NATURE AND THE NATURE RESEARCH JOURNALS PRESS RELEASE
For papers that will be published online on 23 July 2006
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This press release contains:
· Summaries of newsworthy papers:
Infectious disease: Active sites of a hepatitis C virus enzyme revealed - Nature
Large-scale turbulence - Nature Physics
Gleevec may cause heart problems - Nature Medicine
Neutralizing HIV - Nature Structural & Molecular Biology
· Mention of papers to be published at the same time with the same embargo
· Geographical listing of authors
PDFs of all the papers mentioned on this release can be found in the relevant journal's section of http://press.nature.com. Press contacts for the Nature journals are listed at the end of this release.
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**********************************NATURE************************************
(http://www.nature.com/nature)
[1] Infectious disease: Active sites of a hepatitis C virus enzyme revealed
DOI: 10.1038/nature04975
The crystal structure of one of the hepatitis C viral proteins could offer new opportunities for antiviral drug design, report Charles Rice and colleagues in a paper published online this week by Nature. The disease affects an estimated 170 million people worldwide, often leading to cirrhosis and liver cancer.
The viral genome encodes a single polyprotein, which cleaves into proteins including the NS2-3 protease. The crystal structure of the protease catalytic domain reveals a novel structure: it is actually a dimer (resembling a 'butterfly') composed of two identical proteins that each contributes amino acids to two equivalent active sites. The concentration and dimerization of NS2-3 may be a limiting factor in the viral life cycle because the protease is essential for viral replication. Details of the structure may help in the search for small-molecule inhibitors directed against the active site.
Author contact:
Charles Rice (The Rockefeller University, New York, NY, USA)
Tel: +1 212 327 7046; E-mail: [email protected]
Other papers from Nature to be published online at the same time and with the same embargo:
[2] Protein flexibility acclimatizes photosynthetic energy conversion to the ambient temperature
DOI: 10.1038/nature04947
*****************************NATURE PHYSICS******************************
(http://www.nature.com/naturephysics)
[3] Large-scale turbulence
DOI: 10.1038/nphys361
The results from the largest ever simulation of a thermonuclear supernova are reported in the August issue of Nature Physics. Type-Ia supernovae - spectacular explosions from collapsing white-dwarf stars - are used as 'standard candles' to gauge the distance of galaxies and the expansion rate of the universe, so it is important to understand how the flame fronts travel. Explosions of this sort cannot be measured directly so computer simulations are used to reveal the dynamics of the star's combustion.
William Cabot and colleagues carried out the simulation on the IBM BlueGene/L, the fastest supercomputer in the world. They examined the turbulent mixing of fluids of different density, which is the basis of many other problems in oceanography and geophysics. For a fluid, the Reynolds number is a measure of whether the flow is laminar or turbulent. By going to Reynolds numbers well beyond those of previous simulations, the authors find that the growth rate of the turbulent region has an unexpected dependence on the Reynolds number. Their results suggest that we have much to learn regarding highly unstable flows.
Author contact:
Andrew Cook (Lawrence Livermore National Laboratory, Livermore, CA, USA)
Tel: +1 510 423 2856; E-mail: [email protected]
Other papers from Nature Physics to be published online at the same time and with the same embargo:
[4] Effects of topology on network evolution
DOI: 10.1038/nphys359
[5] Superconductivity in CuxTiSe2
DOI: 10.1038/nphys360
[6] Two energy scales and two distinct quasiparticle dynamics in the superconducting state of underdoped cuprates
DOI: 10.1038/nphys362
[7] The effect of Auger heating on intraband carrier relaxation in semiconductor quantum rods
DOI: 10.1038/nphys363
[8] Interaction between optical nano-objects at metallo-dielectric interfaces
DOI: 10.1038/nphys364
*****************************NATURE MEDICINE***********************
(http://www.nature.com/naturemedicine)
[9] Gleevec may cause heart problems
DOI: 10.1038/nm1446
Imatinib mesylate (Gleevec), a drug used to treat chronic myelogenous leukemia (CML), can kill heart cells, according to a paper in the August issue of Nature Medicine.
Imatinib acts by inhibiting the activity of the protein Bcr-Abl, the causal agent in CML. Thomas Force and his colleagues report on ten people who developed severe congestive heart failure while on imatinib and show that mice treated with the drug develop heart pathology. Microscopic and biochemical analyses of human and mice hearts treated with imatinib suggest that the drug is toxic to cardiac cells. This effect seemed to depend on the action of imatinib over Bcr-Abl and not on other targets.
So, a toxic effect on the heart is an unanticipated side effect of imatinib. The authors suggest that patients who are on imatinib should be followed closely for symptoms of cardiac dysfunction.
Author contact:
Thomas Force (Jefferson Medical College, Philadelphia, PA, USA)
Tel: +1 215 503 9520; E-mail: [email protected]
Other papers from Nature Medicine to be published online at the same time and with the same embargo:
[10] A potential molecular mechanism for hypersensitivity caused by formalin-inactivated vaccines
DOI: 10.1038/nm1456
[11] Chronic stress promotes tumor growth and angiogenesis in a mouse model of ovarian carcinoma
DOI: 10.1038/nm1447
[12] Interaction of KAI1 on tumor cells with DARC on vascular endothelium leads to metastasis suppression
DOI: 10.1038/nm1444
[13] Connexin37 protects against atherosclerosis by regulating monocyte adhesion
DOI: 10.1038/nm1441
[14] Quantum dot semiconductor nanocrystals for immunophenotyping by polychromatic flow cytometry
DOI: 10.1038/nm1371
**********************NATURE STRUCTURAL & MOLECULAR BIOLOGY**********************
(http://www.nature.com/natstructmolbiol)
[15] Neutralizing HIV
DOI: 10.1038/nsmb1127
The interaction between a human antibody and a protein found on the surface of the HIV-1 virus is revealed in a study in the August issue of Nature Structural & Molecular Biology. The antibody, called D5, recognises an intermediate version of the protein that controls the process by which HIV-1 fuses with host cell membranes.
To gain entry to a host cell, some viruses must first bind to the target cell surface and fuse their membranes with that of the target cell. The protein responsible for controlling the fusion process, called gp41 in HIV-1, must undergo a series of structural changes as membrane fusion occurs. This exposes 'conserved' regions of the molecule, which are ideal targets for antibodies because their sequences mutate less frequently; they tend to 'look' the same to the antibody even in different HIV strain populations.
Andrea Carfi and colleagues report that the human antibody D5 recognizes a gp41 structural intermediate. Understanding how these molecules interact may potentially aid the development of more potent HIV-1 neutralizing antibodies and therapeutic agents. Because other viruses also fuse with host cell membranes, targeting a fusion protein intermediate may be a useful and widely-applicable strategy for drug treatment and vaccination.
Author contact:
Andrea Carfi (IRBM P. Angeletti, Pomezia, Italy)
Tel: +39 06 9109 3550; E-mail: [email protected]
Other papers from Nature Structural & Molecular Biology to be published online at the same time and with the same embargo:
[16] Proteasome-dependent degradation of Est1p regulates the cell cycle-restricted assembly of telomerase in Saccharomyces cerevisiae
DOI: 10.1038/nsmb1125
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Items from other Nature journals to be published online at the same time and with the same embargo:
NATURE CHEMICAL BIOLOGY (http://www.nature.com/nchembio)
[17] Small molecule inhibitor of p53 binding to mitochondria protects mice from gamma radiation
DOI: 10.1038/nchembio809
NATURE GENETICS (http://www.nature.com/naturegenetics)
[18] Principal components analysis corrects for stratification in genome-wide association studies
DOI: 10.1038/ng1847
[19] Candidate lung tumor susceptibility genes identified through whole-genome association analyses in inbred mice
DOI: 10.1038/ng1849
[20] RNA interference machinery influences the nuclear organization of a chromatin insulator
DOI: 10.1038/ng1850
Nature NEUROSCIENCE (http://www.nature.com/natureneuroscience)
[21] Species-specific calls activate homologs of Broca's and Wernicke's areas in the macaque
DOI: 10.1038/nn1741
[22] Midbrain dopamine neurons encode decisions for future action
DOI: 10.1038/nn1743
Nature IMMUNOLOGY (http://www.nature.com/natureimmunology)
[23] Key function for the Ubc13 E2 ubiquitin-conjugating enzyme in immune receptor signaling
DOI: 10.1038/ni1367
NATURE CELL BIOLOGY (http://www.nature.com/naturecellbiology)
[24] The endocytic pathway mediates cell entry of dsRNA to induce RNAi silencing
DOI: 10.1038/ncb1439
[25] Arp2/3 ATP hydrolysis-catalysed branch dissociation is critical for endocytic force generation
DOI: 10.1038/ncb1443
[26] FilGAP, a Rho- and ROCK-regulated GAP for Rac binds filamin A to control actin remodelling
DOI: 10.1038/ncb1437
[27] Chromatin relaxation in response to DNA double-strand breaks is modulated by a novel ATM- and KAP-1-dependent pathway
DOI: 10.1038/ncb1446
[28] Plasminogen activator inhibitor-1 is a critical downstream target of p53 in the induction of replicative senescence
DOI: 10.1038/ncb1448
[39] The EphB4 receptor suppresses breast cancer cell tumorigenicity through an Abl-Crk pathway
DOI: 10.1038/ncb1438
[30] A regulated interaction with the UIM protein Eps15 implicates parkin in EGF receptor trafficking and PI(3)K-Akt signalling
DOI: 10.1038/ncb1441
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GEOGRAPHICAL LISTING OF AUTHORS
The following list of places refers to the whereabouts of authors on the papers numbered in this release. The listing may be for an author's main affiliation, or for a place where they are working temporarily. Please see the PDF of the paper for full details.
CANADA
Edmonton: 24
Montreal: 30
CZECH REPUBLIC
Nove Hrady: 2
DENMARK
Copenhagen: 27
FRANCE
Gif-sur-Yvette: 6
Orsay: 8
Palaiseau: 6
Paris: 6, 30
INDIA
Andhra Pradesh: 2
ISRAEL
Haifa: 2
Jerusalem: 22
Tel Aviv: 27
ITALY
Pomezia: 15
JAPAN
Akita City: 12
Fukuoka: 23
Osaka: 23
Tokyo: 23, 27
Toyama: 23
POLAND
Gdansk: 5
PORTUGAL
Oeiras: 21
SWITZERLAND
Geneva: 13
THE NETHERLANDS
Amsterdam: 28
Delft: 5
Utrecht: 30
UNITED KINGDOM
London: 10, 21
Oxford: 10, 14
UNITED STATES OF AMERICA
Alabama
Birmingham: 14
California
Berkeley: 25
Foster City: 15
Fremont: 17
La Jolla: 29
Livermore: 3
Los Angeles: 11
Palo Alto: 14
San Francisco: 24
Illinois
Chicago: 4
Springfield: 12
Iowa
Iowa City: 11
Maryland
Bethesda: 14, 21
Baltimore: 20
College Park: 21
Massachusetts
Boston: 9, 13, 18, 26
Cambridge: 18, 21
North Grafton: 9
Missouri
St Louis: 19
New Jersey
Murray Hill: 5
Princeton: 5
Rutgers University: 6
New Mexico
Los Alamos: 7
New York
Albany: 28
New York: 1, 6, 12
Ohio
Cleveland: 17, 27
Pennsylvania
Philadelphia: 2, 9, 14
Pittsburgh: 14
West Point: 15
Tennessee
Nashville: 16
Texas
Houston: 9, 11
Washington
Seattle: 14
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Katherine Anderson (Nature London)
Tel: +44 20 7843 4502; E-mail: [email protected]
Ruth Francis (Senior Press Officer, Nature, London)
Tel: +44 20 7843 4562; E-mail: [email protected]
For media inquiries relating to editorial content/policy for the Nature Research Journals, please contact the journals individually:
Nature Cell Biology (London)
Bernd Pulverer
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Nature Chemical Biology (Boston)
Beatrice Chrystall
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Nature Genetics (New York)
Orli Bahcall
Tel: +1 212 726 9311; E-mail: [email protected]
Nature Immunology (New York)
Laurie Dempsey
Tel: +1 212 726 9372; E-mail: [email protected]
Nature Medicine (New York)
Juan Carlos Lopez
Tel: +1 212 726 9325; E-mail: [email protected]
Nature Neuroscience (New York)
Sandra Aamodt (based in California)
Tel: +1 530 795 3256; E-mail: [email protected]
Nature Physics (London)
Alison Wright
Tel: +44 20 7843 4555; E-mail: [email protected]
Nature Structural & Molecular Biology (New York)
Michelle Montoya
Tel: +1 212 726 9326; E-mail: [email protected]
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