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CaMKII (不作postdog) 于 (Thu Aug 20 12:39:18 2009, 美东) 提到:
发信人: CaMKII (不作postdog), 信区: Biology
标 题: 最新一期Cell两篇北大的文章（尚永丰&汤超）
发信站: BBS 未名空间站 (Thu Aug 20 12:38:55 2009, 美东)
http://www.cell.com/abstract/S0092-8674(09)00710-7
Cell, Volume 138, Issue 4, 660-672, 21 August 2009
doi:10.1016/j.cell.2009.05.050
LSD1 Is a Subunit of the NuRD Complex and Targets the Metastasis Programs in
Breast Cancer
Yan Wang1,Hua Zhang1,Yupeng Chen1,Yimin Sun1,Fen Yang1,Wenhua Yu1,Jing
Liang1,Luyang Sun1,Xiaohan Yang1,Lei Shi1,Ruifang Li1,Yanyan Li1,Yu Zhang1,
Qian Li1,Xia Yi1 and Yongfeng Shang1,,
1 Key Laboratory of Carcinogenesis and Translational Research, Ministry of
Education, Department of Biochemistry and Molecular Biology, Peking
University Health Science Center, Beijing 100191, China
Corresponding author
Summary
Lysine-specific demethylase 1 (LSD1) exerts pathway-specific activity in
animal development and hasbeen linked to several high-risk cancers. Here, we
report that LSD1 is an integral component of theMi-2/nucleosome remodeling
and deacetylase (NuRD) complex. Transcriptional target analysis revealed
that the LSD1/NuRD complexes regulate several cellular signaling pathways
including TGF1 signaling pathway that are critically involved in cell
proliferation, survival, and epithelial-to-mesenchymal transition. We
demonstrated that LSD1 inhibits the invasion of breast cancer cells invitro
and suppresses breast cancer metastatic potential invivo. We found that LSD1
is downregulated in breast carcinomas and that its level of expression is
negatively correlated with that of TGF1. Our data provide a molecular basis
for the interplay of histone demethylation and deacetylation in chromatin
remodeling. By enlisting LSD1, the NuRD complex expands its chromatin
remodeling capacity to include ATPase, histone deacetylase, and histone
demethylase.
另一篇偏理论的：
http://www.cell.com/abstract/S0092-8674(09)00712-0
Cell, Volume 138, Issue 4, 760-773, 21 August 2009
doi:10.1016/j.cell.2009.06.013
Defining Network Topologies that Can Achieve Biochemical Adaptation
Wenzhe Ma1,2,3,Ala Trusina2,3,Hana El-Samad2,4,Wendell A. Lim2,5,,and Chao
Tang1,2,3,4,,
1 Center for Theoretical Biology, Peking University, Beijing 100871, China
2 California Institute for Quantitative Biosciences, University of
California, San Francisco, CA 94158, USA
3 Department of Bioengineering and Therapeutic Sciences, University of
California, San Francisco, CA 94158, USA
4 Department of Biochemistry and Biophysics, University of California, San
Francisco, CA 94158, USA
5 Howard Hughes Medical Institute and Department of Cellular and Molecular
Pharmacology, University of California, San Francisco, CA 94158, USA
Corresponding author
Corresponding author
Summary
Many signaling systems show adaptationthe ability to reset themselves after
responding toa stimulus. We computationally searched all possible three-node
enzyme network topologies to identify those that could perform adaptation.
Only two major core topologies emerge as robust solutions: a negative
feedback loop with a buffering node and an incoherent feedforward loop with
a proportioner node. Minimal circuits containing these topologies are,
within proper regions of parameter space, sufficient to achieve adaptation.
More complex circuits that robustly perform adaptation all contain at least
one of these topologies at their core. This analysis yields a design table
highlighting a finite set of adaptive circuits. Despite the diversity of
possible biochemical networks, it may be common to find that only a finite
set of core topologies can execute a particular function. These design rules
provide a framework for functionally classifying complex natural networks
and a manual for engineering networks.For a video summary of this article,
see the PaperFlickfile with the Supplemental Data available online.
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mingfm (carol) 于 (Thu Aug 20 13:53:07 2009, 美东) 提到:
niu
in
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gausschen (aaaa) 于 (Thu Aug 20 16:47:51 2009, 美东) 提到:
qiang!
in
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mama123 (boy) 于 (Thu Aug 20 20:49:40 2009, 美东) 提到:
都是第一单位. 不错. |
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