AI Article Synopsis
- Phosphatidylserine (PtdSer) plays a crucial role as a cofactor in activating the TAM receptor family (TYRO3, AXL, MERTK) during inflammation and cancer.
- PtdSer binding is essential for the activation of TAMs, which subsequently influences homeostasis, inflammation control, and cancer progression.
- Research is focused on how PtdSer impacts signaling within tumor microenvironments, influencing interactions between tumor cells and immune responses.
Article Abstract
The numerous and diverse biological roles of Phosphatidylserine (PtdSer) are featured in this special issue. This review will focus on PtdSer as a cofactor required for stimulating TYRO3, AXL and MERTK - comprising the TAM family of receptor tyrosine kinases by their ligands Protein S (PROS1) and growth-arrest-specific 6 (GAS6) in inflammation and cancer. As PtdSer binding to TAMs is a requirement for their activation, the biological repertoire of PtdSer is now recognized to be broadened to include functions performed by TAMs. These include key homeostatic roles necessary for preserving a healthy steady state in different tissues, controlling inflammation and further additional roles in diseased states and cancer. The impact of PtdSer on inflammation and cancer through TAM signaling is a highly dynamic field of research. This review will focus on PtdSer as a necessary component of the TAM receptor-ligand complex, and for maximal TAM signaling. In particular, interactions between tumor cells and their immediate environment - the tumor microenvironment (TME) are highlighted, as both cancer cells and TME express TAMs and secrete their ligands, providing a nexus for a multifold of cross-signaling pathways which affects both immune cells and inflammation as well as tumor cell biology and growth. Here, we will highlight the current and emerging knowledge on the implications of PtdSer on TAM signaling, inflammation and cancer.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6881992 | PMC |
| http://dx.doi.org/10.1186/s12964-019-0461-0 | DOI Listing |
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