The tyrosine phosphatase SHP2 increases robustness and information transfer within IL-6-induced JAK/STAT signalling.

ABSTRACT:

Background

Cell-to-cell heterogeneity is an inherent feature of multicellular organisms and is central in all physiological and pathophysiological processes including cellular signal transduction. The cytokine IL-6 is an essential mediator of pro- and anti-inflammatory processes. Dysregulated IL-6-induced intracellular JAK/STAT signalling is associated with severe inflammatory and proliferative diseases. Under physiological conditions JAK/STAT signalling is rigorously controlled and timely orchestrated by regulatory mechanisms such as expression of the feedback-inhibitor SOCS3 and activation of the protein-tyrosine phosphatase SHP2 (PTPN11). Interestingly, the function of negative regulators seems not to be restricted to controlling the strength and timely orchestration of IL-6-ind

SUBMITTER: Fiebelkow J 

PROVIDER: S-EPMC8444181 | biostudies-literature | 2021 Sep

REPOSITORIES: biostudies-literature