Abstract:
:Proteomic studies have suggested a biochemical interaction between α subunit of the large conductance, voltage- and Ca2+-activated potassium channel (BKCaα), and annexin A5 (ANXA5), which we verify here by coimmunoprecipitation and double labelling immunocytochemistry. The observation that annexin is flipped to the outer membrane leaflet of the plasma membrane during apoptosis, together with the knowledge that the intracellular C-terminal of BKCaα contains both Ca2+-binding and a putative annexin-binding motif, prompted us to investigate the functional consequences of this protein partnership to cell death. Membrane biotinylation demonstrated that ANXA5 was flipped to the outer membrane leaflet of HEK 293 cells early in serum deprivation-evoked apoptosis. As expected, serum deprivation caused caspase-3/7 activation and this was accentuated in BKCaα expressing HEK 293 cells. The functional consequences of ANXA5 partnership with BKCaα were striking, with ANXA5 knockdown causing an increase and ANXA5 overexpression causing a decrease, in single BKCa channel Ca2+-sensitivity, measured in inside-out membrane patches by patch-clamp. Taken together, these data suggest a novel model of the early stages of apoptosis where membrane flippage results in removal of the inhibitory effect of ANXA5 on K+ channel activity with the consequent amplification of Ca2+ influx and augmented activation of caspases.
journal_name
Oxid Med Cell Longevjournal_title
Oxidative medicine and cellular longevityauthors
Brazier SP,Telezhkin V,Kemp PJdoi
10.1155/2016/1607092subject
Has Abstractpub_date
2016-01-01 00:00:00pages
1607092eissn
1942-0900issn
1942-0994journal_volume
2016pub_type
杂志文章abstract::Transient receptor potential (TRP) proteins consist of a superfamily of cation channels that have been involved in diverse physiological processes in the brain as well as in the pathogenesis of neurological disease. TRP channels are widely expressed in the brain, including neurons and glial cells, as well as in the ce...
journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章,评审
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journal_title:Oxidative medicine and cellular longevity
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journal_title:Oxidative medicine and cellular longevity
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journal_title:Oxidative medicine and cellular longevity
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journal_title:Oxidative medicine and cellular longevity
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章
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更新日期:2014-01-01 00:00:00
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章,评审
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journal_title:Oxidative medicine and cellular longevity
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章
doi:10.1155/2019/8184656
更新日期:2019-01-30 00:00:00
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章
doi:10.1155/2019/1968539
更新日期:2019-10-22 00:00:00
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章
doi:10.1155/2016/5139458
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journal_title:Oxidative medicine and cellular longevity
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章
doi:10.1155/2018/9524657
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journal_title:Oxidative medicine and cellular longevity
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doi:10.1155/2020/9571490
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章
doi:10.1155/2019/2069250
更新日期:2019-02-13 00:00:00
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章,评审
doi:10.1155/2015/370312
更新日期:2015-01-01 00:00:00
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章
doi:10.1155/2012/185867
更新日期:2012-01-01 00:00:00
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章,评审
doi:10.1155/2016/1067801
更新日期:2016-01-01 00:00:00
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章
doi:10.1155/2016/9707292
更新日期:2016-01-01 00:00:00
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journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章,评审
doi:10.1155/2013/323619
更新日期:2013-01-01 00:00:00
abstract::Virulence of enterohemorrhagic Escherichia coli (EHEC) strains depends on production of Shiga toxins. These toxins are encoded in genomes of lambdoid bacteriophages (Shiga toxin-converting phages), present in EHEC cells as prophages. The genes coding for Shiga toxins are silent in lysogenic bacteria, and prophage indu...
journal_title:Oxidative medicine and cellular longevity
pub_type: 杂志文章,评审
doi:10.1155/2016/3578368
更新日期:2016-01-01 00:00:00