Source:http://linkedlifedata.com/resource/pubmed/id/20826761
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2010-12-1
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pubmed:abstractText |
Acid-sensing ion channels (ASICs) extensively exist in both central and peripheral neuronal systems and contribute to many physiological and pathological processes. The protein that interacts with C kinase 1 (PICK1) was cloned as one of the proteins interacting with protein kinase C (PKC) and colocalized with ASIC1 and ASIC2. Here, we used PICK1 knockout (PICK1-KO) C57/BL6 mice together with the whole cell patch clamp, calcium imaging, RT-PCR, Western blot, and immunocytochemistry techniques to explore the possible change in ASICs and the regulatory effects of PKC on ASICs. The results showed that PICK1 played a key role in regulation of ASIC functions. In PICK1-KO mouse cortical neurons, both the amplitude of ASIC currents and elevation of [Ca(2+)](i) mediated by acid were decreased, which were attributable to the decreased expression of ASIC1a and ASIC2a proteins in the plasma membrane. PKC, a partner protein of PICK1, regulated ASIC functions via PICK1. The agonist and antagonist of PKC only altered ASIC currents and acid-induced increase in [Ca(2+)](i) in wild-type, but not in KO mice. In conclusion, our data provided the direct evidence from PICK1-KO mice that a novel target protein, PICK1, would regulate ASIC function and membrane expression in the brain. In addition, PICK1 played the bridge role between PKC and ASICs.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/ASIC channel,
http://linkedlifedata.com/resource/pubmed/chemical/Carrier Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Nerve Tissue Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Nuclear Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Prkcabp protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase C,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium Channels
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
1522-1563
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
299
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
C1355-62
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pubmed:meshHeading |
pubmed-meshheading:20826761-Animals,
pubmed-meshheading:20826761-Brain,
pubmed-meshheading:20826761-Carrier Proteins,
pubmed-meshheading:20826761-Cerebral Cortex,
pubmed-meshheading:20826761-Membrane Proteins,
pubmed-meshheading:20826761-Mice,
pubmed-meshheading:20826761-Mice, Inbred C57BL,
pubmed-meshheading:20826761-Mice, Knockout,
pubmed-meshheading:20826761-Nerve Tissue Proteins,
pubmed-meshheading:20826761-Neurons,
pubmed-meshheading:20826761-Nuclear Proteins,
pubmed-meshheading:20826761-Protein Kinase C,
pubmed-meshheading:20826761-Sodium Channels
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pubmed:year |
2010
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pubmed:articleTitle |
Disruption of PICK1 attenuates the function of ASICs and PKC regulation of ASICs.
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pubmed:affiliation |
Department of Pharmacology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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