Help:Formatting

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{| class="wikitable" ! Description ! width=40% | You type ! width=40% | You get ! colspan="3" style="background:#ABE" | character (inline) formatting – applies anywhere italic italic bold bold bold & italic bold & italic &lt;nowiki>no markup</nowiki&gt; no markup ! colspan="3" style="background:#ABE" | section formatting – only at the beginning of the line = Level 1 =
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 * Bold text
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 * Escape wiki markup
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 * Headings of different levels

Level 6


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Level 6
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Text below Text above

Text below don't break levels. Any other first character ends the list. don't break levels. Any other first character ends the list. don't break levels.
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 * Start each line
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 * More asterisks gives deeper
 * and deeper levels.
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 * But jumping levels creates empty space.
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 * 1) Start each line
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Any other first character also ends the list.
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of &lt;nowiki> &lt;/nowiki>
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 * this looks like a continuation
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 * instead
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of
 * 1) one
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 * 6) ; three item one
 * three def one
 * 1) four
 * four def one
 * this looks like a continuation
 * and is often used
 * instead
 * instead

Start each line with a space. Text is preformatted and markups can be done
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Proceeding of the National Academy of Sciences - PNAS
Volume 107, Issue 45, Pages 19525 - 19530, 9 November 2010

From the Cover: Bayesian model of dynamic image stabilization in the visual system

Yoram Burak1, Uri Rokni1, Markus Meister1,2, and Haim Sompolinsky1,3


 * 1) Center for Brain Science, Harvard University, Cambridge, MA 02138
 * 2) Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138
 * 3) Interdisciplinary Center for Neural Computation, Hebrew University, Jerusalem 91904, Israel

Humans can resolve the fine details of visual stimuli although the image projected on the retina is constantly drifting relative to the photoreceptor

array. Here we demonstrate that the brain must take this drift into account when performing high acuity visual tasks. Further, we propose a decoding

strategy for interpreting the spikes emitted by the retina, which takes into account the ambiguity caused by retinal noise and the unknown trajectory of

the projected image on the retina. A main difficulty, addressed in our proposal, is the exponentially large number of possible stimuli, which renders the

ideal Bayesian solution to the problem computationally intractable. In contrast, the strategy that we propose suggests a realistic implementation in the

visual cortex. The implementation involves two populations of cells, one that tracks the position of the image and another that represents a stabilized

estimate of the image itself. Spikes from the retina are dynamically routed to the two populations and are interpreted in a probabilistic manner. We

consider the architecture of neural circuitry that could implement this strategy and its performance under measured statistics of human fixational eye

motion. A salient prediction is that in high acuity tasks, fixed features within the visual scene are beneficial because they provide information about

the drifting position of the image. Therefore, complete elimination of peripheral features in the visual scene should degrade performance on high acuity

tasks involving very small stimuli.

Volume 107, Issue 45, Pages 19290 - 193295, 9 November 2010

Graded enhancement of p53 binding to CREB-binding protein (CBP) by multisite phosphorylation

Chul Won Lee, Josephine C. Ferreon, Allan Chris M. Ferreon, Munehito Arai, and Peter E. Wright

Department of Molecular Biology and The Skaggs Institute for Chemical Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037

The transcriptional activity of p53 is regulated by a cascade of posttranslational modifications. Although acetylation of p53 by CREB-binding protein (CBP)/p300 is known to be indispensable for p53 activation, the role of phosphorylation, and in particular multisite phosphorylation, in activation of CBP/p300-dependent p53 transcriptional pathways remains unclear. We investigated the role of single site and multiple site phosphorylation of the p53 transactivation domain in mediating its interaction with CBP and with the ubiquitin ligase HDM2. Phosphorylation at Thr18 functions as an on/off switch to regulate binding to the N-terminal domain of HDM2. In contrast, binding to CBP is modulated by the extent of p53 phosphorylation; addition of successive phosphoryl groups enhances the affinity for the TAZ1, TAZ2, and KIX domains of CBP in an additive manner. Activation of p53-dependent transcriptional pathways requires that p53 compete with numerous cellular transcription factors for binding to limiting amounts of CBP/p300. Multisite phosphorylation represents a mechanism for a graded p53 response, with each successive phosphorylation event resulting in increasingly efficient recruitment of CBP/p300 to p53-regulated transcriptional programs, in the face of competition from cellular transcription factors. Multisite phosphorylation thus acts as a rheostat to enhance binding to CBP/p300 and provides a plausible mechanistic explanation for the gradually increasing p53 response observed following prolonged or severe genotoxic stress.

Volume 107, Issue 45, Pages 19231 - 193236, 9 November 2010

Affinity purification of microRNA-133a with the cardiac transcription factor, Hand2

Ngan K. Vo1, Ryan P. Dalton1, Ning Liu2, Eric N. Olson2, and Richard H. Goodman1


 * 1) Vollum Institute, Oregon Health and Science University, Portland, OR 97239
 * 2) Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9148

Predictions of microRNA-mRNA interactions typically rely on bioinformatic algorithms, but these algorithms only suggest the possibility of microRNA binding and may miss important interactions as well as falsely predict others. We developed an affinity purification approach to empirically identify microRNAs associated with the 3′UTR of the mRNA encoding Hand2, a transcription factor essential for cardiac development. In addition to miR-1, a known regulator of Hand2 expression, we determined that the Hand2 3′UTR also associated with miR-133a, a microRNA cotranscribed with miR-1 in cardiac and muscle cells. Using a sequential binding assay, we showed that miR-1 and miR-133a could occupy the Hand2 3′UTR concurrently. miR-133a inhibited Hand2 expression in tissue culture models, and miR-133a double knockout mice had elevated levels of Hand2 mRNA and protein. We conclude that Hand2 is regulated by miR-133a in addition to miR-1. The affinity purification assay should be generally applicable for identifying other microRNA-mRNA interactions.

Volume 107, Issue 45, Pages 19207 - 193212, 9 November 2010

From the Cover: Electrical detection of pathogenic bacteria via immobilized antimicrobial peptides

Manu S. Mannoor1, Siyan Zhang2, A. James Link2 and Michael C. McAlpine1


 * 1) Department of Mechanical and Aerospace Engineering, Princeton University, Princeton, NJ 08544
 * 2) Department of Chemical and Biological Engineering, Princeton University, Princeton, NJ 08544

The development of a robust and portable biosensor for the detection of pathogenic bacteria could impact areas ranging from water-quality monitoring to testing of pharmaceutical products for bacterial contamination. Of particular interest are detectors that combine the natural specificity of biological recognition with sensitive, label-free sensors providing electronic readout. Evolution has tailored antimicrobial peptides to exhibit broad-spectrum activity against pathogenic bacteria, while retaining a high degree of robustness. Here, we report selective and sensitive detection of infectious agents via electronic detection based on antimicrobial peptide-functionalized microcapacitive electrode arrays. The semiselective antimicrobial peptide magainin I—which occurs naturally on the skin of African clawed frogs—was immobilized on gold microelectrodes via a C-terminal cysteine residue. Significantly, exposing the sensor to various concentrations of pathogenic Escherichia coli revealed detection limits of approximately 1 bacterium/&mu;L, a clinically useful detection range. The peptide-microcapacitive hybrid device was further able to demonstrate both Gram-selective detection as well as interbacterial strain differentiation, while maintaining recognition capabilities toward pathogenic strains of E. coli and Salmonella. Finally, we report a simulated “water-sampling” chip, consisting of a microfluidic flow cell integrated onto the hybrid sensor, which demonstrates real-time on-chip monitoring of the interaction of E. coli cells with the antimicrobial peptides. The combination of robust, evolutionarily tailored peptides with electronic read-out monitoring electrodes may open exciting avenues in both fundamental studies of the interactions of bacteria with antimicrobial peptides, as well as the practical use of these devices as portable pathogen detectors.

Volume 107, Issue 45, Pages 19151 - 19156, 9 November 2010

High-throughput identification of compounds targeting influenza RNA-dependent RNA polymerase activity

Ching-Yao Su1,2, Ting-Jen R. Chenga1, Meng-I. Lin1, Shi-Yun Wang1, Wen-I. Huang1, Shao-Ying Lin-Chu1, Yu-Hou Chen3, Chung-Yi Wu4, Michael M. C. Lai4, Wei-Chieh Cheng1, Ying-Ta Wu1, Ming-Daw Tsai1,3 Yih-Shyun E. Cheng1, and Chi-Huey Wong1,2


 * 1) Genomics Research Center, Academia Sinica, Taipei, 115, Taiwan
 * 2) Institute of Biochemical Sciences, National Taiwan University, Taipei, 106, Taiwan, Republic of China
 * 3) Institute of Biological Chemistry, Academia Sinica, Taipei, 115, Taiwan
 * 4) Institute of Molecular Biology, Academia Sinica, Taipei, 115, Taiwan

As influenza viruses have developed resistance towards current drugs, new inhibitors that prevent viral replication through different inhibitory mechanisms are useful. In this study, we developed a screening procedure to search for new antiinfluenza inhibitors from 1,200,000 compounds and identified previously reported as well as new antiinfluenza compounds. Several antiinfluenza compounds were inhibitory to the influenza RNA-dependent RNA polymerase (RdRP), including nucleozin and its analogs. The most potent nucleozin analog, 3061 (FA-2), inhibited the replication of the influenza A/WSN/33 (H1N1) virus in MDCK cells at submicromolar concentrations and protected the lethal H1N1 infection of mice. Influenza variants resistant to 3061 (FA-2) were isolated and shown to have the mutation on nucleoprotein (NP) that is distinct from the recently reported resistant mutation of Y289H [Kao R, et al. (2010) Nat Biotechnol 28:600]. Recombinant influenza carrying the Y52H NP is also resistant to 3061 (FA-2), and NP aggregation induced by 3061 (FA-2) was identified as the most likely cause for inhibition. In addition, we identified another antiinfluenza RdRP inhibitor 367 which targets PB1 protein but not NP. A mutant resistant to 367 has H456P mutation at the PB1 protein and both the recombinant influenza and the RdRP expressing the PB1 H456P mutation have elevated resistance to 367. Our high-throughput screening (HTS) campaign thus resulted in the identification of antiinfluenza compounds targeting RdRP activity.