Publications by authors named "Xianan Qin"

Filopodia are slender cellular protrusions containing parallel actin bundles involved in environmental sensing and signaling, cell adhesion and migration, and growth cone guidance and extension. Myosin 10 (Myo10), an unconventional actin-based motor protein, was reported to induce filopodial initiation with its motor domain. However, the roles of the multifunctional tail domain of Myo10 in filopodial formation and elongation remain elusive.

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Titanium dioxide (TiO) nanoparticles have been extensively used to modify the optical properties of various types of materials. In particular, they have been intensively loaded onto polymer fibers to quench the light reflection. In situ polymerization and online addition are two common strategies for fabricating TiO-loaded polymer nanocomposite fibers.

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Myosin X forms an antiparallel dimer and moves processively on actin bundles. How the antiparallel dimer affects the stepping mechanism of myosin X remains elusive. Here, we generated several chimeras using domains of myosin V and X and performed single-molecule motility assays.

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The three-dimensional (3D) inter-site distance can be measured by single-molecule localization microscopy. Existing theories and analysis tools for 3D inter-site distance measurement only consider the simplest case where all measured distances are from an identical 3D Rician distribution. There are many problems where the 3D inter-site distance measurement result is made up of multiple components, for example, the measurement of intramolecular distances of deoxyribonucleic acid with multiple possible conformations.

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Many biological processes employ mechanisms involving the locations and interactions of multiple components. Given that most biological processes occur in three dimensions, the simultaneous measurement of three-dimensional locations and interactions is necessary. However, the simultaneous three-dimensional precise localization and measurement of interactions in real time remains challenging.

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Myosin X (Myo10) has several unique design features including dimerization via an anti-parallel coiled coil and a long lever arm, which allow it to preferentially move on actin bundles. To understand the stepping behavior of single Myo10 on actin bundles, we labeled two heads of Myo10 dimers with different fluorophores. Unlike previously described for myosin V (Myo5) and VI (Myo6), which display alternating hand-over-hand stepping, Myo10 frequently took near simultaneous steps of both heads, and less frequently, 2-3 steps of one head before the other head stepped.

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Store-operated Ca entry (SOCE) is a major Ca influx pathway that is controlled by the ER Ca sensor STIM1. Abnormal activation of STIM1 directly influences Ca influx, resulting in severe diseases such as Stormorken syndrome. The inactivation domain of STIM1 (IDstim) has been identified as being essential for Ca-dependent inactivation of STIM1 (CDI) after SOCE occurs.

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STIM1 (a Ca sensor in the endoplasmic reticulum (ER) membrane) and Orai1 (a pore-forming subunit of the Ca-release-activated calcium channel in the plasma membrane) diffuse in the ER membrane and plasma membrane, respectively. Upon depletion of Ca stores in the ER, STIM1 translocates to the ER-plasma membrane junction and binds Orai1 to trigger store-operated Ca entry. However, the motion of STIM1 and Orai1 during this process and its roles to Ca entry is poorly understood.

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The release of neurotransmitters via the fusion between synaptic vesicles and the presynaptic membrane is an essential step in synaptic transmission. Synaptic vesicles generally undergo two distinct modes of exocytosis called full-collapse fusion and kiss-and-run fusion. In kiss-and-run fusion, the fusion pore of the synaptic vesicle opens transiently without the vesicle collapsing fully into the plasma membrane; thus, each synaptic vesicle can be used multiple times to release neurotransmitters.

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Huntington's disease (HD) is an inherited neurodegenerative disorder caused by the abnormal expansion of CAG repeats in the () gene, which leads to progressive loss of neurons starting in the striatum and cortex. One possible mechanism for this selective loss of neurons in the early stage of HD is altered neurotransmission at synapses. Despite the recent finding that presynaptic terminals play an important role in HD, neurotransmitter release at synapses in HD remains poorly understood.

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Huntington's disease (HD) is a dominantly inherited neurodegenerative disease caused by an increase in CAG repeats in the Huntingtin gene (HTT). The striatum is one of the most vulnerable brain regions in HD, and altered delivery of BDNF to the striatum is believed to underlie this high vulnerability. However, the delivery of BDNF to the striatum in HD remains poorly understood.

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Mitochondria are essential for cellular survival and function. In neurons, mitochondria are transported to various subcellular regions as needed. Thus, defects in the axonal transport of mitochondria are related to the pathogenesis of neurodegenerative diseases, and the movement of mitochondria has been the subject of intense research.

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Objective: To evaluate the advantages, disadvantages and their indications of total nasal reconstruction with different techniques.

Methods: A series of total nasal reconstruction were treated with four methods from 1975 to 2003. These methods were tubed flap of arm,midline forehead flap with skin graft, midline forehead flap with bilateral frontotemporal flaps for repairing the donor site, and expanded forehead flap.

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