Progress of solid-phase microextraction coatings and coating techniques.
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Solid-phase microextraction (SPME) has been popular as an environmentally friendly sample pretreatment technique to extract a very wide range of analytes. This is partly owing to the development of SPME coatings. One of the key factors affecting the extraction performances, such as the sensitivity, selectivity, and reproducibility, is the properties of the coatings on SPME fibers. This paper classifies the materials used as SPME coatings and introduces some common preparation techniques of SPME coating in detail, such as sol-gel technique, electrochemical polymerization technique, particle direct pasting technique, restricted access matrix SPME technique, and molecularly imprinted SPME technique. (+info)
In guinea pig sperm, aldolase A forms a complex with actin, WAS, and Arp2/3 that plays a role in actin polymerization.
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Kelch-like 1 protein upregulates T-type currents by an actin-F dependent increase in alpha(1H) channels via the recycling endosome.
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The neuronal protein Kelch-like 1 (KLHL1) is a novel actin-binding protein that modulates neuronal structure and function. KLHL1 knockout mice exhibit dendritic atrophy in cerebellar Purkinje neurons and motor dysfunction. Interestingly, KLHL1 upregulates high and low voltage-gated calcium currents (Ca(V)2.1 and Ca(V)3.2) and interacts with their respective principal subunits, alpha(1A) and alpha(1H). We reported the mechanism of enhanced Ca(V)3.2 (alpha(1H)) current density (and calcium influx) by KLHL1 is due to an increase in channel number (N) that requires the binding of actin. In this report we further elucidate the role of the actin cytoskeleton in this process using pharmacological tools to disrupt or stabilize actin filaments and to prevent protein trafficking and vesicle recycling. Disruption of the cytoskeleton did not affect the basal activity of alpha(1H), but did eliminate its modulation by KLHL1. In contrast, actin-F stabilization on its own increased basal alpha(1H) activity similar to KLHL1 but without synergy in its presence, suggesting KLHL1 requires actin-polymerization to increase alpha(1H) currents. Noise analysis revealed that actin polymerization induced an increase in N and P(o), in contrast to increased N in the presence of KLHL1. Interestingly, pharmacological or genetic disruption of endosomal recycling eliminated the increase in channel number by KLHL1 demonstrating this effect occurs via enhanced alpha(1H) re-insertion through the recycling endosome. Our findings afford insight on a novel mechanism of T-type channel modulation that could have overall functional implications for T-type channel function in the brain. (+info)
Molecular toxicology of substances released from resin-based dental restorative materials.
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