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Madison, WI, United States

Moe A.M.,Laboratory of Cell and Molecular Biology | Golding A.E.,Laboratory of Cell and Molecular Biology | Bement W.M.,Laboratory of Cell and Molecular Biology | Bement W.M.,University of Wisconsin - Madison
Seminars in Cell and Developmental Biology | Year: 2015

Cell repair is attracting increasing attention due to its conservation, its importance to health, and its utility as a model for cell signaling and cell polarization. However, some of the most fundamental questions concerning cell repair have yet to be answered. Here we consider three such questions: (1) How are wound holes stopped? (2) How is cell regeneration achieved after wounding? (3) How is calcium inrush linked to wound stoppage and cell regeneration? © 2015 Elsevier Ltd. Source

Davenport N.R.,Cellular and Molecular Biology | Sonnemann K.J.,Laboratory of Cell and Molecular Biology | Eliceiri K.W.,Laboratory of Cell and Molecular Biology | Eliceiri K.W.,Laboratory for Optical and Computational Instrumentation | And 3 more authors.
Molecular Biology of the Cell | Year: 2016

Cells rapidly reseal after damage, but how they do so is unknown. It has been hypothesized that resealing occurs due to formation of a patch derived from rapid fusion of intracellular compartments at the wound site. However, patching has never been directly visualized. Here we study membrane dynamics in wounded Xenopus laevis oocytes at high spatiotemporal resolution. Consistent with the patch hypothesis, we find that damage triggers rampant fusion of intracellular compartments, generating a barrier that limits influx of extracellular dextrans. Patch formation is accompanied by compound exocytosis, local accumulation and aggregation of vesicles, and rupture of compartments facing the external environment. Subcellular patterning is evident as annexin A1, dysferlin, diacylglycerol, active Rho, and active Cdc42 are recruited to compartments confined to different regions around the wound. We also find that a ring of elevated intracellular calcium overlaps the region where membrane dynamics are most evident and persists for several minutes. The results provide the first direct visualization of membrane patching during membrane repair, reveal novel features of the repair process, and show that a remarkable degree of spatial patterning accompanies damage-induced membrane dynamics. © 2016 van Gent and Kanaar. Source

Zhu H.,Laboratory of Cell and Molecular Biology | Zhang G.,Laboratory of Cell and Molecular Biology | Wang Y.,Chinese Academy of Sciences | Xu N.,Loudi Center Hospital | And 7 more authors.
Cancer Science | Year: 2010

Overexpression of ErbB2 is associated with poor prognosis in breast cancer. Targeting of ErbB2 is a very common therapeutic strategy in ErbB2-overexpressed breast cancer. Herceptin is the first approved and most widely used agent for ErbB2-targeting therapy in breast cancer. Even though the clinical application has been performed for more than 10 years, the exact mechanism underlying how Herceptin exhibits its effects has not been fully elucidated. In this study, we found that Herceptin could inhibit the expression of survivin in ErbB2-overexpressed cell lines. Overexpression of survivin could abrogate the inhibition of cell growth induced by Herceptin. Herceptin could reduce survivin expression at the transcriptional level. The β-catenin/T-cell factor (TCF) pathway played a very crucial role in this cascade. We found that Herceptin could reduce tyrosine phosphorylation levels of ErbB2 and β-catenin. Herceptin treatment induced degradation of β-catenin protein, resulting in reduced binding affinity of β-catenin/TCF4 to the promoter region of survivin. When we cross-mutated the TCF4 binding sites in the promoter region of survivin, the reduction of survivin promoter activity almost diminished. Taken together, we showed that Herceptin could inhibit survivin expression through the ErbB2-β-catenin/TCF4-survivin pathway in ErbB2-overexpressed breast cancer cells. This indicates that there may be a new cascade axis from ErbB2 to survivin. © 2010 Japanese Cancer Association. Source

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