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Megan Robinson
Researcher at University of Texas Southwestern Medical Center
Publications - 20
Citations - 4371
Megan Robinson is an academic researcher from University of Texas Southwestern Medical Center. The author has contributed to research in topics: MAP kinase kinase kinase & MAP2K7. The author has an hindex of 13, co-authored 20 publications receiving 4181 citations. Previous affiliations of Megan Robinson include University of Texas System.
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Journal ArticleDOI
Mitogen-activated protein kinase pathways.
Megan Robinson,Melanie H. Cobb +1 more
TL;DR: Recent advances in the study of mitogen-activated protein kinase cascades include the cloning of genes encoding novel members of the cascades, further definition of the roles of the cascade in responses to extracellular signals, and examination of cross-talk between different cascades.
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Phosphorylation of the MAP kinase ERK2 promotes its homodimerization and nuclear translocation.
Andrei Khokhlatchev,Bertram Canagarajah,Julie L. Wilsbacher,Megan Robinson,Mark A. L. Atkinson,Elizabeth J. Goldsmith,Melanie H. Cobb +6 more
TL;DR: The MAP kinase ERK2 is widely involved in eukaryotic signal transduction and upon activation it translocates to the nucleus of the stimulated cell, where it phosphorylates nuclear targets and forms dimers.
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A constitutively active and nuclear form of the MAP kinase ERK2 is sufficient for neurite outgrowth and cell transformation
TL;DR: Activation of ERK2 is sufficient to cause several transcriptional and phenotypic responses in mammalian cells, and nuclear localization of activated ERK1 is required to induce these events.
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Mutation of position 52 in ERK2 creates a nonproductive binding mode for adenosine 5'-triphosphate.
Megan Robinson,Paul C. Harkins,Jiandong Zhang,Richard Baer,John W. Haycock,Melanie H. Cobb,Elizabeth J. Goldsmith +6 more
TL;DR: The structural and kinetic data show that mutation of K52 created a nonproductive binding mode for ATP and suggest that K52 is essential for orienting ATP for catalysis, which is not currently known in the wild-type ERK2.
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iPSC-derived NK cells maintain high cytotoxicity and enhance in vivo tumor control in concert with T cells and anti-PD-1 therapy.
Frank Cichocki,Ryan Bjordahl,Svetlana Gaidarova,Sajid Mahmood,Ramzey Abujarour,Hongbo Wang,Katie Tuininga,Martin Felices,Zachary Davis,Laura Bendzick,Raedun Clarke,Laurel Stokely,Paul Rogers,Moyar Q. Ge,Megan Robinson,Betsy Rezner,David Robbins,Tom Tong Lee,Dan S. Kaufman,Bruce R. Blazar,Bahram Valamehr,Jeffrey S. Miller +21 more
TL;DR: iNK cells represent an “off-the-shelf” source of cells for immunotherapy with the capacity to target tumors and engage the adaptive arm of the immune system to make a “cold” tumor “hot” by promoting the influx of activated T cells to augment checkpoint inhibitor therapies.