Abstract:
:In the canonical model of JAK/STAT signalling STAT transcription factors are activated by JAK mediated tyrosine phosphorylation following pathway stimulation by external cytokines. Activated STAT molecules then homo- or heterodimerise before translocating to the nucleus where they bind to DNA sequences within the promoters of pathway target genes. DNA-bound STAT dimers then activate transcription of their targets via interaction with components of the basal transcription machinery. Here we describe a missense mutation in the SH2 domain of the single Drosophila STAT92E homologue which results in an amino-acid substitution conserved in both the canonical SH2 domain and STAT-like molecules previously identified in C. elegans and the mosquito Anopheles gambiae. This mutation leads to nuclear accumulation and constitutive DNA binding of Drosophila STAT92E even in the absence of JAK stimulation. Strikingly, this mutant shows only limited transcriptional activity in tissue culture based assays and functions as a dominant-negative at both the phenotypic and molecular levels in vivo. These features represent aspects of both dominant gain-of-function and dominant-negative activities and imply that the functions of DNA binding can be functionally separated from the role of STAT92E as a transcriptional activator. It is thus possible that an alternative post-translational modification, in addition to tyrosine phosphorylation, may be required to allow STAT to act as a transcriptional activator and suggests the existence of an alternative mechanism by which STAT transcriptional activity may be regulated in vivo.
journal_name
Cell Signaljournal_title
Cellular signallingauthors
Karsten P,Plischke I,Perrimon N,Zeidler MPdoi
10.1016/j.cellsig.2005.07.006subject
Has Abstractpub_date
2006-06-01 00:00:00pages
819-29issue
6eissn
0898-6568issn
1873-3913pii
S0898-6568(05)00179-8journal_volume
18pub_type
杂志文章abstract::Interferon-α (IFNα) has enormous potential for anti-proliferative and anti-viral treatments. However, clinical success is still hampered due to its limited bioavailability and thus, lack of sustained modulation of disease-relevant protective programs. Consequently, we here examined whether IFNα immobilized on nanoscal...
journal_title:Cellular signalling
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更新日期:2013-04-01 00:00:00
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pub_type: 杂志文章,评审
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更新日期:2011-06-01 00:00:00
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2011.01.010
更新日期:2011-05-01 00:00:00
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pub_type: 杂志文章
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journal_title:Cellular signalling
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2013.12.011
更新日期:2014-04-01 00:00:00
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2008.05.010
更新日期:2008-09-01 00:00:00
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pub_type: 杂志文章
doi:10.1016/j.cellsig.2016.02.012
更新日期:2016-05-01 00:00:00
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journal_title:Cellular signalling
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doi:10.1016/j.cellsig.2013.09.011
更新日期:2013-12-01 00:00:00
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pub_type: 杂志文章
doi:10.1016/j.cellsig.2015.03.001
更新日期:2015-06-01 00:00:00
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/s0898-6568(00)00090-5
更新日期:2000-07-01 00:00:00
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pub_type: 杂志文章
doi:10.1016/j.cellsig.2020.109549
更新日期:2020-05-01 00:00:00
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journal_title:Cellular signalling
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doi:10.1016/j.cellsig.2019.109461
更新日期:2020-01-01 00:00:00
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pub_type: 杂志文章
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更新日期:1996-03-01 00:00:00
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更新日期:2020-04-01 00:00:00
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journal_title:Cellular signalling
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doi:10.1016/j.cellsig.2011.03.001
更新日期:2011-07-01 00:00:00
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journal_title:Cellular signalling
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journal_title:Cellular signalling
pub_type: 杂志文章,评审
doi:10.1016/j.cellsig.2011.10.007
更新日期:2012-02-01 00:00:00
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