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Your search keyword '"Frelinger, Andrew L."' showing total 36 results
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36 results on '"Frelinger, Andrew L."'

1. Outcomes of hematopoietic stem cell gene therapy for Wiskott-Aldrich syndrome

Author

Labrosse, Roxane, Chu, Julia I., Armant, Myriam A., Everett, John K., Pellin, Danilo, Kareddy, Niharika, Frelinger, Andrew L., Henderson, Lauren A., O’Connell, Amy E., Biswas, Amlan, Coenen-van der Spek, Jet, Miggelbrink, Alexandra, Fiorini, Claudia, Adhikari, Hriju, Berry, Charles C., Cantu, Vito Adrian, Fong, Johnson, Jaroslavsky, Jason, Karadeniz, Derin F., Li, Quan-Zhen, Reddy, Shantan, Roche, Aoife M., Zhu, Chengsong, Whangbo, Jennifer S., Dansereau, Colleen, Mackinnon, Brenda, Morris, Emily, Koo, Stephanie M., London, Wendy B., Baris, Safa, Ozen, Ahmet, Karakoc-Aydiner, Elif, Despotovic, Jenny M., Forbes Satter, Lisa R., Saitoh, Akihiko, Aizawa, Yuta, King, Alejandra, Nguyen, Mai Anh Thi, Vu, Vy Do Uyen, Snapper, Scott B., Galy, Anne, Notarangelo, Luigi D., Bushman, Frederic D., Williams, David A., and Pai, Sung-Yun

Published
2023
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5. The aryl hydrocarbon receptor directs hematopoietic progenitor cell expansion and differentiation

Author

Smith, Brenden W., Rozelle, Sarah S., Leung, Amy, Ubellacker, Jessalyn, Parks, Ashley, Nah, Shirley K., French, Deborah, Gadue, Paul, Monti, Stefano, Chui, David H.K., Steinberg, Martin H., Frelinger, Andrew L., Michelson, Alan D., Theberge, Roger, McComb, Mark E., Costello, Catherine E., Kotton, Darrell N., Mostoslavsky, Gustavo, Sherr, David H., and Murphy, George J.

Published
2013
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7. Platelet activation in cystic fibrosis

Author

O'Sullivan, Brian P., Linden, Matthew D., Frelinger, Andrew L., III, Barnard, Marc R., Spencer-Manzon, Michele, Morris, James E., Salem, Raneem O., Laposata, Michael, and Michelson, Alan D.

Published
2005
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9. Elipsis: A Longitudinal Study of Electronic Patient-Reported Outcomes, Actigraphy and Biomarkers to Identify and Assess at-Home Vaso-Occlusive Crises in Adults and Adolescents with Sickle Cell Disease

Author

Callaghan, Michael U., primary, Hines, Patrick C., additional, Pittman, Debra D, additional, Beidler, David, additional, Rybin, Denis, additional, Zaidi, Ahmar Urooj, additional, White, Jennell, additional, Liu, Ke, additional, Hannan, Bryan, additional, Gao, Xiufeng, additional, Pleil, Andreas M, additional, Barsdorf, Alexandra, additional, David, Martin, additional, Simmons, Melanie, additional, Frelinger, Andrew L, additional, Michelson, Alan D, additional, Clarke, Nick, additional, and Charnigo, Robert J, additional

Published
2017
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13. Hypoxia Reoxygenation Treatment Induces Platelet Hyperactivity and Relieves Calpain-1-Mediated Inhibition of Platelet Aggregation in a Mouse Model of Severe Sickle Cell Disease

Author

Nwankwo, Jennifer O., primary, Warburton, Rod R., additional, Gremmel, Thomas, additional, Gerrits, Anja J., additional, Richey, Lauren J., additional, Hill, Nicholas S., additional, Rivera, Alicia, additional, Jakubowski, Joseph A., additional, Frelinger, Andrew L., additional, and Chishti, Athar H., additional

Published
2015
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17. Effects Of Eltrombopag On Thrombocytopenia, Platelet Function and Bleeding In Patients With Wiskott-Aldrich Syndrome/X-Linked Thrombocytopenia

Author

Gerrits, Anja J, primary, Leven, Emily, additional, Frelinger, Andrew L., additional, Berny-Lang, Michelle A., additional, Tamary, Hannah, additional, Revel-Vilk, Shoshana, additional, Carmichael, Sabrina L., additional, Mitchell, W. Beau, additional, Michelson, Alan D., additional, and Bussel, James B, additional

Published
2013
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20. Clopidogrel Pharmacokinetics and Pharmacodynamics Vary Widely Despite Exclusion or Control of Polymorphisms (CYP2C19, ABCB1, PON1), Non-Compliance, Diet, Smoking, Co-Medications (including Proton Pump Inhibitors), and Pre-Existent Variability in Platelet Function

Author

Frelinger, Andrew L., primary, Bhatt, Deepak L., additional, Lee, Ronald D., additional, Mulford, Darcy J., additional, Wu, Jingtao, additional, Nudurupati, Sai, additional, Nigam, Anu, additional, Lampa, Michael, additional, Brooks, Julie K., additional, Barnard, Marc R., additional, and Michelson, Alan D., additional

Published
2012
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26. In Vivo Effects of Eltrombopag on Human Platelet Function.

Author

Psaila, Bethan, primary, Bussel, James B., additional, Linden, Matthew D., additional, Li, You Fu, additional, Barnard, Marc R., additional, Tate, Chinara M., additional, Page, Lemke K., additional, Frelinger, Andrew L., additional, and Michelson, Alan D., additional

Published
2007
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30. Analysis of Platelet Aggregation Disorders Based on Flow Cytometric Analysis of Membrane Glycoprotein IIb-IIIa With Conformation-Specific Monoclonal Antibodies

Author

Ginsberg, Mark H., Frelinger, Andrew L., Lam, Stephen C-T., Forsyth, Jane, McMillan, Robert, Plow, Edward F., and Shattil, Sanford J.

Abstract

Normal primary platelet aggregation requires agonist-mediated activation of membrane GPIIb-IIIa, binding of fibrinogen to GPIIb-IIIa, and cellular events after ligand binding. PAC1 monoclonal antibody distinguishes between resting and activated states of GPIIb-IIIa, and other antibodies preferentially recognize GPMb (PMI-1) or Ilia (anti-LIBS1) after the binding of fibrinogen or fibrinogen-mimetic peptides, such as GRGOSP. Using these antibodies and platelet flow cytometry, we studied two distinct persistent platelet aggregation abnormalities. Platelets from a thrombasthenia variant, which contained near-normal amounts of GPIIb-IIIa, failed to aggregate or bind PAC1 in response to agonists. In addition, GRGDSP, which binds to normal GPIIb-IIIa without prior cell activation, failed to Increase the binding of PMI-1 or anti-LIBS1 to the thrombasthenia platelets, suggesting a primary defect In ligand binding. Chromatography of detergent-solubilized platelets on a KYGRGDS affinity column confirmed that the patient’s GPIIb-IIIa lacked the fibrinogen binding site. In another patient with myelofibrosis and defective aggregation, PAC1 failed to bind to adenosine diphosphate–stimulated platelets, but did bind when protein kinase C was directly activated with phorbol myristate acetate. Furthermore, the binding of PMI-1 and anti-LIBS1 increased in response to GRGDSP, confirming a defect in agonist-mediated fibrinogen receptor activation rather than in fibrinogen binding or events distal to binding. These studies indicate that this immunochemical approach is useful in classification of clinical abnormalities of platelet aggregation as defects in either (a) fibrinogen receptor activation, (b) fibrinogen binding, or (c) postoccupancy events.

Published
1990
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31. Arg-Gly-Asp–Dependent Occupancy of GPIIb/IIIa by Applaggin: Evidence for Internalization and Cycling of a Platelet Integrin

Author

Wencel-Drake, June D., Frelinger, Andrew L., Dieter, Michael G., and Lam, Stephen C.-T.

Abstract

Using indirect immunofluorescence microscopy we examined the distribution and cycling of GPIIb/IIIa after binding to applaggin, a high-affinity Arg-Gly-Asp (RGD)-containing ligand. Resting, unfixed platelets were incubated with applaggin for 30 minutes at 37°C, and bound applaggin was detected by an affinity-purified rabbit anti-applaggin antibody. Examination of intact cells showed a rim pattern for applaggin, consistent with its binding to the platelet surface. Staining of Triton X-100-permeabilized cells showed an intracellular pool of applaggin. Competition of applaggin binding by either AP-2, an anti-GPIIb/llla monoclonal antibody (MoAb) that blocks fibrinogen binding, or the synthetic peptide RGDW eliminated both surface and intracellular staining, indicating that applaggin is binding to GPIIb/IIIa in an RGD-dependent manner. Inhibition of platelet activation by PGE, and theophylline had no effect on the observed staining patterns, indicating that cellular activation is not required for surface binding and subsequent internalization. To evaluate whether occupancy of functional binding sites on GPIIb/IIIa is required for internalization, we used mAbl 5, an anti-GPIIIa antibody that neither blocks fibrinogen binding nor induces the expression of ligand-induced binding sites on GPIIb/IIIa. In these studies mAbl 5 was internalized in a manner analogous to both AP-2 and applaggin, showing that occupancy of the RGD binding site is not required to initiate receptor internalization. To estimate the size of the newly internalized pool of applaggin, 125l-applaggin-binding studies were performed. Displacement of bound 125I-applaggin by excess unlabeled applaggin or EDTA showed that at least 17% of bound applaggin was nondisplaceable when binding was performed under conditions permitting membrane flow and internalization. These data indicate that GPIIb/IIIa is internalized in unstimulated platelets independent of cellular activation or occupancy of the functional binding site(s) of GPIIb/IIIa by RGD-containing ligands. Thus, internalization of GPIIb/IIIa may represent a mechanism by which the surface expression of this adhesion receptor is regulated.

Published
1993
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32. GLS-409, a Synergistic Inhibitor of Both P2Y1and P2Y12: Efficacy in a Canine Model of Recurrent Coronary Thrombosis and Reversibility of Human Platelet Inhibition

Author

Smolensky Koganov, Elena, Michelson, Alan D, Yanachkov, Ivan B, Yanachkova, Milka I, Wright, George E, Przyklenk, Karin, and Frelinger, Andrew L

Abstract

Introduction.Dual antiplatelet therapy with aspirin and an adenosine diphosphate (ADP) P2Y12receptor inhibitor is a mainstay of pharmacological therapy in acute coronary syndromes. GLS-409 is a novel diadenosine tetraphosphate derivative that inhibits both P2Y1and P2Y12platelet ADP receptors.

Published
2017
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36. Agonist and Antagonist Effects of Diadenosine Tetraphosphate, a Platelet Dense Granule Constituent, on Platelet P2Y1, P2Y12and P2X1Receptors

Author

Chang, Hung, Yanachkov, Ivan B, Michelson, Alan D, Li, YouFu, Barnard, Marc R, Wright, George E, and Frelinger, Andrew L

Abstract

Introduction:Diadenosine 5′,5‴-P1,P4- tetraphosphate (Ap4A) is stored in platelet dense granules, but its effects on platelet function are not well understood. In the current study, we examined the effects of Ap4A on signaling through the human platelet purinergic receptors P2Y1, P2Y12and P2X1.

Published
2008
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