Yip Ai Kia

Anisotropic traction stresses and focal adhesion polarization mediates topography-induced cell elongation

Published date : 30 Jul 2018

Cell elongation and differentiation has been shown to be modulated by topographical cues provided by grating substratum. However, little is known about the mechanisms and forces involved in the grating-induced cell elongation, due to the difficulty in fabricating soft elastic gels that allow 3-dimensional (3D) cell traction stress measurements. In this paper, we present a method to fabricate soft elastic polyacrylamide grating substrates, using an imprinted polyethylene terephthalate mould, for 3D cell traction stress measurements.

type
Journal Paper
journal
Biomaterials, Vol. 181, October 2018, Pg 103-112, doi: 10.1016/j.biomaterials.2018.07.057
Impact Factor
8.806

Cell-Cell Adhesion and Cortical Actin Bending Govern Cell Elongation on Negatively Curved Substrates

Published date : 20 Feb 2018

Physiologically, cells experience and respond to a variety of mechanical stimuli such as rigidity and topography of the extracellular matrix. However, little is known about the effects of substrate curvature on cell behavior. We developed a novel, to our knowledge, method to fabricate cell culture substrates with semicylindrical grooves of negative curvatures (radius of curvature, Rc = 20-100 μm). We found that negative substrate curvatures induced elongation of mesenchymal and epithelial cells along the cylinder axis.

type
Journal Paper
journal
Biophysical Journal 114, Pg 1707-1717, April 10, 2018 doi: 10.1016/j.bpj.2018.02.027
Impact Factor
3.495

MEKK1-dependent phosphorylation of calponin-3 tunes cell contractility

Published date : 15 Aug 2016

MEKK1 (also known as MAP3K1), which plays a major role in MAPK signaling, has been implicated in mechanical processes in cells, such as migration. Here, we identify the actin-binding protein calponin-3 as a new MEKK1 substrate in the signaling that regulates actomyosin-based cellular contractility. MEKK1 colocalizes with calponin-3 at the actin cytoskeleton and phosphorylates it, leading to an increase in the cell-generated traction stress.

type
Journal Paper
journal
Journal of Cell Science, 2016 Oct 1;129(19):3574-3582, doi: 10.1242/jcs.189415
Impact Factor
4.431

p53-mediated activation of the mitochondrial protease HtrA2/Omi prevents cell invasion

Published date : 31 Mar 2014

Oncogenic Ras induces cell transformation and promotes an invasive phenotype. The tumor suppressor p53 has a suppressive role in Ras-driven invasion. However, its mechanism remains to be poorly understood. Here we show that p53 induces activation of the mitochondrial protease high temperature requirement A2 (HtrA2; also known as Omi) and prevents Ras-driven invasion by modulating the actin cytoskeleton.

type
Journal Paper
journal
The Journal of Cell Biology, April 2014, Vol. 204, no. 7, pg 1191-1207, doi: 10.1083/jcb.201309107
Impact Factor
10.822

Loss of p53 enhances NF-κB-dependent lamellipodia formation

Published date : 29 Oct 2013

Tumor suppressor p53 prevents tumorigenesis and tumor growth by suppressing the activation of several transcription factors, including NF-κB and STAT3. On the other hand, p53 stimulates actin cytoskeleton remodeling and integrin related signaling cascades. Here, we examined the p53-mediated link between regulation of the actin cytoskeleton and activation of NF-κB and STAT3 in MCF-7 cells and mouse embryonic fibroblasts (MEFs). In the absence of p53, STAT3 was constitutively activated. This activation was attenuated by depleting the expression of p65, a component of NF-κB.

type
Journal Paper
journal
Journal of Cellular Physiology 2013, doi: 10.1002/jcp.24505
Impact Factor
4.218