LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 6 of total 6

Search options

  1. Article ; Online: TRAF3 enhances type I interferon receptor signaling in T cells by modulating the phosphatase PTPN22.

    Hornick, Emma L / Wallis, Alicia M / Bishop, Gail A

    Science signaling

    2022  Volume 15, Issue 753, Page(s) eabn5507

    Abstract: Type I interferons (IFNs) are among the most powerful tools that host cells deploy against intracellular pathogens. Their effectiveness is due both to the rapid, directly antiviral effects of IFN-stimulated gene products and to the effects of type I IFN ... ...

    Abstract Type I interferons (IFNs) are among the most powerful tools that host cells deploy against intracellular pathogens. Their effectiveness is due both to the rapid, directly antiviral effects of IFN-stimulated gene products and to the effects of type I IFN on responding immune cells. Type I IFN signaling through its receptor, IFNAR, is tightly regulated at multiple steps in the signaling cascade, including at the level of IFNAR downstream effectors, which include the kinase JAK1 and the transcriptional regulator STAT1. Here, we found that tumor necrosis factor receptor (TNFR)-associated factor 3 (TRAF3) enhanced the activation of JAK1 and STAT1 specifically in CD4
    MeSH term(s) Antiviral Agents/metabolism ; Interferon Type I/genetics ; Interferon Type I/metabolism ; Phosphoric Monoester Hydrolases/metabolism ; Receptor, Interferon alpha-beta/genetics ; Receptors, Tumor Necrosis Factor/metabolism ; T-Lymphocytes/metabolism ; TNF Receptor-Associated Factor 3/genetics ; TNF Receptor-Associated Factor 3/metabolism
    Chemical Substances Antiviral Agents ; Interferon Type I ; Receptors, Tumor Necrosis Factor ; TNF Receptor-Associated Factor 3 ; Receptor, Interferon alpha-beta (156986-95-7) ; Phosphoric Monoester Hydrolases (EC 3.1.3.2)
    Language English
    Publishing date 2022-09-27
    Publishing country United States
    Document type Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
    ZDB-ID 2417226-1
    ISSN 1937-9145 ; 1945-0877
    ISSN (online) 1937-9145
    ISSN 1945-0877
    DOI 10.1126/scisignal.abn5507
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  2. Article ; Online: TRAF3 regulation of inhibitory signaling pathways in B and T lymphocytes by kinase and phosphatase localization.

    Wallis, Alicia M / Bishop, Gail A

    Journal of leukocyte biology

    2018  

    Abstract: This brief review presents current understanding of how the signaling adapter protein TRAF3 can both induce and block inhibitory signaling pathways in B and T lymphocytes, via association with kinases and phosphatases, and subsequent regulation of their ... ...

    Abstract This brief review presents current understanding of how the signaling adapter protein TRAF3 can both induce and block inhibitory signaling pathways in B and T lymphocytes, via association with kinases and phosphatases, and subsequent regulation of their localization within the cell. In B lymphocytes, signaling through the interleukin 6 receptor (IL-6R) induces association of TRAF3 with IL-6R-associated JAK1, to which TRAF3 recruits the phosphatase PTPN22 (protein tyrosine phosphatase number 22) to dephosphorylate JAK1 and STAT3, inhibiting IL-6R signaling. An important biological consequence of this inhibition is restraining the size of the plasma cell compartment, as their differentiation is IL-6 dependent. Similarly, in T lymphocytes, interleukin 2 receptor (IL-2R) signaling recruits TRAF3, which in turn recruits the phosphatase TCPTP (T cell protein tyrosine phosphatase) to dephosphorylate JAK3. The resulting inhibition of IL-2R signaling limits the IL-2-dependent size of the T regulatory cell (Treg) compartment. TRAF3 also inhibits type 1 IFN receptor (IFNαR) signaling to T cells by this mechanism, restraining expression of IFN-stimulated gene expression. In contrast, TRAF3 association with two inhibitors of TCR signaling, C-terminal Src kinase (Csk) and PTPN22, promotes their localization to the cytoplasm, away from the membrane TCR complex. TRAF3 thus enhances TCR signaling and downstream T cell activation. Implications are discussed for these regulatory roles of TRAF3 in lymphocytes, as well as potential future directions.
    Language English
    Publishing date 2018-01-17
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 605722-6
    ISSN 1938-3673 ; 0741-5400
    ISSN (online) 1938-3673
    ISSN 0741-5400
    DOI 10.1002/JLB.2MIR0817-339RR
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 603: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  3. Article ; Online: Roles of TRAF3 in T cells: many surprises.

    Yi, Zuoan / Wallis, Alicia M / Bishop, Gail A

    Cell cycle (Georgetown, Tex.)

    2015  Volume 14, Issue 8, Page(s) 1156–1163

    Abstract: Tumor necrosis factor receptor (TNFR)-associated factor 3 (TRAF3) is broadly involved in different receptor-mediated signaling pathways. Considerable progress was made recently in understanding the role of TRAF3 in T cell biology. Here we review these ... ...

    Abstract Tumor necrosis factor receptor (TNFR)-associated factor 3 (TRAF3) is broadly involved in different receptor-mediated signaling pathways. Considerable progress was made recently in understanding the role of TRAF3 in T cell biology. Here we review these new findings about how TRAF3 participates in T cell development and function. The different roles of TRAF3 in distinct immune cells are also compared. That TRAF3 is required for T cell effector functions, and invariant Natural Killer T cell function and development, was unexpected. Another surprising finding is that TRAF3 normally restrains regulatory T cell development. It is now clear that TRAF3 regulates signaling to T cells not only through costimulatory members of the TNFR superfamily, but also through the T cell receptor complex, and cytokine receptors. The diverse roles it plays support the multifaceted nature of this molecule. How TRAF3 mediates integration of different signaling cascades is an important topic for future study.
    MeSH term(s) Animals ; Humans ; Killer Cells, Natural/immunology ; Killer Cells, Natural/metabolism ; NF-kappa B/metabolism ; Receptors, Interleukin-2/metabolism ; Signal Transduction ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/metabolism ; TNF Receptor-Associated Factor 3/deficiency ; TNF Receptor-Associated Factor 3/genetics ; TNF Receptor-Associated Factor 3/metabolism
    Chemical Substances NF-kappa B ; Receptors, Interleukin-2 ; TNF Receptor-Associated Factor 3
    Language English
    Publishing date 2015-03-03
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2146183-1
    ISSN 1551-4005 ; 1538-4101 ; 1554-8627
    ISSN (online) 1551-4005
    ISSN 1538-4101 ; 1554-8627
    DOI 10.1080/15384101.2015.1021524
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 5881: 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)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  4. Article ; Online: TRAF3 deficiency promotes metabolic reprogramming in B cells.

    Mambetsariev, Nurbek / Lin, Wai W / Wallis, Alicia M / Stunz, Laura L / Bishop, Gail A

    Scientific reports

    2016  Volume 6, Page(s) 35349

    Abstract: The adaptor protein TNF receptor-associated factor 3 (TRAF3) is a critical regulator of B lymphocyte survival. B cell-specific TRAF3 deficiency results in enhanced viability and is associated with development of lymphoma and multiple myeloma. We show ... ...

    Abstract The adaptor protein TNF receptor-associated factor 3 (TRAF3) is a critical regulator of B lymphocyte survival. B cell-specific TRAF3 deficiency results in enhanced viability and is associated with development of lymphoma and multiple myeloma. We show that TRAF3 deficiency led to induction of two proteins important for glucose metabolism, Glut1 and Hexokinase 2 (HXK2). This was associated with increased glucose uptake. In the absence of TRAF3, anaerobic glycolysis and oxidative phosphorylation were increased in B cells without changes in mitochondrial mass or reactive oxygen species. Chemical inhibition of glucose metabolism or glucose deprivation substantially attenuated the enhanced survival of TRAF3-deficient B cells, with a decrease in the pro-survival protein Mcl-1. Changes in Glut1 and Mcl-1 levels, glucose uptake and B cell number in the absence of TRAF3 were all dependent upon NF-κB inducing kinase (NIK). These results indicate that TRAF3 deficiency suffices to metabolically reprogram B cells, a finding that improves our understanding of the role of TRAF3 as a tumor suppressor, and suggests potential therapeutic strategies.
    MeSH term(s) Animals ; B-Lymphocytes/metabolism ; Cellular Reprogramming/genetics ; Glucose/genetics ; Glucose/metabolism ; Glucose Transporter Type 1/genetics ; Glucose Transporter Type 1/metabolism ; Hexokinase/genetics ; Hexokinase/metabolism ; Lymphoma/genetics ; Lymphoma/pathology ; Mice, Knockout ; Multiple Myeloma/genetics ; Multiple Myeloma/pathology ; Myeloid Cell Leukemia Sequence 1 Protein/genetics ; Myeloid Cell Leukemia Sequence 1 Protein/metabolism ; Protein Serine-Threonine Kinases/genetics ; Protein Serine-Threonine Kinases/metabolism ; Reactive Oxygen Species/metabolism ; TNF Receptor-Associated Factor 3/deficiency ; TNF Receptor-Associated Factor 3/genetics ; TNF Receptor-Associated Factor 3/metabolism ; NF-kappaB-Inducing Kinase
    Chemical Substances Glucose Transporter Type 1 ; Mcl1 protein, mouse ; Myeloid Cell Leukemia Sequence 1 Protein ; Reactive Oxygen Species ; Slc2a1 protein, mouse ; TNF Receptor-Associated Factor 3 ; Hexokinase (EC 2.7.1.1) ; hexokinase 2, mouse (EC 2.7.1.1) ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2016-10-18
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/srep35349
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  5. Article ; Online: TRAF3 enhances TCR signaling by regulating the inhibitors Csk and PTPN22.

    Wallis, Alicia M / Wallace, Ellie C / Hostager, Bruce S / Yi, Zuoan / Houtman, Jon C D / Bishop, Gail A

    Scientific reports

    2017  Volume 7, Issue 1, Page(s) 2081

    Abstract: The adaptor protein TNF receptor associated factor (TRAF) 3 is required for effective TCR signaling and normal T cell effector functions, and associates with the CD3/CD28 complex upon activation. To determine how TRAF3 promotes proximal TCR signaling, we ...

    Abstract The adaptor protein TNF receptor associated factor (TRAF) 3 is required for effective TCR signaling and normal T cell effector functions, and associates with the CD3/CD28 complex upon activation. To determine how TRAF3 promotes proximal TCR signaling, we studied TRAF3-deficient mouse and human T cells, which showed a marked reduction in activating phosphorylation of the TCR-associated kinase Lck. The impact of TRAF3 on this very early signaling event led to the hypothesis that TRAF3 restrains one or both of two known inhibitors of Lck, C-terminal Src kinase (Csk) and protein tyrosine phosphatase N22 (PTPN22). TRAF3 associated with Csk, promoting the dissociation of Csk from the plasma membrane. TRAF3 also associated with and regulated the TCR/CD28 induced localization of PTPN22. Loss of TRAF3 resulted in increased amounts of both Csk and PTPN22 in T cell membrane fractions and decreased association of PTPN22 with Csk. These findings identify a new role for T cell TRAF3 in promoting T cell activation, by regulating localization and functions of early TCR signaling inhibitors.
    MeSH term(s) Animals ; Cell Line, Tumor ; Cell Membrane/metabolism ; Cells, Cultured ; HEK293 Cells ; Humans ; Mice ; Mice, Inbred C57BL ; Protein Binding ; Protein Transport ; Protein Tyrosine Phosphatase, Non-Receptor Type 22/metabolism ; Receptors, Antigen, T-Cell/metabolism ; Signal Transduction ; T-Lymphocytes/metabolism ; TNF Receptor-Associated Factor 3/genetics ; TNF Receptor-Associated Factor 3/metabolism ; src-Family Kinases/metabolism
    Chemical Substances Receptors, Antigen, T-Cell ; TNF Receptor-Associated Factor 3 ; CSK tyrosine-protein kinase (EC 2.7.10.2) ; src-Family Kinases (EC 2.7.10.2) ; Protein Tyrosine Phosphatase, Non-Receptor Type 22 (EC 3.1.3.48) ; Ptpn22 protein, mouse (EC 3.1.3.48)
    Language English
    Publishing date 2017-05-18
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-017-02280-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  6. Article ; Online: Foxk1 promotes cell proliferation and represses myogenic differentiation by regulating Foxo4 and Mef2.

    Shi, Xiaozhong / Wallis, Alicia M / Gerard, Robert D / Voelker, Kevin A / Grange, Robert W / DePinho, Ronald A / Garry, Mary G / Garry, Daniel J

    Journal of cell science

    2012  Volume 125, Issue Pt 22, Page(s) 5329–5337

    Abstract: In response to severe injury, adult skeletal muscle exhibits a remarkable regenerative capacity due to a resident muscle stem/progenitor cell population. While a number of factors are expressed in the muscle progenitor cell (MPC) population, the ... ...

    Abstract In response to severe injury, adult skeletal muscle exhibits a remarkable regenerative capacity due to a resident muscle stem/progenitor cell population. While a number of factors are expressed in the muscle progenitor cell (MPC) population, the molecular networks that govern this cell population remain an area of active investigation. In this study, utilizing knockdown techniques and overexpression of Foxk1 in the myogenic lineage, we observed dysregulation of Foxo and Mef2 downstream targets. Utilizing an array of technologies, we establish that Foxk1 represses the transcriptional activity of Foxo4 and Mef2 and physically interacts with Foxo4 and Mef2, thus promoting MPC proliferation and antagonizing the myogenic lineage differentiation program, respectively. Correspondingly, knockdown of Foxk1 in C2C12 myoblasts results in cell cycle arrest, and Foxk1 overexpression in C2C12CAR myoblasts retards muscle differentiation. Collectively, we have established that Foxk1 promotes MPC proliferation by repressing Foxo4 transcriptional activity and inhibits myogenic differentiation by repressing Mef2 activity. These studies enhance our understanding of the transcriptional networks that regulate the MPC population and muscle regeneration.
    MeSH term(s) Animals ; Cell Cycle ; Cell Cycle Proteins ; Cell Differentiation ; Cell Proliferation ; DNA/metabolism ; Forkhead Transcription Factors/metabolism ; MEF2 Transcription Factors ; Male ; Mice ; Mice, Knockout ; Muscle Development ; Muscle, Skeletal/cytology ; Muscle, Skeletal/physiology ; Myogenic Regulatory Factors/metabolism ; Protein Binding ; Regeneration ; Repressor Proteins/metabolism ; Transcription, Genetic
    Chemical Substances Cell Cycle Proteins ; Forkhead Transcription Factors ; FoxO4 protein, mouse ; Foxk1 protein, mouse ; MEF2 Transcription Factors ; Mef2c protein, mouse ; Myogenic Regulatory Factors ; Repressor Proteins ; DNA (9007-49-2)
    Language English
    Publishing date 2012-09-06
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2993-2
    ISSN 1477-9137 ; 0021-9533
    ISSN (online) 1477-9137
    ISSN 0021-9533
    DOI 10.1242/jcs.105239
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 1200: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 14: Show issues

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

To top