Publications

• Tuning Cytokine Receptor Signaling by Re-orienting Dimer Geometry with Surrogate Ligands
  Moraga, I., Wernig, G., Wilmes, S., Gryshkova, V., Richter, C. P., & Garcia, K. C. (2015). Tuning Cytokine Receptor Signaling by Re-orienting Dimer Geometry with Surrogate Ligands. CELL, 160(6), 1196-1208.
• STAT5 Is Crucial to Maintain Leukemic Stem Cells in Acute Myelogenous Leukemias Induced by MOZ-TIF2
  Tam, W. F., Haehnel, P. S., Schueler, A., Lee, B. H., Okabe, R., & Kindler, T. (2013). STAT5 Is Crucial to Maintain Leukemic Stem Cells in Acute Myelogenous Leukemias Induced by MOZ-TIF2. CANCER RESEARCH, 73(1), 373-384.
• Anti-CD47 antibodies promote phagocytosis and inhibit the growth of human myeloma cells
  Kim, D., Wang, J., Willingham, S. B., Martin, R., Wernig, G., & Weissman, I. L. (2012). Anti-CD47 antibodies promote phagocytosis and inhibit the growth of human myeloma cells. LEUKEMIA, 26(12), 2538-2545.
• EXEL-8232, a small-molecule JAK2 inhibitor, effectively treats thrombocytosis and extramedullary hematopoiesis in a murine model of myeloproliferative neoplasm induced by MPLW515L Wernig, G., Kharas, M. G., Mullally, A., Leeman, D. S., Okabe, R., & Gilliland, D. G. (2012). EXEL-8232, a small-molecule JAK2 inhibitor, effectively treats thrombocytosis and extramedullary hematopoiesis in a murine model of myeloproliferative neoplasm induced by MPLW515L. LEUKEMIA, 26(4), 720-727.
  
• Physiological Jak2V617F Expression Causes a Lethal Myeloproliferative Neoplasm with Differential Effects on Hematopoietic Stem and Progenitor Cells Mullally, A., Lane, S. W., Ball, B., Megerdichian, C., Okabe, R., & Ebert, B. L. (2010). Physiological Jak2V617F Expression Causes a Lethal Myeloproliferative Neoplasm with Differential Effects on Hematopoietic Stem and Progenitor Cells. CANCER CELL, 17(6), 584-596.
  
• High-throughput sequence analysis of the tyrosine kinome in acute myeloid leukemia Loriaux, M. M., Levine, R. L., Tyner, J. W., Froehling, S., Scholl, C., & Druker, B. J. (2008). High-throughput sequence analysis of the tyrosine kinome in acute myeloid leukemia. BLOOD, 111(9), 4788-4796.
  
• The Jak2V617F oncogene associated with myeloproliferative diseases requires a functional FERM domain for transformation and for expression of the Myc and Pim proto-oncogenes Wernig, G., Gonneville, J. R. R., Crowley, B. J., Rodrigues, M. S., Reddy, M. M., & Sattler, M. (2008). The Jak2V617F oncogene associated with myeloproliferative diseases requires a functional FERM domain for transformation and for expression of the Myc and Pim proto-oncogenes. BLOOD, 111(7), 3751-3759.
  
• Efficacy of TG101348, a selective JAK2 inhibitor, in treatment of a murine model of JAK2V617F-induced polycythemia vera Werning, G., Kharas, M. G., Okabe, R., Moore, S. A., Leeman, D. S., & Gilliland, D. G. (2008). Efficacy of TG101348, a selective JAK2 inhibitor, in treatment of a murine model of JAK2V617F-induced polycythemia vera. CANCER CELL, 13(4), 311-320.
  
• JAK2T875N is a novel activating mutation that results in myeloproliferative disease with features of megakaryoblastic leukemia in a murine bone marrow transplantation model Mercher, T., Wernig, G., Moore, S. A., Levine, R. L., Gu, T.-L., & Gilliland, D. G. (2006). JAK2T875N is a novel activating mutation that results in myeloproliferative disease with features of megakaryoblastic leukemia in a murine bone marrow transplantation model. BLOOD, 108(8), 2770-2779.
  
• MPLW515L is anovel somatic activating mutation in myelofibrosis with myeloid metaplasia Pikman, Y., Lee, B. H., Mercher, T., McDowell, E., Ebert, B. L., & Levine, R. L. (2006). MPLW515L is anovel somatic activating mutation in myelofibrosis with myeloid metaplasia. PLOS MEDICINE, 3(7), 1140-1151.
  
• Expression of Jak2V617F causes a polycythemia vera-like disease with associated myelofibrosis in a murine bone marrow transplant model Wernig, G., Mercher, T., Okabe, R., Levine, R. L., Lee, B. H., & Gilliland, D. G. (2006). Expression of Jak2V617F causes a polycythemia vera-like disease with associated myelofibrosis in a murine bone marrow transplant model. BLOOD, 107(11), 4274-4281.
  
• Role of JAK-STAT signaling in the pathogenesis of myeloproliferative disorders. Levine, R. L., & Wernig, G. (2006). Role of JAK-STAT signaling in the pathogenesis of myeloproliferative disorders. Hematology / the Education Program of the American Society of Hematology. American Society of Hematology. Education Program, 233-?.
  
• Expression of a homodimeric type I cytokine receptor is required for JAK2V617F-mediated transformation Lu, X. H., Levine, R., Tong, W., Wernig, G., Pikman, Y., & Lodish, H. (2005). Expression of a homodimeric type I cytokine receptor is required for JAK2V617F-mediated transformation. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 102(52), 18962-18967.
  
• The vast majority of bone-marrow-derived cells integrated into mdx muscle fibers are silent despite long-term engraftment Wernig, G., Janzen, V., SCHAFER, R., Zweyer, M., Knauf, U., & Wernig, A. (2005). The vast majority of bone-marrow-derived cells integrated into mdx muscle fibers are silent despite long-term engraftment. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 102(33), 11852-11857.
  
• Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis Levine, R. L., Wadleigh, M., Cools, J., Ebert, B. L., Wernig, G., & Gilliland, D. G. (2005). Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis. CANCER CELL, 7(4), 387-397.
  
• Correction of CFTR malfunction and stimulation of Ca2+- activated Cl- channels restore HCO3- secretion in cystic fibrosis bile ductular cells Zsembery, A., Jessner, W., Sitter, G., Spirli, C., Strazzabosco, M., & Graf, J. (2002). Correction of CFTR malfunction and stimulation of Ca2+- activated Cl- channels restore HCO3- secretion in cystic fibrosis bile ductular cells. HEPATOLOGY, 35(1), 95-104.