Isoform 1, isoform 2 and T1-TrpRS have aminoacylation activity while T2-TrpRS lacks it. Isoform 2, T1-TrpRS and T2-TrpRS possess angiostatic activity whereas isoform 1 lacks it. T2-TrpRS inhibits fluid shear stress-activated responses of endothelial cells. Regulates ERK, Akt, and eNOS activation pathways that are associated with angiogenesis, cytoskeletal reorganization and shear stress-responsive gene expression. ATP + L-tryptophan + tRNA(Trp) = AMP + diphosphate + H(+) + L-tryptophanyl-tRNA(Trp) Homodimer (PubMed:28369220). Isoform 1 and isoform 2 interact with an oxidized form of GAPDH. GAPDH stimulates the aminoacylation activity of isoform 2 (PubMed:15628863). By IFNG/IFN-gamma. Proteolytic cleavage generates 2 forms; T1-TrpRS and T2-TrpRS. The disease is caused by variants affecting the gene represented in this entry. Belongs to the class-I aminoacyl-tRNA synthetase family.