Abstract：
:Receptor for Activated C-Kinase 1 (RACK1) belongs to the WD40 family of proteins, known to act as scaffolding proteins in interaction networks. Accordingly, RACK1 is found to have numerous interacting partners ranging from kinases and signaling proteins to membrane bound receptors and ion channels. Interestingly, RACK1 has also been identified as a ribosomal protein present in all eukaryotic ribosomes. Structures of eukaryotic ribosomes have shown RACK1 to be located at the back of the head of the small ribosomal subunit. This suggests that RACK1 could act as a ribosomal scaffolding protein recruiting regulators of translation to the ribosome, and several studies have in fact found RACK1 to play a role in regulation of translation. To fully understand the role of RACK1 we need to understand whether the many reported interaction partners of RACK1 bind to free or ribosomal RACK1. In this review we provide a structural analysis of ribosome-bound RACK1 to provide a basis for answering this fundamental question. Our analysis shows that RACK1 is tightly bound to the ribosome through highly conserved and specific interactions confirming RACK1 as an integral ribosomal protein. Furthermore, we have analyzed whether reported binding sites for RACK1 interacting partners with a proposed role in translational control are accessible on ribosomal RACK1. Our analysis shows that most of the interaction partners with putative regulatory functions have binding sites that are available on ribosomal RACK1, supporting the role of RACK1 as a ribosomal signaling hub. We also discuss the possible role for RACK1 in recruitment of ribosomes to focal adhesion sites and regulation of local translation during cell spreading and migration.
journal_name
Cell Signaljournal_title
Cellular signallingauthors
Nielsen MH,Flygaard RK,Jenner LBdoi
10.1016/j.cellsig.2017.01.026subject
Has Abstractpub_date
2017-07-01 00:00:00pages
272-281eissn
0898-6568issn
1873-3913pii
S0898-6568(17)30032-3journal_volume
35pub_type
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journal_title：Cellular signalling
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journal_title：Cellular signalling
pub_type： 杂志文章,评审
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journal_title：Cellular signalling
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journal_title：Cellular signalling
pub_type： 杂志文章,评审
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更新日期：2007-07-01 00:00:00
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journal_title：Cellular signalling
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journal_title：Cellular signalling
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journal_title：Cellular signalling
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journal_title：Cellular signalling
pub_type： 杂志文章
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更新日期：2015-01-01 00:00:00
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journal_title：Cellular signalling
pub_type： 杂志文章
doi：10.1016/j.cellsig.2005.08.019
更新日期：2006-07-01 00:00:00
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journal_title：Cellular signalling
pub_type： 杂志文章
doi：10.1016/j.cellsig.2008.02.018
更新日期：2008-07-01 00:00:00
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journal_title：Cellular signalling
pub_type： 杂志文章
doi：10.1016/j.cellsig.2005.03.006
更新日期：2005-12-01 00:00:00
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journal_title：Cellular signalling
pub_type： 杂志文章
doi：10.1016/j.cellsig.2013.02.007
更新日期：2013-05-01 00:00:00
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journal_title：Cellular signalling
pub_type： 杂志文章
doi：10.1016/j.cellsig.2018.07.008
更新日期：2018-11-01 00:00:00
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journal_title：Cellular signalling
pub_type： 杂志文章
doi：10.1016/j.cellsig.2017.12.008
更新日期：2018-03-01 00:00:00
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journal_title：Cellular signalling
pub_type： 杂志文章,评审
doi：10.1016/j.cellsig.2004.05.014
更新日期：2005-01-01 00:00:00
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journal_title：Cellular signalling
pub_type： 杂志文章
doi：10.1016/0898-6568(94)90049-3
更新日期：1994-08-01 00:00:00
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journal_title：Cellular signalling
pub_type： 杂志文章
doi：10.1016/j.cellsig.2006.12.015
更新日期：2007-06-01 00:00:00
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journal_title：Cellular signalling
pub_type： 杂志文章
doi：10.1016/j.cellsig.2016.05.018
更新日期：2016-09-01 00:00:00
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journal_title：Cellular signalling
pub_type： 杂志文章
doi：10.1016/s0898-6568(03)00132-3
更新日期：2004-02-01 00:00:00
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journal_title：Cellular signalling
pub_type： 杂志文章
doi：10.1016/j.cellsig.2019.03.018
更新日期：2019-07-01 00:00:00
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journal_title：Cellular signalling
pub_type： 杂志文章
doi：10.1016/j.cellsig.2009.09.022
更新日期：2010-01-01 00:00:00
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journal_title：Cellular signalling
pub_type： 杂志文章
doi：10.1016/j.cellsig.2020.109875
更新日期：2021-03-01 00:00:00
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journal_title：Cellular signalling
pub_type： 杂志文章
doi：10.1016/j.cellsig.2005.05.015
更新日期：2006-04-01 00:00:00
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journal_title：Cellular signalling
pub_type： 杂志文章
doi：10.1016/0898-6568(93)90080-6
更新日期：1993-07-01 00:00:00
abstract：:Oral squamous cell carcinoma (OSCC) is characterized by genomic and epigenomic alterations. However, the mechanisms underlying oral squamous cell carcinoma tumorigenesis and progression remain to be elucidated. Long non-coding RNAs (lncRNAs), circular RNAs (circRNAs), and extracellular RNAs (exRNAs) are emerging group...
journal_title：Cellular signalling
pub_type： 杂志文章,评审
doi：10.1016/j.cellsig.2017.10.009
更新日期：2018-01-01 00:00:00
abstract：:G protein-coupled receptors (GPCRs) constitute the largest and most diverse protein family in the human genome with over 800 members identified to date. They play critical roles in numerous cellular and physiological processes, including cell proliferation, differentiation, neurotransmission, development and apoptosis...
journal_title：Cellular signalling
pub_type： 杂志文章,评审
doi：10.1016/j.cellsig.2017.09.005
更新日期：2018-01-01 00:00:00
abstract：:The kidney is one of the fastest-aging organs, and renal senescence has become a major disease affecting human health. Renal cellular senescence is regulated by the joint action of multiple signal transduction pathways. The previous study by our research group found that the Janus kinase 2 (JAK2)/signal transducer and...
journal_title：Cellular signalling
pub_type： 杂志文章
doi：10.1016/j.cellsig.2018.10.021
更新日期：2019-01-01 00:00:00
