Karim Dib

Background

About Karim Dib

My research interest is broadly signal transduction in relation with inflammation, cancer, and metabolic diseases. This field of investigation was initiated during my Ph.D (Unit 96 INSERM, France). In this laboratory, I studied the regulation of Gs and Gi proteins in thyroid cells in response to the hormone TSH and in astrocytes in response to beta 2 adrenergic agonists to better understand production of thyroid hormones by thyroid cells and release by astrocytes of gliotransmitters which signal to neurons. Next, during my Post-Doctoral training, I investigated the mechanism by which insulin regulates its metabolic and mitogenic pathways. This work has allowed me to better understand the physiopathology of obesity and diabetes (University of Cambridge, UK). At Lund University (Sweden), I investigated the regulation of monomeric GTPases in neutrophils to better understand how inflammatory functions of these cells are regulated. I continued working on signalling pathways in leukocytes at Queen’s University Belfast when I was appointed Senior Lecturer/Associate Professor. Recently, I opened up a new field of investigation by showing presence of the histamine four receptor (H4R) in human neutrophils with anti-inflammatory functions. Present work is aimed at investigating the role of the H4R in the regulation of phagocytosis. I also developed a research project at the Max Planck Institute for Biochemistry (Germany) as a Marie Curie Fellow. I identified mu1A adaptin, a protein of the AP-1 complex, as a novel protein interacting with L-selectin tail. AP-1 mediates bi-directional transport of proteins between the trans-Golgi network and early endosomes via clathrin-coated-vesicles. I am currently investigating how phosphorylation of L-selectin cytoplasmic tail regulates association with mu1A adaptin and how this is relevant to L-selectin-dependent leukocyte adhesion and rolling along the vascular endothelium and migration to sites of infection.