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Siglec-E is a negative regulator of acute pulmonary neutrophil inflammation and suppresses CD11b β2- integrin–dependent signaling by Sarah J. McMillan, Ritu S. Sharma, Emma J. McKenzie, Hannah E. Richards, Jiquan Zhang, Alan Prescott, and Paul R. Crocker Blood Volume 121(11):2084-2094 March 14, 2013 ©2013 by American Society of Hematology
Generation of siglec-E–deficient mice. Sarah J. McMillan et al. Blood 2013;121:2084-2094 ©2013 by American Society of Hematology
LPS-induced airway inflammation in siglec-E–deficient mice. Sarah J. McMillan et al. Blood 2013;121:2084-2094 ©2013 by American Society of Hematology
Chemotactic responses and requirement for CD11b in exaggerated neutrophil recruitment of siglec-E–deficient mice exposed to LPS. (A) CXCL1 and CXCL2 levels were measured in serum, bronchoalveolar lavage (BAL) fluid, and lung tissue homogenate by enzyme-link... Sarah J. McMillan et al. Blood 2013;121:2084-2094 ©2013 by American Society of Hematology
Siglec-E does not regulate “inside-out” signaling of CD11b in neutrophils. Sarah J. McMillan et al. Blood 2013;121:2084-2094 ©2013 by American Society of Hematology
Siglec-E is preferentially localized in areas of high CD11b staining on neutrophils spreading over fibrinogen. Sarah J. McMillan et al. Blood 2013;121:2084-2094 ©2013 by American Society of Hematology
Siglec-E is a negative regulator of CD11b-dependent phosphorylation of Syk and p38 MAP kinase. Sarah J. McMillan et al. Blood 2013;121:2084-2094 ©2013 by American Society of Hematology
Siglec-E associates with SHP-1 in the absence of tyrosine phosphorylation. Sarah J. McMillan et al. Blood 2013;121:2084-2094 ©2013 by American Society of Hematology
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Introduction ●Cux1 is a transcriptional repressor gene and part of the network controlling G1-S phase transition. It represses the expression of the cyclin.
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