Publications

• 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., Hoegemeier, O., … 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), 11852–57.
• 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., George, T., … 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), 720–27.
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• 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., Al-Shahrour, F., … 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.
  
• 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.
  
• 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., Huntly, B. J. P., … 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.
  
• 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., Zarnegar, S., … 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.
  
• 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), 4274–81.
  
• 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., Frohling, S., … 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., Gozo, M., … Levine, R. L. (2006). MPLW515L is anovel somatic activating mutation in myelofibrosis with myeloid metaplasia. PLOS MEDICINE, 3(7), 1140–1151.
  
• 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-?
  
• 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., Hudon, H. E., … 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.
  
• 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., Stoffregen, E. P., … Druker, B. J. (2008). High-throughput sequence analysis of the tyrosine kinome in acute myeloid leukemia. BLOOD, 111(9), 4788–96.
  
• 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., Cullen, D. E., … 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), 311–20.
  
• 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., Zhu, N., … 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.
  
• Tuning Cytokine Receptor Signaling by Re-orienting Dimer Geometry with Surrogate Ligands Moraga, I., Wernig, G., Wilmes, S., Gryshkova, V., Richter, C. P., Hong, W.-J., … Garcia, K. C. (2015). Tuning Cytokine Receptor Signaling by Re-orienting Dimer Geometry with Surrogate Ligands. CELL, 160(6), 1196–1208.
  
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• Unifying mechanism for different fibrotic diseases Wernig, G., Chen, S.-Y., Cui, L., Van Neste, C., Tsai, J. M., Kambham, N., … Weissman, I. L. (2017). Unifying mechanism for different fibrotic diseases. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 114(18), 4757–62.
  
• Unifying Mechanism of fibrotic diseases Wernig, G., & Weissman, I. L. (2017). Unifying Mechanism of fibrotic diseases. Proceedings of the National Academy of Science, 114(18).
  
• Doxycyline Improves Wound Healing via Nonantibiotic Associated Mechanisms Moore, A. L., Murphy, M. P., Irizarry, D. M., Brett, E. A., Wernig, G., & Longaker, M. T. (2017). Doxycyline Improves Wound Healing via Nonantibiotic Associated Mechanisms. JOURNAL OF THE AMERICAN COLLEGE OF SURGEONS, 225(4), S162–S163.
  
• Stem cell therapy for treatment of ischemic optic neuropathy Mesentier-Louro, L. A., Yang, N., Shariati, A., Domizi, P. D., Dodd, R., Wernig, G., … Liao, Y. J. (2018). Stem cell therapy for treatment of ischemic optic neuropathy. INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE, 59(9).
  
• EXEL-8232, a Small Molecule JAK2 inhibitor, Effectively Treats Thrombocytosis and Extramedullary Hematopoiesis in a Murine Model of Myeloproliferative Disease Induced by MPLW515L Wernig, G., Kharas, M., Clary, D., Gilliland, G., & George, T. (2011). EXEL-8232, a Small Molecule JAK2 inhibitor, Effectively Treats Thrombocytosis and Extramedullary Hematopoiesis in a Murine Model of Myeloproliferative Disease Induced by MPLW515L. LABORATORY INVESTIGATION, 91, 329A.
  
• Direct targeting of the mouse optic nerve for therapeutic delivery. Mesentier-Louro, L. A., Dodd, R., Domizi, P., Nobuta, H., Wernig, M., Wernig, G., & Liao, Y. J. (2018). Direct targeting of the mouse optic nerve for therapeutic delivery. Journal of Neuroscience Methods.
  
• Reduced Scar Thickness Achieved by Topical Doxycycline Is Mediated by Specific Skin Fibroblast Populations and Not Immune Cell Infiltrate Moore, A. L., Murphy, M. P., Irizarry, D. M., Des Jardins-Park, H. E., Duoto, B. A., Mascharak, S., … Longaker, M. T. (2018). Reduced Scar Thickness Achieved by Topical Doxycycline Is Mediated by Specific Skin Fibroblast Populations and Not Immune Cell Infiltrate. JOURNAL OF THE AMERICAN COLLEGE OF SURGEONS, 227(4), S210–S211.
  
• Mouse Model with cJUN Over-Expression Eludes to Deep Dermal Fibroblast Expansion and Immune Cell Recruitment as the Biologic Mechanism of Hypertrophic Scarring Moore, A. L., Duoto, B. A., Des Jardins-Park, H. E., Mascharak, S., Wernig, G., & Longaker, M. T. (2018). Mouse Model with cJUN Over-Expression Eludes to Deep Dermal Fibroblast Expansion and Immune Cell Recruitment as the Biologic Mechanism of Hypertrophic Scarring. JOURNAL OF THE AMERICAN COLLEGE OF SURGEONS, 227(4), S208.
  
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