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William J. Murphy

Researcher at Texas A&M University

Publications -  320
Citations -  27304

William J. Murphy is an academic researcher from Texas A&M University. The author has contributed to research in topics: Genome & Immune system. The author has an hindex of 80, co-authored 293 publications receiving 25360 citations. Previous affiliations of William J. Murphy include Pontifícia Universidade Católica do Rio Grande do Sul & Texas College.

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Cloning Thymic Precursor Cells: Demonstration That Individual Pro-T1 Cells Have Dual T–NK Potential and Individual Pro-T2 Cells Have Dual αβ–γδ T Cell Potential

TL;DR: This work shows that commitment of a cell to the αβ versus γδ lineages does not precede rearrangement of the TCR genes (which occurs immediately after the pro-T2 stage), and shows the existence of a common T/NK precursor cell in the thymus.
Journal Article

CD16 Cross-Linking Blocks Rearrangement of the TCRβ Locus and Development of αβ T Cells and Induces Development of NK Cells from Thymic Progenitors

TL;DR: It is suggested that common lymphoid precursors can respond to environmental signals to commit to the αβT vs NK developmental pathways.
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A conserved segmental duplication within ELA.

TL;DR: Striking sequence conservation throughout Perissodactyl evolution is consistent with a functional role for at least some of the genes included within this segmental duplication.
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Emerging Frontiers in the Study of Molecular Evolution.

TL;DR: A collection of the editors of Journal of Molecular Evolution have gotten together to pose a set of key challenges and future directions for the field of molecular evolution, including challenges and new directions in prebiotic chemistry and the RNA world.

NCI First International Workshop on The Biology, Prevention, and Treatment of Relapse After Allogeneic Hematopoietic Stem Cell Transplantation: Report from the Committee on the Biology Underlying Recurrence of Malignant Disease following Allogeneic HSCT:

TL;DR: In this article, the basic biology and potential application to exploit adaptive T cell responses, minor histocompatibility antigens, contraction and suppression mechanisms that hinder immune responses, adaptive B cell responses and innate NK cell responses are discussed.