2 research outputs found
Achieving 100% Utilization of Reduced Graphene Oxide by Layer-by-Layer Assembly: Insight into the Capacitance of Chemically Derived Graphene in a Monolayer State
Face-to-face restacking is one of
the main reasons for low surface
utilization of multilayered graphene. In this study, multilayered
reduced graphene oxide/polymer architecture was fabricated by gas
phase or chemical reduction of thin films composed of graphene oxide
monolayers using polyÂ(diallyldimethylammonium) as the cationic binder
deposited by layer-by-layer self-assembly. The electrochemical behavior
of the thin films in acidic and neutral electrolytes was investigated
by using cyclic voltammetry and electrochemical impedance spectroscopy.
A transmission line model was adopted to simulate the electrochemical
impedance data. The electrochemical data were analyzed and deconvoluted
into charge storage due to non-Faradaic electrical double layer capacitance
and pseudocapacitance arising from Faradaic surface redox reactions.
Pseudocapacitance observed in acidic electrolyte is proportional to
the amount of surface functional groups. An overall volumetric capacitance
as high as 364 F cm<sup>–3</sup> was achieved for the nanoarchitecture,
and it is shown that the electrical double layer capacitance of a
monolayer of graphene oxide is 20 μF cm<sup>–2</sup>,
regardless of the number of layers deposited. This can be interpreted
as full capacitive utilization of reduced graphene oxide sheets in
the multilayered reduced graphene oxide films
Substrate rigidity-dependent positive feedback regulation between YAP and ROCK2
<p>Extracellular matrix (ECM) stiffness influences gene expression, leading to modulation of various cellular functions. While ROCK2 regulates actomyosin activity as well as cell migration and proliferation, expression of ROCK2 is increased in response to stiffening ECM. However, the mechanism underlying rigidity-dependent <i>ROCK2</i> expression remains elusive. Here, we show that YAP, a mechanically regulated transcription coactivator, upregulates <i>ROCK2</i> expression in an ECM rigidity-dependent manner. YAP interacted with the <i>ROCK2</i> promoter region in an actomyosin activity-dependent manner. Knockdown of <i>YAP</i> decreased <i>ROCK2</i> expression while activity of the <i>ROCK2</i> promoter was upregulated by expressing constitutively active YAP. Furthermore, we found that <i>ROCK2</i> expression promotes transcriptional activation by YAP. Our results reveal a novel positive feedback loop between YAP and ROCK2, which is modulated by ECM stiffness.</p