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10.1242/jcs.200006

http://scihub22266oqcxt.onion/10.1242/jcs.200006
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C5358343!5358343!28154159
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suck abstract from ncbi


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pmid28154159      J+Cell+Sci 2017 ; 130 (6): 1110-21
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  • The T cell IFT20 interactome reveals new players in immune synapse assembly #MMPMID28154159
  • Galgano D; Onnis A; Pappalardo E; Galvagni F; Acuto O; Baldari CT
  • J Cell Sci 2017[Mar]; 130 (6): 1110-21 PMID28154159show ga
  • Sustained signalling at the immune synapse (IS) requires the synaptic delivery of recycling endosome-associated T cell antigen receptors (TCRs). IFT20, a component of the intraflagellar transport system, controls TCR recycling to the IS as a complex with IFT57 and IFT88. Here, we used quantitative mass spectrometry to identify additional interaction partners of IFT20 in Jurkat T cells. In addition to IFT57 and IFT88, the analysis revealed new binding partners, including IFT54 (also known as TRAF3IP1), GMAP-210 (also known as TRIP11), Arp2/3 complex subunit-3 (ARPC3), COP9 signalosome subunit-1 (CSN1, also known as GPS1) and ERGIC-53 (also known as LMAN1). A direct interaction between IFT20 and both IFT54 and GMAP-210 was confirmed in pulldown assays. Confocal imaging of antigen-specific conjugates using T cells depleted of these proteins by RNA interference showed that TCR accumulation and phosphotyrosine signalling at the IS were impaired in the absence of IFT54, ARPC3 or ERGIC-53. Similar to in IFT20-deficient T cells, this defect resulted from a reduced ability of endosomal TCRs to polarize to the IS despite a correct translocation of the centrosome towards the antigen-presenting cell contact. Our data underscore the traffic-related role of an IFT20 complex that includes components of the intracellular trafficking machinery in IS assembly.
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