L
Lin Ji
Researcher at Capital Normal University
Publications - 216
Citations - 7654
Lin Ji is an academic researcher from Capital Normal University. The author has contributed to research in topics: Lung cancer & Tumor suppressor gene. The author has an hindex of 47, co-authored 195 publications receiving 6966 citations. Previous affiliations of Lin Ji include University of Texas MD Anderson Cancer Center & Scripps Research Institute.
Papers
More filters
Journal ArticleDOI
Differential transmission of actin motion within focal adhesions
TL;DR: Interactions between vinculin, talin, and actin filaments appear to constitute a slippage interface between the cytoskeleton and integrins, generating a molecular clutch that is regulated during the morphodynamic transitions of cell migration.
Journal ArticleDOI
Traction stress in focal adhesions correlates biphasically with actin retrograde flow speed
Margaret L. Gardel,Benedikt Sabass,Benedikt Sabass,Lin Ji,Gaudenz Danuser,Ulrich S. Schwarz,Ulrich S. Schwarz,Clare M. Waterman +7 more
TL;DR: F-actin speed is a fundamental regulator of traction force at FAs during cell migration, independent of changes in FA protein density, age, stress magnitude, assembly/disassembly status, or subcellular position induced by pleiotropic perturbations to Rho family guanosine triphosphatase signaling and myosin II activity.
Journal ArticleDOI
Myosin II contributes to cell-scale actin network treadmilling through network disassembly
Cyrus A. Wilson,Mark A. Tsuchida,Greg M. Allen,Erin L. Barnhart,Kathryn T. Applegate,Patricia T. Yam,Patricia T. Yam,Lin Ji,Kinneret Keren,Kinneret Keren,Gaudenz Danuser,Gaudenz Danuser,Julie A. Theriot +12 more
TL;DR: The results establish the importance of myosin II as an enzyme for actin network disassembly and propose that gradual formation and reorganization of an actomyosin network provides an intrinsic destruction timer, enabling long-range coordination of act in network treadmilling in motile cells.
Journal Article
Induction of apoptosis and inhibition of tumorigenicity and tumor growth by adenovirus vector-mediated fragile histidine triad (FHIT) gene overexpression.
TL;DR: The results suggest that the FHIT gene, when delivered at high efficiency by a recombinant adenoviral vector, functions as a tumor suppressor gene both in vitro and in vivo.
Journal ArticleDOI
Actin–myosin network reorganization breaks symmetry at the cell rear to spontaneously initiate polarized cell motility
Patricia T. Yam,Cyrus A. Wilson,Lin Ji,Benedict Hebert,Erin L. Barnhart,Natalie A. Dye,Paul W. Wiseman,Gaudenz Danuser,Julie A. Theriot +8 more
TL;DR: It is indicated that large-scale actin–myosin network reorganization and contractility at the cell rear initiate spontaneous symmetry breaking and polarized motility of keratocytes.