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Molecular Pharmacology

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Research ArticleArticle

Targeting a PAR4 carboxyl terminal motif to regulate platelet function

Rithwik Ramachandran, Koichiro Mihara, Pierre Thibeault, Christina M Vanderboor, Bjoern Petri, Mahmoud Saifeddine, Michel Bouvier and Morley D. Hollenberg
Molecular Pharmacology January 26, 2017, mol.116.106526; DOI: https://doi.org/10.1124/mol.116.106526
Rithwik Ramachandran
1 University of Western Ontario;
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Koichiro Mihara
2 University of Calgary;
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Pierre Thibeault
1 University of Western Ontario;
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Christina M Vanderboor
1 University of Western Ontario;
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Bjoern Petri
2 University of Calgary;
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Mahmoud Saifeddine
2 University of Calgary;
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Michel Bouvier
3 University of Montreal;
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Morley D. Hollenberg
4 The University of Calgary
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Data Supplement

Files in this Data Supplement:

  • Supplemental Data -

    Supplementary Figure 1 - AYPGKF-NH2 triggered calcium signaling in HEK cells transiently expressing wt-PAR4-YFP, QC-PAR4-YFP and dRS-PAR4-YFP

    Supplementary Figure 2 - (A) HEK cells expressing wt or dRS-PAR4 can activate ERK and P38 MAPK signaling in response to 100-mu-M AYPGKF-NH2 treatment for 10 minutes

    Supplementary Figure 3 - BRET detection of (A) Thrombin and (B) AYPGKF-NH2 triggered beta-arrestin recruitment to QC-PAR4

    Supplementary Figure 4 - BRET detection of beta-arrestin1/2 recruitment to PAR2 in the presence and absence of RAG8

  • Supplementary Video 1 -

    FeCl3 triggered thrombosis in-vivo in SRQ8 treated control animals and RAG8 treated animals. Data are representative of three independent experiments

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