Institution
American Association for the Advancement of Science
Nonprofit•Washington D.C., District of Columbia, United States•
About: American Association for the Advancement of Science is a nonprofit organization based out in Washington D.C., District of Columbia, United States. It is known for research contribution in the topics: Science education & Government. The organization has 353 authors who have published 897 publications receiving 18841 citations. The organization is also known as: AAAS.
Topics: Science education, Government, Public policy, Cancer, Higher education
Papers published on a yearly basis
Papers
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TL;DR: This Podcast features an interview with William Pryor and Srinivasa Subramaniam, authors of a Research Article that appears in the 28 October 2014 issue of Science Signaling, about how the huntingtin protein (Htt) stimulates signaling that contributes to Huntington's disease–like symptoms in mice.
Abstract: This Podcast features an interview with William Pryor and Srinivasa Subramaniam, authors of a Research Article that appears in the 28 October 2014 issue of Science Signaling , about how the huntingtin protein (Htt) stimulates signaling that contributes to Huntington9s disease–like symptoms in mice. Htt is ubiquitously expressed and contains an amino-terminal polyglutamine tract. Whereas normal forms of Htt contain up to 35 glutamine residues in this region, forms of Htt in Huntington9s disease patients contain more than 36 glutamine residues. Expansion of the polyglutamine tract is sufficient to cause disease, because increasing the number of glutamines in this region in mice causes motor defects and other pathologies typical of Huntington9s disease. Although it is clear that expansion of the polyglutamine tract of Htt contributes to Huntington9s disease, it is not clear how normal forms of Htt function in cell biology or how polyglutamine-expanded forms of Htt cause disease. Pryor et al . report that Htt promotes anabolic signaling through the mechanistic target of rapamycin complex 1 (mTORC1) and that polyglutamine-expanded forms of Htt enhance mTORC1 signaling. Increasing mTORC1 signaling in a mouse model of Huntington9s disease led to earlier onset of disease symptoms.
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TL;DR: Findings identify proteins that could potentially be targeted to prevent dry mouth in patients undergoing radiation therapy by inhibiting store-operated Ca2+ entry and interfering with saliva production.
Abstract: This Podcast features a conversation with Indu Ambudkar, senior author of a Research Resource that appears in the 6 June 2017 issue of Science Signaling , about how activation of the cation channel TRPM2 is involved in radiation-induced dry mouth. Patients who receive radiation therapy for head and neck cancers often develop dry mouth as a side effect, and this condition is frequently permanent. Radiation does not kill cells in the salivary gland, yet it causes the acinar cells of the gland to reduce the amount of saliva they secrete. Liu et al . found that radiation-induced activation of the cation channel TRPM2 triggered cleavage of the endoplasmic reticulum Ca 2+ sensor STIM1, thus inhibiting store-operated Ca 2+ entry and interfering with saliva production. These findings identify proteins that could potentially be targeted to prevent dry mouth in patients undergoing radiation therapy. Listen to Podcast
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TL;DR: This is a conversation with Jean-Paul Vincent about a Research Article published in the 6 October 2009 issue of Science Signaling about graded distribution of Wingless.
Abstract: This is a conversation with Jean-Paul Vincent about a Research Article published in the 6 October 2009 issue of Science Signaling.
01 Oct 1938
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TL;DR: A small-molecule transporter and a potassium channel cooperate to modulate the composition of cerebrospinal fluid and seizure susceptibility and identified a mechanism whereby the SMIT1-KCNQ1- KCNE2 complex removes excess myo-inositol from the CSF.
Abstract: This Podcast features an interview with Geoffrey Abbott, author of a Research Article that appears in the 4 March 2014 issue of Science Signaling , about a potassium channel and a solute transporter that contribute to seizure susceptibility. Mice lacking the potassium channel regulatory subunit KCNE2 have cardiac arrhythmia and are prone to seizures. Abbott et al . report that the cerebrospinal fluid (CSF) from Kcne2 −/− mice had decreased abundance of myo -inositol compared to CSF from wild-type mice, and administering myo -inositol rescued seizure susceptibility in Kcne2 −/− mice. KNCE2 colocalized with the potassium channel pore-forming subunit KCNQ1 and the myo -inositol transporter SMIT1 in the choroid plexus, the tissue that produces and secretes CSF. The authors identified a mechanism whereby the SMIT1-KCNQ1-KCNE2 complex removes excess myo -inositol from the CSF.
Authors
Showing all 359 results
Name | H-index | Papers | Citations |
---|---|---|---|
Kendall N. Houk | 112 | 997 | 54877 |
M. Cooke | 110 | 915 | 52792 |
Federica Sallusto | 107 | 244 | 66684 |
Peter Agre | 104 | 248 | 39051 |
Michael B. Yaffe | 102 | 379 | 41663 |
Abul K. Abbas | 88 | 251 | 34965 |
Jose M. F. Moura | 80 | 647 | 25819 |
Marcia C. Linn | 72 | 337 | 25744 |
Eli Y. Adashi | 66 | 442 | 17139 |
William H. Press | 63 | 180 | 102433 |
Richard A. Berk | 58 | 293 | 15288 |
James L. Salzer | 56 | 111 | 11437 |
Robert E. Kopp | 56 | 199 | 10227 |
Herbert C. Kelman | 52 | 155 | 12853 |
Gerard Gilfoyle | 50 | 255 | 8716 |