Le tirosin fosfatasi nella regolazione delle funzioni leucocitarie (2022/2023)

Course code
cod wi: DT000433
Name of lecturer
Alessio Montresor
Coordinator
Alessio Montresor
Number of ECTS credits allocated
0.5
Academic sector
MED/04 - EXPERIMENTAL MEDICINE AND PATHOPHYSIOLOGY
Language of instruction
Italian
Location
VERONA
Period
Anno accademico 2022/2023 Dottorato di ricerca dal Oct 1, 2022 al Sep 30, 2023.

Lesson timetable

Go to lesson schedule

Learning outcomes

The objective of the course is to provide students with basic knowledge relating to the molecular mechanisms of leukocyte recruitment which represents a fundamental event in various pathological conditions of an inflammatory or neoplastic nature. Specifically, the lesson will cover in detail the role of integrin activation in this process. Integrin activation, which manifests itself as an increase in the affinity of integrins for ligands, is regulated by complex molecular mechanisms of signal transduction, which involve kinases and phosphatases. Phosphorylation constitutes a fundamental mechanism for signal transduction and the balance of enzymatic activity between kinases and phosphatases determines the levels of protein phosphorylation and regulates their activation. Protein phosphatases are divided based on substrate specificity and are grouped into tyrosine phosphatases (PTPs) and serine-threonine phosphatases (PSTPs). The PTPRG tyrosine phosphatase belongs to the group of receptor-like tyrosine phosphatases (RPTPs), with phosphatase activity in the intracellular domain (ICD). Data produced by the research laboratories coordinated by the course teachers have recently revealed that the activation of PTPRG prevents, in human monocytes, integrin adhesion and activation induced by chemotactic factors and inhibits the transition of LFA-1 towards high affinity state, through dephosphorylation of the JAK2 kinase. Furthermore, in human B lymphocytes from healthy donors and patients with chronic lymphocytic leukemia (CLL), PTPRG activation prevents integrin adhesion and activation, via inhibition of JAK2 and BTK kinases. Finally, PTPRG activation induces apoptosis selectively in leukemic cells, while B lymphocytes from healthy donors remain viable, with the possibility therefore that PTPRG may function as a tumor suppressor gene in CLL.

Syllabus

- Classification of phosphatases; - Description of the activity of phosphatases; - Description of the main classes of tyrosine phosphatases; - Description of the tyrosine phosphatase PTPRG and its role in pathogenetic contexts.

Assessment methods and criteria

Not expected.

Studying

Share