NATURE AND THE NATURE RESEARCH JOURNALS PRESS RELEASE
For papers that will be published online on 11 April 2010
This press release is copyrighted to the Nature journals mentioned below.
This press release contains:
· Summaries of newsworthy papers:
Medicine: Resolving inflammatory pain
Nature: Ovarian hormones drive stem cell proliferation
Immunology: Influenza ‘channels’ the immune response
Neuroscience: Failure of cannibalization in Huntington disease
Genetics: Variants associated with kidney function
Neuroscience: Anxious interactions
· 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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[1] Medicine: Resolving inflammatory pain
DOI: 10.1038/nm.2123
Resolvins, naturally-occurring lipids derived from omega-3 fatty acids, may represent a new class of painkillers for treating inflammatory pain, suggests a report published online this week in Nature Medicine. The scientists propose that resolvins may prove effective as analgesics by reducing inflammation and acting in the spinal cord to prevent chronic pain.
Inflammatory pain, such as arthritic and post-operative pain, is triggered by tissue injury, leading to the release of compounds that increase inflammation and act within the spinal cord to cause persistent pain.
Ru-Rong Ji and colleagues found that two resolvins, RvE1 and RvD1, which are naturally produced from certain omega-3 fatty acids, reduce inflammatory pain symptoms when administered to mice. The team showed that RvE1 was 10,000 times more potent at alleviating pain than its parent compound; moreover, an artificial compound, Chemerin, which binds to the same receptor as RvE1 and RvD1 also significantly reduced pain symptoms. Aside from their established anti-inflammatory effects, they also found that RvE1 acts in the spinal cord to prevent persistent neuronal activation which normally causes chronic pain. These analgesic effects were seen without any alterations in normal sensitivity to pain.
Author contact:
Ru-Rong Ji (Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA)
Tel: +1 617 732 8852; E-mail: [email protected]
[2] Nature: Ovarian hormones drive stem cell proliferation
DOI: 10.1038/nature09027
Research published in Nature this week shows that the hormones oestrogen and progesterone increase the number of mammary stem cells in mice, even though these cells lack the receptors for these hormones. This might account for the increased incidence of breast cancer associated with pregnancy.
The ovarian hormones oestrogen and progesterone increase breast cancer risk but the cellular mechanisms are unclear. Jane Visvader and colleagues show that the size of the mammary stem cell pool in mice is regulated by steroid hormone signalling. The hormones drive an increase in mammary stem cell numbers, whereas ovariectomy or treatment with an oestrogen synthesis inhibitor impairs the repopulating ability of the cells.
In contrast, pregnancy led to an increase in the number of these cells. The authors speculate that this may lead to the clonal expansion of a mutated cell, leading to cancer.
Author contact:
Jane Visvader (The Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia)
Tel: +61 3 9345 2494; E-mail: [email protected]
[3] Immunology: Influenza ‘channels’ the immune response
DOI: 10.1038/ni.1861
How the influenza virus triggers the inflammasome, an essential component in a host's defense against this the virus, is reported in a paper appearing online this week in Nature Immunology. These findings may aid in our ability to design effective interventions and treatments for the influenza virus infection.
Akiko Iwasaki and colleagues showed that the influenza virus M2 protein--an ion channel previously shown to be important for influenza virus pathogenesis--stimulates the inflammasome pathway. M2 channel activity was both necessary and sufficient for influenza activation of inflammasomes. Furthermore, M2-mediated inflammasome activation required its localization to the Golgi body organelle within the cell.
Future research will be required to see if other viruses use similar ion channels to activate the inflammasome.
Author contact:
Akiko Iwasaki (Yale University School of Medicine, New Haven, CT, USA)
Tel: +1 203 785 2919; E-mail: [email protected]
[4] Neuroscience: Failure of cannibalization in Huntington disease
DOI: 10.1038/nn.2528
The inability to get rid of mutant protein accumulation in Huntington’s disease (HD) is because the neuronal protein degradation machinery fails to recognize and package proteins for destruction. The work published online this week in Nature Neuroscience suggests potential therapeutic targets that may be beneficial for HD.
One of the cellular hallmarks of HD is the accumulation of the mutant protein Huntingtin which eventually leads to cell death in the brain. Normally, excess protein accumulation can be removed by a cellular process called autophagy in which cells digest their own components along with any proteins that are tagged for degradation. Abnormal autophagy is also seen in other neurodegenerative disorders.
Using cells collected from HD patients and mouse models of HD, Ana Maria Cuervo and colleagues show that the cellular ‘vehicles’ which deliver proteins to the degradation machinery, fail to recognize their cargoes. Because mutant Huntingtin is not cleared away properly, the scientists attribute this cellular defect to an increase of protein aggregates that is characteristic of HD cells.
Author contact:
Ana Maria Cuervo (Albert Einstein College of Medicine, Bronx, NY, USA)
Tel: +1 718 430 2689; E-mail: [email protected]
[5] & [6] Genetics: Variants associated with kidney function
DOI: 10.1038/ng.568
DOI: 10.1038/ng.566
Genetic variants that influence kidney function are reported in two new studies published online this week in Nature Genetics.
Chronic kidney disease (CKD) is characterized by a gradual loss of kidney function over time and can lead to end-stage renal disease (ESRD), in which the kidneys can no longer function. An important clinical measurement of kidney function for patients diagnosed with, or at risk of, CKD is the glomerular filtration rate (GFR). Typically, the GFR is estimated from blood levels of creatinine, a waste product that is normally removed from the blood by the kidneys.
Caroline Fox and colleagues report on a genome-wide analysis of 67,093 individuals of European ancestry, followed by further analysis of 22,922 Europeans. The scientists identify 13 new genetic loci that influence renal function, as estimated by GFR and seven other genetic loci that affect creatinine production and secretion. John Chambers and colleagues analyzed the genomes of 23,182 Europeans, with further analysis of 16,427 individuals, and identified four loci that are associated with blood creatinine levels. All four loci reported by Chambers and colleagues are included in the 20 loci reported by Fox and colleagues.
Author contacts:
Caroline S Fox (The National Heart Lung and Blood Institute, Framingham, MA, USA) Author paper [5]
Tel: +1 508 935 3447; E-mail: [email protected]
John Chambers (Imperial College, London, UK) Author paper [6]
Tel: +44 7866 365776; E-mail: [email protected]
[7] Neuroscience: Anxious interactions
DOI: 10.1038/nn.2529
Cross-talk between two compounds—serotonin and corticotrophin-releasing factor—is important to control anxiety-like behaviour in mice reports a study published online this week in Nature Neuroscience.
Both corticotrophin-releasing factor (CRF) and serotonin signaling have been implicated in anxious behavior, but it was previously unknown how these two pathways may interact at a cellular level to regulate anxiety.
Stephen Ferguson and colleagues used molecular and biochemical techniques to show that the corticotrophin-releasing factor type 1 receptor (CRFR1) forms a complex with the type 2 serotonin receptor (5-HT2) in mouse neurons. The CRFR1 receptor “helps” the 5-HT2 receptors that have been recycled inside the neuron get back to the neuron’s surface. To demonstrate the behavioural relevance of this interaction, the authors injected CRF into the prefrontal cortex of mice, and followed this with an injection of a 5-HT2 receptor agonist. These mice showed an increase in anxiety-like behaviours. However, these compounds had no effect on the mice’s behavior when each compound was administered alone, suggesting that the specific interaction between the CRFR1 and 5-HT2 receptor led to the increase in anxiety-like behavior.
Author contact:
Stephen Ferguson (University of Western Ontario, London, Canada)
Tel: +1 519 931 5706; E-mail: [email protected]
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Items from other Nature journals to be published online at the same time and with the same embargo:
Nature (http://www.nature.com/nature)
[8] IkBf regulates TH17 development by cooperating with ROR nuclear receptors
DOI: 10.1038/nature08922
[9] Ku is a 59-dRP/AP lyase that excises nucleotide damage near broken ends
DOI: 10.1038/nature08926
[10] Tracking G-protein-coupled receptor activation using genetically encoded infrared probes
DOI: 10.1038/nature08948
NATURE CELL BIOLOGY (http://www.nature.com/naturecellbiology)
[11] Deciphering the transcription complex critical for RhoA gene expression and cancer metastasis
DOI: 10.1038/ncb2047
[12] GEMC1 is a TopBP1-interacting protein required for chromosomal DNA replication
DOI: 10.1038/ncb2050
[13] Shugoshin–PP2A counteracts casein-kinase-1-dependent cleavage of Rec8 by separase
DOI: 10.1038/ncb2052
NATURE CHEMICAL BIOLOGY (http://www.nature.com/nchembio)
[14] A vancomycin photoprobe identifies the His kinase VanSsc as a vancomycin receptor
DOI: 10.1038/nchembio.350
[15] The role of conformational entropy in molecular recognition by calmodulin
DOI: 10.1038/nchembio.347
[16] Small molecule kinase inhibitors provide insight into Mps1 cell cycle function
DOI: 10.1038/nchembio.345
NATURE CHEMISTRY (http://www.nature.com/nchem)
[17] Isolation of crystalline carbene-stabilized P2-radical cations and P2-dications
DOI: 10.1038/nchem.617
[18] Assembly of a metal–organic framework by sextuple intercatenation of discrete adamantane-like cages
DOI: 10.1038/nchem.618
NATURE GENETICS (http://www.nature.com/naturegenetics)
[19] Genome-wide association study on systemic sclerosis identifies CD247 as a novel susceptibility locus
DOI: 10.1038/ng.565
NATURE GEOSCIENCE (http://www.nature.com/ngeo)
[20] Crustal deformation of the eastern Tibetan plateau revealed by magnetotelluric imaging
DOI: 10.1038/ngeo830
NATURE IMMUNOLOGY (http://www.nature.com/natureimmunology)
[21] The zinc-finger protein MAZR is part of the transcription factor network that controls the CD4 versus CD8 lineage fate of double-positive thymocytes
DOI: 10.1038/ni.1860
[22] CD4+CD8+ immature thymocytes primed by c-Myb for selection into the iNKT lineage
DOI: 10.1038/ni.1865
NATURE MATERIALS (http://www.nature.com/naturematerials)
[23] Free-floating ultra-thin two-dimensional crystals from sequence-specific peptoid polymers
DOI: 10.1038/nmat2742
[24] The thermodynamic origin of hysteresis in insertion batteries
DOI: 10.1038/nmat2730
Nature MEDICINE (http://www.nature.com/naturemedicine)
[25] Multispectral scanning during endoscopy guides biopsy of dysplasia in Barrett's esophagus
DOI: 10.1038/nm.2138
NATURE METHODS (http://www.nature.com/nmeth)
[26] In situ detection and genotyping of individual mRNA molecules
DOI: 10.1038/nmeth.1448
[27] Streptavidin variant with slower biotin dissociation rate and increased mechanostability
DOI: 10.1038/nmeth.1450
[28] Using buoyant mass to measure the growth of single cells
DOI: 10.1038/nmeth.1452
NATURE NANOTECHNOLOGY (http://www.nature.com/nnano)
[29] Observation and control of blinking nitrogen-vacancy centres in discrete nanodiamonds
DOI: 10.1038/nnano.2010.56
[30] Biologically templated photocatalytic nanostructures for sustained light-driven water oxidation
DOI: 10.1038/nnano.2010.57
[31] Tuning payload delivery in tumour cylindroids using gold nanoparticles
DOI: 10.1038/nnano.2010.58
[32] Understanding amyloid aggregation by statistical analysis of atomic force microscopy images
DOI: 10.1038/nnano.2010.59
Nature NEUROSCIENCE (http://www.nature.com/natureneuroscience)
[33] PKMz maintains memories by regulating GluR2-dependent AMPA receptor trafficking
DOI: 10.1038/nn.2531
[34] Real-time visualization of complexin during single exocytic events
DOI: 10.1038/nn.2532
Nature PHYSICS (http://www.nature.com/naturephysics)
[35] Delocalization of a disordered bosonic system by repulsive interactions
DOI: 10.1038/nphys1635
[36] Direct observation of magnetic monopole defects in an artificial spin-ice system
DOI: 10.1038/nphys1628
[37] Why do particle clouds generate electric charges?
DOI: 10.1038/nphys1631
Nature STRUCTURAL & MOLECULAR BIOLOGY (http://www.nature.com/natstructmolbiol)
[38] Structural conversion of neurotoxic amyloid-beta1–42 oligomers to fibrils
DOI: 10.1038/nsmb.1799
[39] Opening of tandem calponin homology domains regulates their affinity for F-actin
DOI: 10.1038/nsmb.1789
[40] Structures of influenza A proteins and insights into antiviral drug targets
DOI: 10.1038/nsmb.1779
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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.
AUSTRALIA
Brisbane: 29
Clayton: 2, 29
Fitzroy: 2
Parkville: 2
Sydney: 29
AUSTRIA
Graz: 5
Innsbruck: 5
Salzburg: 5
Vienna: 19, 21, 39
BELGIUM
Antwerp: 19
Brussels: 6
Ghent: 19
Leuven: 19
BRAZIL
Fortaleza: 37
CANADA:
Edmonton: 20
Hamilton: 5, 14
London: 4, 6
Montreal: 33
Ottawa: 4, 28
Toronto: 28
Vancouver: 33
CHINA
Beijing: 5, 20
Dalian: 20
Fuzhou: 18
Guangzhou: 11
Kunming: 20
CROATIA
Split: 5
Zagreb: 5
FINLAND
Helsinki: 6
Oulu: 6
FRANCE
Montpellier: 4
GERMANY
Aachen: 6
Berlin: 19, 24
Bochum: 19
Cologne: 19
Freiburg: 5, 10
Greifswald: 5
Hannover: 19
Homburg: 34
Kiel: 5
Leipzig: 5
Lubeck: 5
Mainz: 5
Mannheim: 5
Marburg: 17
Munich: 5
Neuherberg: 5
Regensburg: 5
Ulm: 5
ICELAND
Kopavogur: 5
Reykjavik: 5
ITALY
Bolzano: 5
Brescia: 19
Cagliari: 6
Milan: 19
Rome: 35
Sesto Fiorentino: 35
JAPAN
Fukuoka: 3, 11
Obu: 21
Osaka: 8, 38
Sendai: 8
Shiga: 2
Tokyo: 8, 13
Yokohama: 21
NETHERLANDS
Amsterdam: 6
Groningen: 6
Hattem: 6
Leiden: 5, 6
Nijmegen: 19
Rotterdam: 5
Utrecht: 16, 19
Zwolle: 6
SERBIA
Belgrade: 6
SLOVENIA
Ljubljana: 24, 39
SPAIN
Barcelona: 7, 19
Cayalunya: 10
Granada: 19
Madrid: 19
Santander: 19
Sevilla: 19
SWEDEN
Lund: 19
Malmo: 6
Stockholm: 6, 19
Uppsala: 5, 26
SWITZERLAND
Basel: 5
Fribourg: 32
Geneva: 5
Lausanne: 6, 32
Villigen: 10
Zurich: 32, 37
TAIWAN
Kaohsiung: 11
Taichung: 11
Tainan: 11
UNITED KINGDOM
Bristol: 6
Carshalton: 6
Cambridge: 5, 6, 10, 14
Edinburgh: 5
Glasgow: 6, 19
Hertfordshire: 12
Hinxton: 6
Leicester: 6
London: 5, 36
Manchester: 19
Middlesex: 6
Newcastle: 19
Norwich: 14
Oxford: 5, 6, 16, 27
Southampton: 6
UNITED STATES OF AMERICA
California
Berkeley: 23
Los Angeles: 5, 19
Riverside: 17
San Diego: 16
San Francisco: 5
Connecticut
New Haven: 3, 34, 38
Florida
Miami: 5, 27
Illinois
Chicago: 19
Kansas
Pittsburgh: 5
Louisiana
New Orleans: 18
Maryland
Baltimore: 5, 6, 19
Bethesda: 5
Massachusetts
Amherst: 31
Bedford: 25
Boston: 1, 5, 11, 16, 25, 28
Cambridge: 28, 30
Framingham: 5
Michigan
Ann Arbor: 5, 6
Minnesota
Rochester: 5
Missouri
St Louis: 5
New Jersey
East Hanover: 7
Piscataway: 37, 40
New York
Bronx: 7
Brooklyn: 33
Manhasset: 19
New York: 7, 10
Stony Brook: 38
North Carolina
Chapel Hill: 4, 9
Research Triangle Park: 8
Winston-Salem: 5
Oklahoma
Oklahoma City: 22
Pennsylvania
King of Prussia: 6
Philadelphia: 15
Texas
Austin: 40
Houston: 5, 11, 19
San Antonio: 9
Virginia
Charlottesville: 22, 39
Washington
Seattle: 5, 19
PRESS CONTACTS…
For media inquiries relating to embargo policy for all the Nature Research Journals:
Rachel Twinn (Nature London)
Tel: +44 20 7843 4658; E-mail: [email protected]
Neda Afsarmanesh (Nature New York)
Tel: +1 212 726 9231; E-mail: [email protected]
Ruth Francis (Head of Press, 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)
Sowmya Swaminathan
Tel: +44 20 7843 4656; E-mail: [email protected]
Nature Chemical Biology (Boston)
Sarah Daniels
Tel: +1 617 475 9241, E-mail: [email protected]
Nature Chemistry (London)
Stuart Cantrill
Tel: +44 20 7014 4018; E-mail: [email protected]
Nature Genetics (New York)
Myles Axton
Tel: +1 212 726 9324; E-mail: [email protected]
Nature Geoscience (London)
Heike Langenberg
Tel: +44 20 7843 4042; E-mail: [email protected]
Nature Immunology (New York)
Laurie Dempsey
Tel: +1 212 726 9372; E-mail: [email protected]
Nature Materials (London)
Vincent Dusastre
Tel: +44 20 7843 4531; E-mail: [email protected]
Nature Medicine (New York)
Juan Carlos Lopez
Tel: +1 212 726 9325; E-mail: [email protected]
Nature Methods (New York)
Hugh Ash
Tel: +1 212 726 9627; E-mail: [email protected]
Nature Nanotechnology (London)
Peter Rodgers
Tel: +44 20 7014 4019; Email: [email protected]
Nature Neuroscience (New York)
Kalyani Narasimhan
Tel: +1 212 726 9319; E-mail: [email protected]
Nature Photonics (Tokyo)
Oliver Graydon
Tel: +81 3 3267 8776; E-mail: [email protected]
Nature Physics (London)
Alison Wright
Tel: +44 20 7843 4555; E-mail: [email protected]
Nature Structural & Molecular Biology (New York)
Sabbi Lall
Tel: +1 212 726 9326; E-mail: [email protected]
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