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HIV-1 nef limits communication between linker of activated T cells and SLP-76 to reduce formation of SLP-76-signaling microclusters following TCR stimulation
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| Veröffentlicht in: | The journal of immunology 189(2012), 4, Seite 1898-1910 |
|---|---|
| Personen und Körperschaften: | , , , , |
| Titel: | HIV-1 nef limits communication between linker of activated T cells and SLP-76 to reduce formation of SLP-76-signaling microclusters following TCR stimulation/ Libin Abraham, Peter Bankhead, Xiaoyu Pan, Ulrike Engel, and Oliver T. Fackler |
| Format: | E-Book-Kapitel |
| Sprache: | Englisch |
| veröffentlicht: |
August 2, 2012
|
| Gesamtaufnahme: |
: The journal of immunology, 189(2012), 4, Seite 1898-1910
, volume:189 |
| Quelle: | Verbunddaten SWB Lizenzfreie Online-Ressourcen |
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| 245 | 1 | 0 | |a HIV-1 nef limits communication between linker of activated T cells and SLP-76 to reduce formation of SLP-76-signaling microclusters following TCR stimulation |c Libin Abraham, Peter Bankhead, Xiaoyu Pan, Ulrike Engel, and Oliver T. Fackler |
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| 520 | |a Signal initiation by engagement of the TCR triggers actin rearrangements, receptor clustering, and dynamic organization of signaling complexes to elicit and sustain downstream signaling. Nef, a pathogenicity factor of HIV, disrupts early TCR signaling in target T cells. To define the mechanism underlying this Nef-mediated signal disruption, we employed quantitative single-cell microscopy following surface-mediated TCR stimulation that allows for dynamic visualization of distinct signaling complexes as microclusters (MCs). Despite marked inhibition of actin remodeling and cell spreading, the induction of MCs containing TCR-CD3 or ZAP70 was not affected significantly by Nef. However, Nef potently inhibited the subsequent formation of MCs positive for the signaling adaptor Src homology-2 domain-containing leukocyte protein of 76 kDa (SLP-76) to reduce MC density in Nef-expressing and HIV-1-infected T cells. Further analyses suggested that Nef prevents formation of SLP-76 MCs at the level of the upstream adaptor protein, linker of activated T cells (LAT), that couples ZAP70 to SLP-76. Nef did not disrupt pre-existing MCs positive for LAT. However, the presence of the viral protein prevented de novo recruitment of active LAT into MCs due to retargeting of LAT to an intracellular compartment. These modulations in MC formation and composition depended on Nef’s ability to simultaneously disrupt both actin remodeling and subcellular localization of TCR-proximal machinery. Nef thus employs a dual mechanism to disturb early TCR signaling by limiting the communication between LAT and SLP-76 and preventing the dynamic formation of SLP-76-signaling MCs. | ||
| 700 | 1 | |a Bankhead, Peter |e VerfasserIn |0 (DE-588)1074487397 |0 (DE-627)832263850 |0 (DE-576)413998622 |4 aut | |
| 700 | 1 | |a Pan, Xiaoyu |e VerfasserIn |0 (DE-588)102668188X |0 (DE-627)727056190 |0 (DE-576)37196766X |4 aut | |
| 700 | 1 | |a Engel, Ulrike |e VerfasserIn |0 (DE-588)1123163480 |0 (DE-627)879999721 |0 (DE-576)48164525X |4 aut | |
| 700 | 1 | |a Fackler, Oliver Till |e VerfasserIn |0 (DE-588)1026682444 |0 (DE-627)727057391 |0 (DE-576)178094501 |4 aut | |
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| 900 | |a Fackler, Oliver T. | ||
| 900 | |a Fackler, O. T. | ||
| 900 | |a Pan, Xiao-Yu | ||
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| author | Abraham, Libin, Bankhead, Peter, Pan, Xiaoyu, Engel, Ulrike, Fackler, Oliver Till |
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| contents | Signal initiation by engagement of the TCR triggers actin rearrangements, receptor clustering, and dynamic organization of signaling complexes to elicit and sustain downstream signaling. Nef, a pathogenicity factor of HIV, disrupts early TCR signaling in target T cells. To define the mechanism underlying this Nef-mediated signal disruption, we employed quantitative single-cell microscopy following surface-mediated TCR stimulation that allows for dynamic visualization of distinct signaling complexes as microclusters (MCs). Despite marked inhibition of actin remodeling and cell spreading, the induction of MCs containing TCR-CD3 or ZAP70 was not affected significantly by Nef. However, Nef potently inhibited the subsequent formation of MCs positive for the signaling adaptor Src homology-2 domain-containing leukocyte protein of 76 kDa (SLP-76) to reduce MC density in Nef-expressing and HIV-1-infected T cells. Further analyses suggested that Nef prevents formation of SLP-76 MCs at the level of the upstream adaptor protein, linker of activated T cells (LAT), that couples ZAP70 to SLP-76. Nef did not disrupt pre-existing MCs positive for LAT. However, the presence of the viral protein prevented de novo recruitment of active LAT into MCs due to retargeting of LAT to an intracellular compartment. These modulations in MC formation and composition depended on Nef’s ability to simultaneously disrupt both actin remodeling and subcellular localization of TCR-proximal machinery. Nef thus employs a dual mechanism to disturb early TCR signaling by limiting the communication between LAT and SLP-76 and preventing the dynamic formation of SLP-76-signaling MCs. |
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| spelling | Abraham, Libin VerfasserIn (DE-588)1030448566 (DE-627)735277958 (DE-576)378265873 aut, HIV-1 nef limits communication between linker of activated T cells and SLP-76 to reduce formation of SLP-76-signaling microclusters following TCR stimulation Libin Abraham, Peter Bankhead, Xiaoyu Pan, Ulrike Engel, and Oliver T. Fackler, August 2, 2012, 13, Text txt rdacontent, Computermedien c rdamedia, Online-Ressource cr rdacarrier, Gesehen am 22.05.2017, Signal initiation by engagement of the TCR triggers actin rearrangements, receptor clustering, and dynamic organization of signaling complexes to elicit and sustain downstream signaling. Nef, a pathogenicity factor of HIV, disrupts early TCR signaling in target T cells. To define the mechanism underlying this Nef-mediated signal disruption, we employed quantitative single-cell microscopy following surface-mediated TCR stimulation that allows for dynamic visualization of distinct signaling complexes as microclusters (MCs). Despite marked inhibition of actin remodeling and cell spreading, the induction of MCs containing TCR-CD3 or ZAP70 was not affected significantly by Nef. However, Nef potently inhibited the subsequent formation of MCs positive for the signaling adaptor Src homology-2 domain-containing leukocyte protein of 76 kDa (SLP-76) to reduce MC density in Nef-expressing and HIV-1-infected T cells. Further analyses suggested that Nef prevents formation of SLP-76 MCs at the level of the upstream adaptor protein, linker of activated T cells (LAT), that couples ZAP70 to SLP-76. Nef did not disrupt pre-existing MCs positive for LAT. However, the presence of the viral protein prevented de novo recruitment of active LAT into MCs due to retargeting of LAT to an intracellular compartment. These modulations in MC formation and composition depended on Nef’s ability to simultaneously disrupt both actin remodeling and subcellular localization of TCR-proximal machinery. Nef thus employs a dual mechanism to disturb early TCR signaling by limiting the communication between LAT and SLP-76 and preventing the dynamic formation of SLP-76-signaling MCs., Bankhead, Peter VerfasserIn (DE-588)1074487397 (DE-627)832263850 (DE-576)413998622 aut, Pan, Xiaoyu VerfasserIn (DE-588)102668188X (DE-627)727056190 (DE-576)37196766X aut, Engel, Ulrike VerfasserIn (DE-588)1123163480 (DE-627)879999721 (DE-576)48164525X aut, Fackler, Oliver Till VerfasserIn (DE-588)1026682444 (DE-627)727057391 (DE-576)178094501 aut, Enthalten in The journal of immunology Bethesda, Md. : Soc., 1916 189(2012), 4, Seite 1898-1910 Online-Ressource (DE-627)269535217 (DE-600)1475085-5 (DE-576)079963838 1550-6606 nnns, volume:189 year:2012 number:4 pages:1898-1910 extent:13, http://dx.doi.org/10.4049/jimmunol.1200652 Verlag Resolving-System kostenfrei Volltext, http://www.jimmunol.org/content/189/4/1898 Verlag kostenfrei Volltext, http://dx.doi.org/10.4049/jimmunol.1200652 LFER, LFER 2017-06-08T00:00:00Z |
| spellingShingle | Abraham, Libin, Bankhead, Peter, Pan, Xiaoyu, Engel, Ulrike, Fackler, Oliver Till, HIV-1 nef limits communication between linker of activated T cells and SLP-76 to reduce formation of SLP-76-signaling microclusters following TCR stimulation, Signal initiation by engagement of the TCR triggers actin rearrangements, receptor clustering, and dynamic organization of signaling complexes to elicit and sustain downstream signaling. Nef, a pathogenicity factor of HIV, disrupts early TCR signaling in target T cells. To define the mechanism underlying this Nef-mediated signal disruption, we employed quantitative single-cell microscopy following surface-mediated TCR stimulation that allows for dynamic visualization of distinct signaling complexes as microclusters (MCs). Despite marked inhibition of actin remodeling and cell spreading, the induction of MCs containing TCR-CD3 or ZAP70 was not affected significantly by Nef. However, Nef potently inhibited the subsequent formation of MCs positive for the signaling adaptor Src homology-2 domain-containing leukocyte protein of 76 kDa (SLP-76) to reduce MC density in Nef-expressing and HIV-1-infected T cells. Further analyses suggested that Nef prevents formation of SLP-76 MCs at the level of the upstream adaptor protein, linker of activated T cells (LAT), that couples ZAP70 to SLP-76. Nef did not disrupt pre-existing MCs positive for LAT. However, the presence of the viral protein prevented de novo recruitment of active LAT into MCs due to retargeting of LAT to an intracellular compartment. These modulations in MC formation and composition depended on Nef’s ability to simultaneously disrupt both actin remodeling and subcellular localization of TCR-proximal machinery. Nef thus employs a dual mechanism to disturb early TCR signaling by limiting the communication between LAT and SLP-76 and preventing the dynamic formation of SLP-76-signaling MCs. |
| swb_id_str | 488837790 |
| title | HIV-1 nef limits communication between linker of activated T cells and SLP-76 to reduce formation of SLP-76-signaling microclusters following TCR stimulation |
| title_auth | HIV-1 nef limits communication between linker of activated T cells and SLP-76 to reduce formation of SLP-76-signaling microclusters following TCR stimulation |
| title_full | HIV-1 nef limits communication between linker of activated T cells and SLP-76 to reduce formation of SLP-76-signaling microclusters following TCR stimulation Libin Abraham, Peter Bankhead, Xiaoyu Pan, Ulrike Engel, and Oliver T. Fackler |
| title_fullStr | HIV-1 nef limits communication between linker of activated T cells and SLP-76 to reduce formation of SLP-76-signaling microclusters following TCR stimulation Libin Abraham, Peter Bankhead, Xiaoyu Pan, Ulrike Engel, and Oliver T. Fackler |
| title_full_unstemmed | HIV-1 nef limits communication between linker of activated T cells and SLP-76 to reduce formation of SLP-76-signaling microclusters following TCR stimulation Libin Abraham, Peter Bankhead, Xiaoyu Pan, Ulrike Engel, and Oliver T. Fackler |
| title_in_hierarchy | HIV-1 nef limits communication between linker of activated T cells and SLP-76 to reduce formation of SLP-76-signaling microclusters following TCR stimulation / Libin Abraham, Peter Bankhead, Xiaoyu Pan, Ulrike Engel, and Oliver T. Fackler, |
| title_short | HIV-1 nef limits communication between linker of activated T cells and SLP-76 to reduce formation of SLP-76-signaling microclusters following TCR stimulation |
| title_sort | hiv 1 nef limits communication between linker of activated t cells and slp 76 to reduce formation of slp 76 signaling microclusters following tcr stimulation |
| url | http://dx.doi.org/10.4049/jimmunol.1200652, http://www.jimmunol.org/content/189/4/1898 |