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Published byEsther Carr Modified over 9 years ago
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The β2 integrin–kindlin-3 interaction is essential for T-cell homing but dispensable for T-cell activation in vivo by Vicky Louise Morrison, Matthew MacPherson, Terhi Savinko, Hwee San Lek, Alan Prescott, and Susanna Carola Fagerholm Blood Volume 122(8):1428-1436 August 22, 2013 ©2013 by American Society of Hematology
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The TTT motif in the β2 integrin tail mediates kindlin-3 binding. Vicky Louise Morrison et al. Blood 2013;122:1428-1436 ©2013 by American Society of Hematology
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Generation and phenotype of β2TTT/AAA integrin knock-in mice. Vicky Louise Morrison et al. Blood 2013;122:1428-1436 ©2013 by American Society of Hematology
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β2TTT/AAA integrin knock-in T cells display impaired adhesion. Vicky Louise Morrison et al. Blood 2013;122:1428-1436 ©2013 by American Society of Hematology
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Loss of β2–kindlin-3 interactions in CD4 T cells results in impaired adhesion strengthening and impaired migration on ICAM-1 in vitro. Vicky Louise Morrison et al. Blood 2013;122:1428-1436 ©2013 by American Society of Hematology
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Loss of β2–kindlin-3 interactions in CD4 T cells results in altered homing in vivo. Vicky Louise Morrison et al. Blood 2013;122:1428-1436 ©2013 by American Society of Hematology
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β2TTT/AAA integrin knock-in CD4 T-cell activation in vitro and in vivo is normal. Vicky Louise Morrison et al. Blood 2013;122:1428-1436 ©2013 by American Society of Hematology
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