Abstract:
:Tau tubulin kinase 2 (TTBK2) is a kinase known to phosphorylate tau and tubulin. It has recently drawn much attention due to its involvement in multiple important cellular processes. Here, we review the current understanding of TTBK2, including its sequence, structure, binding sites, phosphorylation substrates, and cellular processes involved. TTBK2 possesses a casein kinase 1 (CK1) kinase domain followed by a ~900 amino acid segment, potentially responsible for its localization and substrate recruitment. It is known to bind to CEP164, a centriolar protein, and EB1, a microtubule plus-end tracking protein. In addition to autophosphorylation, known phosphorylation substrates of TTBK2 include tau, tubulin, CEP164, CEP97, and TDP-43, a neurodegeneration-associated protein. Mutations of TTBK2 are associated with spinocerebellar ataxia type 11. In addition, TTBK2 is essential for regulating the growth of axonemal microtubules in ciliogenesis. It also plays roles in resistance of cancer target therapies and in regulating glucose and GABA transport. Reported sites of TTBK2 localization include the centriole/basal body, the midbody, and possibly the mitotic spindles. Together, TTBK2 is a multifunctional kinase involved in important cellular processes and demands augmented efforts in investigating its functions.
journal_name
Biomed Res Intjournal_title
BioMed research internationalauthors
Liao JC,Yang TT,Weng RR,Kuo CT,Chang CWdoi
10.1155/2015/575170subject
Has Abstractpub_date
2015-01-01 00:00:00pages
575170eissn
2314-6133issn
2314-6141journal_volume
2015pub_type
杂志文章,评审abstract::Increasing studies have revealed that long noncoding RNAs (lncRNAs) are not transcriptional noise but play important roles in the regulation of a wide range of biological processes, and the dysregulation of lncRNA genes is associated with disease development. Alzheimer's disease (AD) is a chronic neurodegenerative dis...
journal_title:BioMed research international
pub_type: 杂志文章
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journal_title:BioMed research international
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journal_title:BioMed research international
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journal_title:BioMed research international
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journal_title:BioMed research international
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journal_title:BioMed research international
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journal_title:BioMed research international
pub_type: 杂志文章
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journal_title:BioMed research international
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journal_title:BioMed research international
pub_type: 杂志文章,评审
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journal_title:BioMed research international
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journal_title:BioMed research international
pub_type: 杂志文章
doi:10.1155/2015/508342
更新日期:2015-01-01 00:00:00
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journal_title:BioMed research international
pub_type: 杂志文章
doi:10.1155/2015/948131
更新日期:2015-01-01 00:00:00
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journal_title:BioMed research international
pub_type: 杂志文章
doi:10.1155/2014/921549
更新日期:2014-01-01 00:00:00
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pub_type: 杂志文章
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journal_title:BioMed research international
pub_type: 杂志文章
doi:10.1155/2015/917640
更新日期:2015-01-01 00:00:00
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journal_title:BioMed research international
pub_type: 杂志文章,随机对照试验
doi:10.1155/2018/8925345
更新日期:2018-11-01 00:00:00
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journal_title:BioMed research international
pub_type: 杂志文章
doi:10.1155/2019/2019846
更新日期:2019-06-19 00:00:00
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journal_title:BioMed research international
pub_type: 杂志文章,评审
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journal_title:BioMed research international
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journal_title:BioMed research international
pub_type: 杂志文章
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更新日期:2015-01-01 00:00:00
abstract:Background:Liver ischaemia-reperfusion injury (IRI) remains a problem in liver transplantation. Interleukin-4 (IL-4) has been found to reduce liver IRI, but the exact mechanism remains unclear. Methods:Donor livers were infused with recombinant IL-4 or normal saline during cold storage, and the hepatocellular apoptosi...
journal_title:BioMed research international
pub_type: 杂志文章
doi:10.1155/2020/2953068
更新日期:2020-03-18 00:00:00
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journal_title:BioMed research international
pub_type: 杂志文章
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journal_title:BioMed research international
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:BioMed research international
pub_type: 杂志文章
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journal_title:BioMed research international
pub_type: 杂志文章
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更新日期:2020-01-21 00:00:00
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journal_title:BioMed research international
pub_type: 临床试验,杂志文章
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更新日期:2019-05-28 00:00:00