E
Edward J. Banigan
Researcher at Massachusetts Institute of Technology
Publications - 44
Citations - 2197
Edward J. Banigan is an academic researcher from Massachusetts Institute of Technology. The author has contributed to research in topics: Chromatin & Lamin. The author has an hindex of 18, co-authored 38 publications receiving 1513 citations. Previous affiliations of Edward J. Banigan include Northwestern University & Georgetown University.
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Journal ArticleDOI
Generalized Levy walks and the role of chemokines in migration of effector CD8+ T cells
Tajie H. Harris,Edward J. Banigan,David A. Christian,Christoph Konradt,Elia D. Tait Wojno,Kazumi Norose,Emma H. Wilson,Beena John,Wolfgang Weninger,Wolfgang Weninger,Andrew D. Luster,Andrea J. Liu,Christopher A. Hunter +12 more
TL;DR: CD8+ T-cell behaviour is similar to Lévy strategies reported in organisms ranging from mussels to marine predators and monkeys, and CXCL10 aids T cells in shortening the average time taken to find rare targets.
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Chromatin and lamin A determine two different mechanical response regimes of the cell nucleus
TL;DR: Micromanipulation force measurements of single isolated nuclei at physiological strains and strain rates reveal two distinct cell nuclear mechanical regimes differentially governed by chromatin and lamin A.
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Chromatin histone modifications and rigidity affect nuclear morphology independent of lamins
Andrew D. Stephens,Patrick Z. Liu,Edward J. Banigan,Edward J. Banigan,Luay M. Almassalha,Vadim Backman,Stephen A. Adam,Robert D. Goldman,John F. Marko +8 more
TL;DR: Chromatin decompaction via increasing euchromatin or decreasing heterochromatin results in a softer nucleus and abnormal nuclear blebbing, independent of lamin perturbations, and rescuing nuclear morphology in lamin-perturbed cells that present abnormal nuclear morphology.
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Chromatin’s physical properties shape the nucleus and its functions
TL;DR: These findings reveal how chromatin's physical properties can regulate cellular function and drive abnormal nuclear morphology and dysfunction in disease.
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Loop extrusion: theory meets single-molecule experiments.
TL;DR: It is discussed how SSMC complexes may perform their functions on chromatin in vivo, and surprisingly, condensin extrudes loops asymmetrically, challenging previous models.