MER proto-oncogene tyrosine-protein kinase receptor (Mer)

The MER proto-oncogene tyrosine-protein kinase receptor (Mer or MerTK) is a transmembrane receptor tyrosine kinase and a member of the TAM family (Tyro3, Axl, Mer). It comprises extracellular immunoglobulin-like domains, fibronectin type III domains, a transmembrane region, and a cytoplasmic kinase domain[1][2][4]. Mer regulates critical physiological processes including the clearance of apoptotic cells (efferocytosis) by macrophages and other phagocytes, and subsequent suppression of inflammation through inhibition of NF-κB signaling and cytokine production[1][2][3][4][6]. Ligands such as Gas6 and Protein S activate Mer, triggering intracellular signaling pathways that promote anti-inflammatory responses and tissue repair, but can also contribute to immune evasion in cancer[1][2][3]. Dysregulation or inhibition of Mer has implications in autoimmunity, cancer progression, and chronic inflammation, making it a significant therapeutic target under investigation in oncology and immunology[1][2][4][6].

Other names

MER proto-oncogene tyrosine-protein kinaseMERTKc-MerTyrosine-protein kinase MerMerTKMER receptor tyrosine kinaseMER TKProto-oncogene c-Mer

Kinase inhibition (prevention of receptor autophosphorylation and downstream signaling); Blocking ligand binding (prevent activation by endogenous ligands); Immune checkpoint blockade (enhancing anti-tumor immunity by preventing immunosuppressive Mer signaling); Phagocytosis inhibition (in macrophages, blocks efferocytosis that could promote immune evasion)