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检索条件"任意字段=第十一届全国钙信号和细胞功能研讨会"

共 78 条记录，以下是11-20 订阅

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GPCR biased signaling and TRP channels

GPCR biased signaling and TRP channels

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第十一届全国钙信号和细胞功能研讨会

作者： Xiao Yu Zonglai Liang Chunhua Liu Zheng Gong Yijing Wang Jin-Peng Sun Department of Physiology Shandong University School of Medicine Department of Biochemisry and Molecular Biology Shandong University School of Medicine Qilu Hospital Shandong University School of Medicine Department of Physiology Taishan Medical University

G protein-coupled receptors transduce the extracellular siganls through G proteins or betaarrestin-mediated pathways, participating in a variety of pathophysiological processes. TRP channels also play important roles in widespread pathophysiological processes. The GPCRTRP interactions have received increasing attention because of the findings that GPCR downstream signaling can stimulate TRP channels or regulate TRP channel activities. While G protein-mediated second messenger signaling regulates TRP channel activation directly, arrestins were found to promote TRP channel internalization or modulate TRP channel activities through second messenger systems. Here we use G protein or beta-arrestin-biased GPCR agonists to investigate the function of G protein or beta-arrestin signaling in TRP channel activities.

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Polycystin 2 is required for glucose deprivation induced Autophagy in human embryonic stem cell derived cardiomyocytes

Polycystin 2 is required for glucose deprivation induced Aut...

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第十一届全国钙信号和细胞功能研讨会

作者： Jun Lu Xiaoqiang Yao Li Ka Shing Institute of Health Science and School of Biomedical Sciences The Chinese University of Hong Kong

Autophagy is a ubiquitous process for protein and organelle recycling, critical to numerous forms of stress responsiveness. The activities of m TOR and AMPK, two major regulators of autophagy, are dysregulated in autosomal dominant polycystic kidney disease（ADPKD） which caused by Polycytin 2（PKD2） mutation. Therefore we hypothesized that PKD2 is possible candidate for autophagy regulation in human embryonic stem cell derived cardiomyocytes（h ESC-CMs）. The PKD2 was silenced in h ESC-CMs by sh RNA lentivirus-mediated transduction. Short-term glucose deprivation, which mimicked myocardial ischemia, induced robust accumulation LC3 lipidation in scramble h ESC-CMs. However, this phenomenon was attenuated in cardiomyoytes lacking PKD2. These results demonstrate that PKD2 is a novel regulator of autophagy in h ESC-CMs during glucose deprivation.

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Perisaccadic visual receptive field remapping and visual stability

Perisaccadic visual receptive field remapping and visual sta...

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第十一届全国钙信号和细胞功能研讨会

作者： Cong Zhang Lin Yang Mingsha Zhang State Key Laboratory of Cognitive Neuroscience and Learning IDG/Mc Govern Institute for Brain Research Beijing Normal University

Humans and monkeys have access to an accurate representation of visual space despite a constantly moving eye. One mechanism by which the brain accomplishes this is by remapping visual receptive fields around the time of a saccade. In this process a neuron can be excited by a probe stimulus in the current receptive field, and also simultaneously by a probe stimulus in the location that will be brought into the neuron's receptive field by the saccade(the future receptive field), even before saccade begins. Here we show that perisaccadic neuronal excitability is not limited to the current and future receptive fields, but encompasses the entire region of visual space across which the current receptive field will be swept by the saccade. A computational model shows that this receptive field expansion is consistent with the propagation of a wave of activity across the cerebral cortex as saccade planning and remapping proceed.

关键词： Perisaccadic visual receptive field remapping and visual stability

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Mechanisms of STIM-ORAI signaling

Mechanisms of STIM-ORAI signaling

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第十一届全国钙信号和细胞功能研讨会

作者： Patrick Hogan La Jolla Institute for Allergy ＆ Immunology

STIM-ORAI-dependent calcium entry is a prominent physiological signalling mechanism in T lymphocytes and in other *** basic pathway controlling calcium entry is straightforward: When the ER-anchored protein STIM1 senses a decline in ER-luminal calcium concentration, it directly engages and activates the plasma membrane calcium channel ORAI1. Theefficiency of STIM1-ORAI1 signalling is further tightly regulated by plasma membrane lipids and cellular modulatory proteins. Work from dozens of laboratories has unravelledmany aspects of STIMORAI signalling. However, the processes of channel gating and modulation remain incompletely understood, largely because the slow onset of physiologically-triggered current and the small single-channel conductance have precluded the use of standard electrophysiological approaches. We have tailored recombinant STIM1 and ORAI1 proteins to probe these processes in cellular assays and in parallel assays with the purified proteins. This approach provides new insights into STIM1 and ORAI1 activation mechanisms, ORAI1 channel gating, andits modulation.

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第十一届全国钙信号和细胞功能研讨会

作者： Yong-Jie Wang LI Sun Zhen-Xing Zuo Hui-Fang Shang Zeng-Mei Liu Zhi-Hui Feng Xiang-Yao LI Institute of Neuroscience and Collaborative Innovation Center for Brain Science School of Medicine Zhejiang University Key Laboratory of Biomedical Information Engineering of the Ministry of Education School of Life Science and Technology Xi'an Jiaotong University Department of Neurosurgery First Affiliated Hospital Medical College of Xi'an Jiaotong University

Chronic pain affects about 15-30% people in our society. Previous studies showed that the enhanced excitatory synaptic transmissions in both the spinal cord and superspinal brain areas, such as the anterior cingulate cortex and amygdala were involved in the maintenance of chronic pain, while the detail neuronal mechanisms kept unclear. In the current study, the involvements of apoptosis related protein 3 to the maintenance were investigated by the combining of different approaches, including the genetic, behavioral, biochemical, and molecular approaches. Our data suggest that the apoptosis related protein 3 is one of the key factors that regulate both the evoked and spontaneous pain via the apoptosis in the anterior cingulate cortex.

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Neuronal mechanisms of declarative association memory in the primate medial temporal lobe

Neuronal mechanisms of declarative association memory in the...

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第十一届全国钙信号和细胞功能研讨会

作者： Yuji Naya Peking University

Declarative memory is our "everyday-language memory" and enables us to describe the things that we remember. Other collections of memory are referred to as non-declarative memory. Both of these memory systems involve a form of association memory that connects one thing to another. However, while declarative association brings us sensory or declarative information when we recollect, non-declarative association couples a cue stimulus directly to a behavioral or autonomic response. Accumulating neuropsychological studies of human patients and animal experiments demonstrate that the declarative association memory is supported by medial temporal lobe（MTL） areas. In order to study the neuronal mechanismsfor the declarative association memory, we conducted single-unit recordings from the MTL areas of non-human primates during animals performed memory behavioral tasks that require item-item association memory（"pair-association task"） or item-time association memory（"temporalorder task"）. We found the perirhinal cortex in the MTL plays a critical role for either withindomain or between-domain declarative association memory depending on the task requirement.

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Presynaptic Calcium Mechanism of Homeostatic Synaptic Plasticity

Presynaptic Calcium Mechanism of Homeostatic Synaptic Plasti...

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第十一届全国钙信号和细胞功能研讨会

作者： Cong Jian Zhao Southwest Hospital/Southwest Eye Hospital Third Military Medical University Key Lab of Visual Damage and Regeneration ＆ Restoration of Chongqing

To monitor the dynamic presynaptic calcium signal, various GECIs（genetic engineering calcium indicator） are genetically tagged with external lumen of presynaptic proteins including Synaptobrevin（VAMP2）, Synaptophysin（Sy）, or Synaptotagmin I（Syt I）. Take advantage of the latest GECIs, allowing us dissect the influx of presynaptic calcium evoked by 1 action potential. Furthermore, calcium microdomain of zebrafish retinal bipolar cell can be revealed under TIRF microscopy. To access whether presynaptic mechanism underlying homeostatic synaptic plasticity, we have combined the use of two fluorescent proteins in cultured neurons: a calcium reporter localized to synaptic vesicles, Sy GCa MP, and a reporter of vesicle fusion, Syp Hy. We find that a modulation in the activity of the network causes changes in the amount of calcium entering the synaptic bouton in response to an action potential and changes in the probability of vesicle fusion. The release probability of homeostatic plasticity varied as the third power of calcium influx. These results suggest that changes of presynaptic calcium signal govern synaptic strength of homeostatic changes.

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Long-term chronic Two-photon Calcium Imaging on Awake Macaque Monkey

Long-term chronic Two-photon Calcium Imaging on Awake Macaqu...

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第十一届全国钙信号和细胞功能研讨会

作者： Shiming Tang Ming Li Fang Liu Hongfei Jiang Peking University School of Life Sciences and Peking-Tsinghua Center for Life Sciences IDG/Mc Govern Institute for Brain Research at Peking University

We have established long-term chronic two-photon calcium imaging on awake macaque monkey. A Genetically-encoded calcium indicator AAV-GCa MP5 was injected into the primary visual cortex V1 of monkey. The neurons were densely transduced after 45 days. Nearly 2000 infected neurons could be clearly identified within a single optical section. High quality twophoton imaging could be maintained for months. Thousands individual neurons exhibited robust visual responses during the long-term imaging period. Simultaneous intracellular recording and two-photon calcium imaging confirmed that the fluorescence activity reflected neural activity. The calcium signal was linearly related to neural firing rates across a large range from 20 to 150 Hz. This technology provides a window to access cortical neuron populations to single dendritic spine on awake monkey, and also allows further using in varying cortical areas, with varying genetic tools and during varying cognitive processing in primates.

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Move Ca2+ signaling to the tips, P68 RNA helicase-CaM interaction in cell migration

Move Ca2+ signaling to the tips, P68 RNA helicase-CaM intera...

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第十一届全国钙信号和细胞功能研讨会

作者： Haizhen Wang Xueliang Gao Jenny Yang Zhi-Ren Liu Georgia State University

P68 RNA helicase（p68） is a prototypical RNA helicase. The protein has been implicated in various cellular processes, including gene transcription, RNA processing, viral infection, and cell morphology maintain and *** present evidence here to show that, by interacting with Ca-calmodulin（Ca M）, p68 plays a role in cancer metastasis andcell migration. Our results demonstrate that the p68-CaM interaction is essential for the formation of lamellipodia and filopodia in the migrating cells. P68 interacts with microtubule in the presence of Ca M. Our experiments show that interacting with microtubules stimulates p68 ATPase activity. Further, microtubule gliding assays demonstrate that p68, in the presence of Ca M, can function as a microtubule motor. This motor activity may allow p68 to transport Ca M to the leading edge of migrating cells.A peptide fragment that spans the IQ motif of p68 strongly inhibits cancer metastasis in two different animal models. The peptide interrupts p68 and Ca M interaction and inhibits cell migration. The results suggest that p68 and Ca M interaction is a potential target to interference with cancer metastasis, a potential target for development of cancer treatment.

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Biophysics and neurobiological mechanism of genetic epilepsy led by KCNT1 channel mutations

Biophysics and neurobiological mechanism of genetic epilepsy...

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第十一届全国钙信号和细胞功能研讨会

作者： Fang-Fang Zhang Yan Li Yun Xu Xiao-Yun Zhao Fei-Fei Zhang Qiong-Yao Tang Zhe Zhang Xuzhou Medical University

So far, 23 sodium-activated potassium channel(KCNT1, Slack) genetic mutants have been reported are associated with severe early-onset epilepsy patients. The changes in biophysical properties of these mutants and the underlying mechanisms causing disease remain elusive. Here, we have studied 13 mutations of them. We found that 7 of them increase, whereas one mutation decreases, the channel's sodium sensitivity. Two of the mutants exhibit channel overactivity only when the intracellular Na(+)([Na(+)]i) concentration is ～80 m M. In contrast, single-channel data reveal that 12 mutants increase the maximal open probability(Po). We conclude that these mutant channels lead to channel over-activity predominantly by increasing the ability of sodium binding to activate the channel, which is indicated by its maximal Po. The sodium sensitivity of these epilepsy causing mutants probably determines the [Na(+)]i concentration at which these mutants exert their pathological effects. In vivo study revealed that Slack channel KO mice demonstrate resistance to certain type of epilepsy model.

关键词： Biophysics and neurobiological mechanism of genetic epilepsy led by KCNT1 channel mutations

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