1,4,5-Trisphosphate Receptors ; NF-kappa B ; NOD1 protein, human ; Nod1 Signaling Adaptor Protein ; EIF2AK3 protein, human (EC 2.7.11.1) ; eIF-2 Kinase (EC 2.7.11.1)
    Language English
    Publishing date 2019-07-23
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 218698-6
    ISSN 1098-5522 ; 0019-9567
    ISSN (online) 1098-5522
    ISSN 0019-9567
    DOI 10.1128/IAI.00826-18
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: NOD1 and NOD2 signalling links ER stress with inflammation.

    Keestra-Gounder, A Marijke / Byndloss, Mariana X / Seyffert, Núbia / Young, Briana M / Chávez-Arroyo, Alfredo / Tsai, April Y / Cevallos, Stephanie A / Winter, Maria G / Pham, Oanh H / Tiffany, Connor R / de Jong, Maarten F / Kerrinnes, Tobias / Ravindran, Resmi / Luciw, Paul A / McSorley, Stephen J / Bäumler, Andreas J / Tsolis, Renée M

    Nature

    2016  Volume 532, Issue 7599, Page(s) 394–397

    Abstract: ... a major role in inducing inflammation during ER stress. Here we show that NOD1 and NOD2, two members ... link between innate immunity and ER-stress-induced inflammation. ... of the NOD-like receptor family of PRRs, are important mediators of ER-stress-induced inflammation in mouse ...

    Abstract Endoplasmic reticulum (ER) stress is a major contributor to inflammatory diseases, such as Crohn disease and type 2 diabetes. ER stress induces the unfolded protein response, which involves activation of three transmembrane receptors, ATF6, PERK and IRE1α. Once activated, IRE1α recruits TRAF2 to the ER membrane to initiate inflammatory responses via the NF-κB pathway. Inflammation is commonly triggered when pattern recognition receptors (PRRs), such as Toll-like receptors or nucleotide-binding oligomerization domain (NOD)-like receptors, detect tissue damage or microbial infection. However, it is not clear which PRRs have a major role in inducing inflammation during ER stress. Here we show that NOD1 and NOD2, two members of the NOD-like receptor family of PRRs, are important mediators of ER-stress-induced inflammation in mouse and human cells. The ER stress inducers thapsigargin and dithiothreitol trigger production of the pro-inflammatory cytokine IL-6 in a NOD1/2-dependent fashion. Inflammation and IL-6 production triggered by infection with Brucella abortus, which induces ER stress by injecting the type IV secretion system effector protein VceC into host cells, is TRAF2, NOD1/2 and RIP2-dependent and can be reduced by treatment with the ER stress inhibitor tauroursodeoxycholate or an IRE1α kinase inhibitor. The association of NOD1 and NOD2 with pro-inflammatory responses induced by the IRE1α/TRAF2 signalling pathway provides a novel link between innate immunity and ER-stress-induced inflammation.
    MeSH term(s) Animals ; Bacterial Outer Membrane Proteins/metabolism ; Brucella abortus/immunology ; Brucella abortus/pathogenicity ; Cell Line ; Dithiothreitol/pharmacology ; Endoplasmic Reticulum/drug effects ; Endoplasmic Reticulum/pathology ; Endoplasmic Reticulum Stress/drug effects ; Endoribonucleases/antagonists & inhibitors ; Female ; Humans ; Immunity, Innate ; Inflammation/chemically induced ; Inflammation/metabolism ; Interleukin-6/biosynthesis ; Male ; Mice ; Mice, Inbred C57BL ; NF-kappa B/metabolism ; Nod1 Signaling Adaptor Protein/immunology ; Nod1 Signaling Adaptor Protein/metabolism ; Nod2 Signaling Adaptor Protein/immunology ; Nod2 Signaling Adaptor Protein/metabolism ; Protein-Serine-Threonine Kinases/antagonists & inhibitors ; Receptors, Pattern Recognition/metabolism ; Signal Transduction/drug effects ; TNF Receptor-Associated Factor 2/metabolism ; Taurochenodeoxycholic Acid/pharmacology ; Thapsigargin/pharmacology ; Unfolded Protein Response/drug effects
    Chemical Substances Bacterial Outer Membrane Proteins ; Interleukin-6 ; NF-kappa B ; Nod1 Signaling Adaptor Protein ; Nod2 Signaling Adaptor Protein ; Receptors, Pattern Recognition ; TNF Receptor-Associated Factor 2 ; Taurochenodeoxycholic Acid (516-35-8) ; tauroursodeoxycholic acid (60EUX8MN5X) ; Thapsigargin (67526-95-8) ; ERN1 protein, human (EC 2.7.11.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; Endoribonucleases (EC 3.1.-) ; Dithiothreitol (T8ID5YZU6Y)
    Language English
    Publishing date 2016-04-21
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/nature17631
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    Zs.MO 244: Show issues

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  4. Article ; Online: Proteome profiling of triple negative breast cancer cells overexpressing NOD1 and NOD2 receptors unveils molecular signatures of malignant cell proliferation.

    Velloso, Fernando J / Campos, Alexandre R / Sogayar, Mari C / Correa, Ricardo G

    BMC genomics

    2019  Volume 20, Issue 1, Page(s) 152

    Abstract: ... in vitro. To further investigate the pathways linking NOD1 and NOD2 signaling to tumorigenesis in TNBC ... new light on the molecular pathways that may be modulating tumorigenesis via NOD1 and NOD2 signaling ... in TNBC. Up- and downregulation of several proteins associated to inflammation and stress response ...

    Abstract Background: Triple negative breast cancer (TNBC) is a malignancy with very poor prognosis, due to its aggressive clinical characteristics and lack of response to receptor-targeted drug therapy. In TNBC, immune-related pathways are typically upregulated and may be associated with a better prognosis of the disease, encouraging the pursuit for immunotherapeutic options. A number of immune-related molecules have already been associated to the onset and progression of breast cancer, including NOD1 and NOD2, innate immune receptors of bacterial-derived components which activate pro-inflammatory and survival pathways. In the context of TNBC, overexpression of either NOD1or NOD2 is shown to reduce cell proliferation and increase clonogenic potential in vitro. To further investigate the pathways linking NOD1 and NOD2 signaling to tumorigenesis in TNBC, we undertook a global proteome profiling of TNBC-derived cells ectopically expressing each one of these NOD receptors.
    Results: We have identified a total of 95 and 58 differentially regulated proteins in NOD1- and NOD2-overexpressing cells, respectively. We used bioinformatics analyses to identify enriched molecular signatures aiming to integrate the differentially regulated proteins into functional networks. These analyses suggest that overexpression of both NOD1 and NOD2 may disrupt immune-related pathways, particularly NF-κB and MAPK signaling cascades. Moreover, overexpression of either of these receptors may affect several stress response and protein degradation systems, such as autophagy and the ubiquitin-proteasome complex. Interestingly, the levels of several proteins associated to cellular adhesion and migration were also affected in these NOD-overexpressing cells.
    Conclusions: Our proteomic analyses shed new light on the molecular pathways that may be modulating tumorigenesis via NOD1 and NOD2 signaling in TNBC. Up- and downregulation of several proteins associated to inflammation and stress response pathways may promote activation of protein degradation systems, as well as modulate cell-cycle and cellular adhesion proteins. Altogether, these signals seem to be modulating cellular proliferation and migration via NF-κB, PI3K/Akt/mTOR and MAPK signaling pathways. Further investigation of altered proteins in these pathways may provide more insights on relevant targets, possibly enabling the immunomodulation of tumorigenesis in the aggressive TNBC phenotype.
    MeSH term(s) Cell Proliferation ; Computational Biology/methods ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Gene Ontology ; Humans ; Nod1 Signaling Adaptor Protein/genetics ; Nod1 Signaling Adaptor Protein/metabolism ; Nod2 Signaling Adaptor Protein/genetics ; Nod2 Signaling Adaptor Protein/metabolism ; Protein Interaction Mapping ; Protein Interaction Maps ; Proteome ; Proteomics/methods ; Transcriptome ; Triple Negative Breast Neoplasms/genetics ; Triple Negative Breast Neoplasms/metabolism ; Triple Negative Breast Neoplasms/pathology
    Chemical Substances NOD1 protein, human ; NOD2 protein, human ; Nod1 Signaling Adaptor Protein ; Nod2 Signaling Adaptor Protein ; Proteome
    Language English
    Publishing date 2019-02-21
    Publishing country England
    Document type Journal Article
    ISSN 1471-2164
    ISSN (online) 1471-2164
    DOI 10.1186/s12864-019-5523-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: NOD1 and NOD2: New Functions Linking Endoplasmic Reticulum Stress and Inflammation.

    Byndloss, Mariana X / Keestra-Gounder, Arina Marijke / Bäumler, Andreas J / Tsolis, Renée M

    DNA and cell biology

    2016  Volume 35, Issue 7, Page(s) 311–313

    Abstract: ... stress signals to elicit inflammation. Given the known roles of both ER stress and NOD2 in chronic ... receptors, NOD1 and NOD2, previously shown to sense bacterial peptidoglycan, were found to transduce ER ... known as ER stress, which activates the host cell's unfolded protein response (UPR) to restore ...

    Abstract Although viruses have long been known to subvert the endoplasmic reticulum (ER) for their replication, recent work has shown that this strategy is also used by bacterial pathogens and parasites to promote their intracellular growth. The ensuing disruption of cellular processes triggers a condition known as ER stress, which activates the host cell's unfolded protein response (UPR) to restore homeostasis. Recent work has linked the UPR, in particular the arm of this response that depends on the ER-resident sensor IRE1, to innate immunity and inflammation. Surprisingly, two intracellular innate immune receptors, NOD1 and NOD2, previously shown to sense bacterial peptidoglycan, were found to transduce ER stress signals to elicit inflammation. Given the known roles of both ER stress and NOD2 in chronic inflammatory diseases, including inflammatory bowel disease and type 2 diabetes, this new link has important implications for understanding the basis for these pathologies.
    MeSH term(s) Animals ; Endoplasmic Reticulum/metabolism ; Endoplasmic Reticulum Stress/physiology ; Humans ; Immunity, Innate/immunology ; Inflammation/immunology ; Inflammation/metabolism ; Nod1 Signaling Adaptor Protein/immunology ; Nod1 Signaling Adaptor Protein/metabolism ; Nod2 Signaling Adaptor Protein/immunology ; Nod2 Signaling Adaptor Protein/metabolism
    Chemical Substances NOD1 protein, human ; NOD2 protein, human ; Nod1 Signaling Adaptor Protein ; Nod2 Signaling Adaptor Protein
    Language English
    Publishing date 2016-07
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1024454-2
    ISSN 1557-7430 ; 0198-0238 ; 1044-5498
    ISSN (online) 1557-7430
    ISSN 0198-0238 ; 1044-5498
    DOI 10.1089/dna.2016.3396
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