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Jeffrey J. Lange

Researcher at Stowers Institute for Medical Research

Publications -  56
Citations -  912

Jeffrey J. Lange is an academic researcher from Stowers Institute for Medical Research. The author has contributed to research in topics: Biology & Gene. The author has an hindex of 16, co-authored 46 publications receiving 651 citations. Previous affiliations of Jeffrey J. Lange include Washington University in St. Louis & Kansas State University.

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Egr-5 is a post-mitotic regulator of planarian epidermal differentiation

TL;DR: The planarian epidermis is established as a novel paradigm to uncover the molecular mechanisms regulating ASC specification in vivo and a conserved early growth response family transcription factor, egr-5, that is essential for epidermal differentiation is identified.
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wtf genes are prolific dual poison-antidote meiotic drivers

TL;DR: A complex landscape of meiotic drive genes on chromosome 3 of the fission yeasts Schizosaccharomyces kambucha and S. pombe is demonstrated, suggesting that the wtf multigene family proliferated due to meioticDrive and highlights the power of selfish genes to shape genomes, even while imposing tremendous costs to fertility.
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The membrane-associated proteins FCHo and SGIP are allosteric activators of the AP2 clathrin adaptor complex

TL;DR: It is demonstrated that the membrane-associated proteins FCHo and SGIP1 convert AP2 into an open, active conformation by rearrangement of the F-BAR domain or the µ-homology domain that directly binds AP2.
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Quantifying Nucleation In Vivo Reveals the Physical Basis of Prion-like Phase Behavior

TL;DR: It is shown that kinetic barriers limit the nucleation of ordered self-assemblies and that the persistence of the barriers with respect to concentration relates to structure, suggesting that nucleation barriers govern cytoplasmic inheritance, subcellular organization, and proteotoxicity.
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Dynamic regulation of Nanog and stem cell-signaling pathways by Hoxa1 during early neuro-ectodermal differentiation of ES cells

TL;DR: A model whereby direct inputs of Nanog and Hoxa1 on shared targets and mutual repression between HoxA1 and the core pluripotency network provides a molecular mechanism that modulates the fine balance between the alternate states of pluripOTency and differentiation is proposed.