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  • Gaestel, Matthias  (5)
  • Menon, Manoj B.  (5)
  • 2020-2024  (5)
  • 1
    Online Resource
    Online Resource
    Editorial: Emerging Functions of Septins—Volume II
    Frontiers Media SA ; 2022
    In:  Frontiers in Cell and Developmental Biology Vol. 10 ( 2022-6-16)
    Details
    In: Frontiers in Cell and Developmental Biology, Frontiers Media SA, Vol. 10 ( 2022-6-16)
    Type of Medium: Online Resource
    ISSN: 2296-634X
    URL: Article
    DOI: 10.3389/fcell.2022.949824
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2737824-X
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  • 2
    Online Resource
    Online Resource
    PRMT5-mediated regulatory arginine methylation of RIPK3
    Springer Science and Business Media LLC ; 2023
    In:  Cell Death Discovery Vol. 9, No. 1 ( 2023-01-19)
    Details
    In: Cell Death Discovery, Springer Science and Business Media LLC, Vol. 9, No. 1 ( 2023-01-19)
    Abstract: The TNF receptor-interacting protein kinases (RIPK)-1 and 3 are regulators of extrinsic cell death response pathways, where RIPK1 makes the cell survival or death decisions by associating with distinct complexes mediating survival signaling, caspase activation or RIPK3-dependent necroptotic cell death in a context-dependent manner. Using a mass spectrometry-based screen to find new components of the ripoptosome/necrosome, we discovered the protein-arginine methyltransferase (PRMT)-5 as a direct interaction partner of RIPK1. Interestingly, RIPK3 but not RIPK1 was then found to be a target of PRMT5-mediated symmetric arginine dimethylation. A conserved arginine residue in RIPK3 (R486 in human, R415 in mouse) was identified as the evolutionarily conserved target for PRMT5-mediated symmetric dimethylation and the mutations R486A and R486K in human RIPK3 almost completely abrogated its methylation. Rescue experiments using these non-methylatable mutants of RIPK3 demonstrated PRMT5-mediated RIPK3 methylation to act as an efficient mechanism of RIPK3-mediated feedback control on RIPK1 activity and function. Therefore, this study reveals PRMT5-mediated RIPK3 methylation as a novel modulator of RIPK1-dependent signaling.
    Type of Medium: Online Resource
    ISSN: 2058-7716
    URL: Article
    DOI: 10.1038/s41420-023-01299-z
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 2842546-7
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    Online Resource
  • 3
    Online Resource
    Online Resource
    Image5.JPEG
    Frontiers Media SA ; 2022
    In:  Frontiers in Cell and Developmental Biology Vol. 9 ( 2022-1-6)
    Details
    In: Frontiers in Cell and Developmental Biology, Frontiers Media SA, Vol. 9 ( 2022-1-6)
    Abstract: By crossing septin7 -floxed mice with Lyz2 -Cre mice carrying the Cre recombinase inserted in the Lysozyme-M ( Lyz2 ) gene locus we aimed the specific deletion of septin7 in myeloid cells, such as monocytes, macrophages and granulocytes. Septin7 flox/flox : Lyz2- Cre mice show no alterations in the myeloid compartment. Septin7 -deleted macrophages (BMDMs) were isolated and analyzed. The lack of Septin7 expression was confirmed and a constitutive double-nucleation was detected in Septin7-deficient BMDMs indicating a defect in macrophage cytokinesis. However, phagocytic function of macrophages as judged by uptake of labelled E. coli particles and LPS-stimulated macrophage activation as judged by induction of TNF mRNA expression and TNF secretion were not compromised. In addition to myeloid cells, Lyz2-Cre is also active in type II pneumocytes (AT2 cells). We monitored lung adenocarcinoma formation in these mice by crossing them with the conditional knock-in Kras -LSL-G12D allele. Interestingly, we found that control mice without septin7 depletion die after 3–5 weeks, while the Septin7-deficient animals survived 11 weeks or even longer. Control mice sacrificed in the age of 4 weeks display a bronchiolo-alveolar hyperplasia with multiple adenomas, whereas the Septin7-deficient animals of the same age are normal or show only a weak multifocal brochiolo-alveolar hyperplasia. Our findings indicate an essential role of Septin7 in macrophage cytokinesis but not in macrophage function. Furthermore, septin7 seems absolutely essential for oncogenic Kras -driven lung tumorigenesis making it a potential target for anti-tumor interventions.
    Type of Medium: Online Resource
    ISSN: 2296-634X
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.3389/fcell.2021.795798
    DOI: 10.3389/fcell.2021.795798.s001
    DOI: 10.3389/fcell.2021.795798.s002
    DOI: 10.3389/fcell.2021.795798.s003
    DOI: 10.3389/fcell.2021.795798.s004
    DOI: 10.3389/fcell.2021.795798.s005
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2737824-X
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  • 4
    Online Resource
    Online Resource
    Image_4.tif
    Frontiers Media SA ; 2023
    In:  Frontiers in Immunology Vol. 14 ( 2023-9-12)
    Details
    In: Frontiers in Immunology, Frontiers Media SA, Vol. 14 ( 2023-9-12)
    Abstract: Autophagy plays an important role in recognizing and protecting cells from invading intracellular pathogens such as Salmonella . In this work, we investigated the role of p38 MAPK /MK2 in modulating the host cell susceptibility to Salmonella infection. Inhibition of p38 MAPK or MK2 led to a significant increase of bacterial counts in Salmonella infected mouse embryonic fibroblasts (MEFs), as well as in MK2-deficient ( Mk2 -/- ) cells. Furthermore, western blot analysis showed that Mk2 -/- cells have lower level of LC3 lipidation, which is the indicator of general autophagy compared to Mk2 -rescued cells. In Mk2 -/- cells, we also observed lower activated TANK-binding kinase-1 phosphorylation on Ser172 and p62/SQTM1-Ser403 phosphorylation, which are important to promote the translocation of p62 to ubiquitinated microbes and required for efficient autophagy of bacteria. Furthermore, immunofluorescence analysis revealed reduced colocalization of Salmonella with LC3 and p62 in MEFs. Inhibition of autophagy with bafilomycin A1 showed increased bacterial counts in treated cells compared to control cell. Overall, these results indicate that p38 MAPK /MK2-mediated protein phosphorylation modulates the host cell susceptibility to Salmonella infection by affecting the autophagy pathways.
    Type of Medium: Online Resource
    ISSN: 1664-3224
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.3389/fimmu.2023.1245443
    DOI: 10.3389/fimmu.2023.1245443.s001
    DOI: 10.3389/fimmu.2023.1245443.s002
    DOI: 10.3389/fimmu.2023.1245443.s003
    DOI: 10.3389/fimmu.2023.1245443.s004
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2023
    detail.hit.zdb_id: 2606827-8
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  • 5
    Online Resource
    Online Resource
    5-Iodotubercidin sensitizes cells to RIPK1-dependent necroptosis by interfering with NFκB signaling
    Springer Science and Business Media LLC ; 2023
    In:  Cell Death Discovery Vol. 9, No. 1 ( 2023-07-26)
    Details
    In: Cell Death Discovery, Springer Science and Business Media LLC, Vol. 9, No. 1 ( 2023-07-26)
    Abstract: Receptor-interacting protein kinases (RIPK)-1 and -3 play crucial roles in cell fate decisions and are regulated by multiple checkpoint controls. Previous studies have identified IKK1/2- and p38/MK2-dependent checkpoints that phosphorylate RIPK1 at different residues to inhibit its activation. In this study, we investigated TNF-induced death in MAPK-activated protein kinase 2 (MK2)-deficient cells and found that MK2 deficiency or inactivation predominantly leads to necroptotic cell death, even without caspase inhibition. While RIPK1 inhibitors can rescue MK2-deficient cells from necroptosis, inhibiting RIPK3 seems to switch the process to apoptosis. To understand the underlying mechanism of this switch, we screened a library of 149 kinase inhibitors and identified the adenosine analog 5-Iodotubercidin (5-ITu) as the most potent compound that sensitizes MK2-deficient MEFs to TNF-induced cell death. 5-ITu also enhances LPS-induced necroptosis when combined with MK2 inhibition in RAW264.7 macrophages. Further mechanistic studies revealed that 5-ITu induces RIPK1-dependent necroptosis by suppressing IKK signaling in the absence of MK2 activity. These findings highlight the role for the multitarget kinase inhibitor 5-ITu in TNF-, LPS- and chemotherapeutics-induced necroptosis and its potential implications in RIPK1-targeted therapies.
    Type of Medium: Online Resource
    ISSN: 2058-7716
    URL: Article
    DOI: 10.1038/s41420-023-01576-x
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 2842546-7
    Location Call Number Limitation Availability
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