Integrin CD11c/CD18 α-chain phosphorylation is functionally important.

J Biol Chem

From the Division of Biochemistry and Biotechnology, Department of Biosciences, University of Helsinki, 00014 Helsinki, Finland.

Published: November 2013

CD11c/CD18 (αXβ2, p150/95, or complement receptor 4, CR4) is a monocyte/macrophage-enriched integrin that has been reported to bind to a variety of ligands. These include cell surface proteins, extracellular matrix proteins, and soluble ligands. The regulation of ligand binding to CD11c/CD18 has remained poorly understood. Previous work has shown that both α-chain and β-chain phosphorylations of CD11a/CD18 and CD11b/CD18 are needed for activity, but no corresponding studies on CD11c/CD18 have been performed. In this study, we have identified the phosphorylation site of CD11c as Ser-1158 and show that it is pivotal for adherence and phagocytosis.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3829194PMC
http://dx.doi.org/10.1074/jbc.C113.497446DOI Listing

Publication Analysis

Top Keywords

integrin cd11c/cd18
4
cd11c/cd18 α-chain
4
α-chain phosphorylation
4
phosphorylation functionally
4
functionally cd11c/cd18
4
cd11c/cd18 αxβ2
4
αxβ2 p150/95
4
p150/95 complement
4
complement receptor
4
receptor cr4
4

Similar Publications

The Complement System is composed of more than 40 proteins that act in innate and adaptive immunity. C3 is the most abundant one and C3-deficient patients are more susceptible to recurrent and severe infections. Several studies have demonstrated the importance of C3 in controlling infections.

View Article and Find Full Text PDF

CD11c is not required by microglia to convey neuroprotection after prion infection.

PLoS One

November 2023

Laboratory of Neurological Infections and Immunity, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana, United States of America.

Prion diseases are caused by the misfolding of a normal host protein that leads to gliosis, neuroinflammation, neurodegeneration, and death. Microglia have been shown to be critical for neuroprotection during prion infection of the central nervous system (CNS), and their presence extends survival in mice. How microglia impart these benefits to the infected host are unknown.

View Article and Find Full Text PDF

Transglutaminase 2 associated with PI3K and PTEN in a membrane-bound signalosome platform blunts cell death.

Cell Death Dis

March 2023

Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Debrecen, Egyetem tér 1, Debrecen, H-4032, Hungary.

Atypically expressed transglutaminase 2 (TG2) has been identified as a poor prognostic factor in a variety of cancers. In this study, we evaluated the contribution of TG2 to the prolonged cell survival of differentiated acute promyelocytic leukaemia (APL) cells in response to the standard treatment with combined retinoic acid (ATRA) and arsenic trioxide (ATO). We report that one advantage of ATRA + ATO treatment compared to ATRA alone diminishes the amount of activated and non-activated CD11b/CD18 and CD11c/CD18 cell surface integrin receptors.

View Article and Find Full Text PDF

Activation of the integrin phagocytic receptors CR3 (αβ, CD11b/CD18) and CR4 (αβ, CD11c/CD18) requires Rap1 activation and RIAM function. RIAM controls integrin activation by recruiting Talin to β subunits, enabling the Talin-Vinculin interaction, which in term bridges integrins to the actin-cytoskeleton. RIAM also recruits VASP to phagocytic cups and facilitates VASP phosphorylation and function promoting particle internalization.

View Article and Find Full Text PDF

Neonates are highly susceptible to bacterial infections, which represent a major source of mortality and morbidity in this age category. It is recognized that β2 integrins play a critical role in innate immunity by mediating leukocyte vascular adhesion, transmigration and bacterial phagocytosis. Therefore, we aimed to assess if the impaired immune functions seen in newborns may derive, in part, from a transient insufficient β2 integrin expression.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!