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Aminoacyl-Transfer RNA Synthetase Deficiency Promotes Angiogenesis via the Unfolded Protein Response Pathway
Author(s) -
Daniel Castranova,
Andrew Davis,
Brigid D. Lo,
Mayumi F. Miller,
Paul J. Paukstelis,
Matthew Swift,
Van N. Pham,
Jesús TorresVázquez,
Kameha Bell,
Kenna M. Shaw,
Makoto Kamei,
Brant M. Weinstein
Publication year - 2016
Publication title -
arteriosclerosis thrombosis and vascular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.007
H-Index - 270
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/atvbaha.115.307087
Subject(s) - unfolded protein response , atf6 , xbp1 , endoplasmic reticulum , angiogenesis , microbiology and biotechnology , downregulation and upregulation , atf4 , biology , protein biosynthesis , protein kinase a , integrated stress response , protein kinase r , transcription factor , signal transduction , rna , zebrafish , chemistry , kinase , messenger rna , biochemistry , cancer research , mitogen activated protein kinase kinase , translation (biology) , gene , rna splicing
Understanding the mechanisms regulating normal and pathological angiogenesis is of great scientific and clinical interest. In this report, we show that mutations in 2 different aminoacyl-transfer RNA synthetases, threonyl tRNA synthetase (tars(y58)) or isoleucyl tRNA synthetase (iars(y68)), lead to similar increased branching angiogenesis in developing zebrafish.

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