Table 2.
Ligands and roles of Ecto-F1-ATPase
Cells/tissues | Ligands | Proposed roles | Ref. |
K562, A549, Raji | ? | NK/LAK-mediated tumor cell lysis | [38] |
HUVEC | Angiostatin HDL/apoA-I | Cell survival through ATP production | [40,60,66] |
FC6 | Cell survival through purinergic receptor activation | ||
Control of blood pressure | |||
Hepatocytes | HDL/apoA-I | HDL endocytosis | [30] |
3T3-L1, HaCat | ? | Cell survival | [41,43] |
Tumor cells | Vγ9/Vδ2 TCR, apoA-I, MHC-I | Tumor cell recognition by Vγ9/Vδ2 T cells/presentation of phosphoantigens | [31,33,46,67] |
Tonsils (mouse) | Enterostatin | Food intake regulation | [44] |
Neurons | APP, Amyloid β-peptide | Synaptic plasticity regulation | [45] |
Major roles of Ecto-F1-ATPase described in the literature, as well as ligands involved, are summarized here. MHC-I: Major histocompatibility complex class I; NK: Natural killer; LAK: Lymphokine activated killer; HDL: High density lipoprotein; apoA-I: Apolipoprotein A-I; FC6: Coupling factor 6; ATP: Adenosine triphosphate; APP: Amyloid precursor protein. Cells/tissues are of human origin unless otherwise noted. K562: Erythroleukemia; A549: Lung adenocarcinoma; Raji: Burkitt’s lymphoma; HUVEC: Human umbilical vein endothelial cells; 3T3-L1: Murine fibroblasts (differentiated into adipocytes); HaCat: Immortalized human keratinocytes.