Loss of the Rap1 effector RIAM results in leukocyte adhesion deficiency due to impaired β2 integrin function in mice
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چکیده
منابع مشابه
Loss of the Rap1 effector RIAM results in leukocyte adhesion deficiency due to impaired β2 integrin function in mice.
Talin is an integrin adaptor, which controls integrin activity in all hematopoietic cells. How intracellular signals promote talin binding to the integrin tail leading to integrin activation is still poorly understood, especially in leukocytes. In vitro studies identified an integrin activation complex whose formation is initiated by the interaction of active, guanosine triphosphate (GTP)-bound...
متن کاملLoss of the Rap1 effector RIAM results in leukocyte adhesion deficiency due to impaired b2 integrin function in mice
Integrins are a/b heterodimeric transmembrane receptors that are expressed on all cells. They provide stable adhesion of cells to the extracellular matrix or to other cell counter receptors by forming complex adhesion sites, which serve as signaling platforms (outside-in signaling) that induce cell polarity, migration, survival, and proliferation. Because integrins reside in an inactive state, ...
متن کاملLAD-III, a leukocyte adhesion deficiency syndrome associated with defective Rap1 activation and impaired stabilization of integrin bonds.
Recently, we reported a rare leukocyte adhesion deficiency (LAD) associated with severe defects in integrin activation by chemokine signals, despite normal ligand binding of leukocyte integrins.(1) We now report that the small GTPase, Rap1, a key regulator of inside-out integrin activation is abnormally regulated in LAD Epstein-Barr virus (EBV) lymphocyte cells. Both constitutive and chemokine-...
متن کاملThe critical cytoplasmic regions of the αL/β2 integrin in Rap1-induced adhesion and migration
متن کامل
Rap1 and its effector RIAM are required for lymphocyte trafficking.
Regulation of integrins is critical for lymphocyte adhesion to endothelium and trafficking through secondary lymphoid organs. Inside-out signaling to integrins is mediated by the small GTPase Rap1. Two effectors of Rap1 regulate integrins, RapL and Rap1 interacting adaptor molecule (RIAM). Using mice conditionally deficient in both Rap1a and Rap1b and mice null for RIAM, we show that the Rap1/R...
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ژورنال
عنوان ژورنال: Blood
سال: 2015
ISSN: 0006-4971,1528-0020
DOI: 10.1182/blood-2015-05-647453