News tips from the Journal of Biological Chemistry

April 10, 2007

The following article was featured as a "Paper of the Week" by the Journal of Biological Chemistry's Editors, meaning that it belongs to the top one percent of papers reviewed in a year in significance and overall importance.

New Insight into Viral Infection

Researchers provide new details on how a key protein used to fight viruses works, raising new hopes to improve treatments against viral infection.

When a virus infects the cells of an organism, the immune system generates proteins called interferons that prevent the virus from replicating in nearby cells. Prompted by the interferons, the nearby cells produce proteins called RNA-dependent protein kinases (PKR) that bind to viral RNA and inhibit it.

Joseph D. Puglisi and colleagues provide new insight into how PKR may be activated.

They show the molecular details of the various regions of the protein, and how their functions change upon sensing RNAs.

Article: "Molecular Framework for the Activation of RNA-Dependent Protein Kinase" by Sean A. McKenna, Darrin A. Lindhout, Insil Kim, Corey W. Liu, Vladimir M. Gelev, Gerhard Wagner, and Joseph D. Puglisi

MEDIA CONTACT: Joseph D. Puglisi, Department of Structural Biology and Stanford
Magnetic Resonance Laboratory, Stanford University School of Medicine, Stanford, CA; tel: 650-498-4397; e-mail: puglisi@stanford.edu


Cardiac Stem Cells Not Affected by Acute Heart Failure

Acute heart failure does not affect heart stem cells, making them available to contribute to cardiac recovery following an acute episode of cardiac dysfunction, according to researchers.

Heart failure, a disease in which the heart's ventricles cannot fill with or eject blood, is the leading cause of death in the United States. One of the promising ways to treat patients with the disease is by using their own heart's stem cells, but it hasn't been established whether the stem cells themselves were also damaged by acute manifestations of this disease.

Bernardo Nadal-Ginard and colleagues show that by injecting a single excessive dose of Isoproterenol -- a chemical that induces acute diffuse heart damage -- in rats, heart muscle cells are progressively damaged but the heart's stem cells are left unaffected. These results suggest that the stem cells may help heal the heart after an acute episode and could also be used to treat patients with chronic heart failure.

Article: "Acute Beta-adrenergic Overload Produces Myocyte Damage through Calcium Leakage from the Ryanodine Receptor 2 (RyR2) but Spares Cardiac Stem Cells" by Georgina M. Ellison, Daniele Torella, Ioannis Karakikes, Saranya Purushothaman, Antonio Curcio, Cosimo Gasparri, Ciro Indolfi, N. Tim Cable, David F. Goldspink, and Bernardo Nadal-Ginard.

MEDIA CONTACT: Bernardo Nadal-Ginard, The Zena and Michael A. Wiener Cardiovascular Institute and Marie-Jose and Henry R. Kravis Center for Cardiovascular Health, Mount Sinai School of Medicine, New York, New York; tel: 212-241-6543; e-mail: bernardo.nadalginard@mssm.edu


New Chemical Effective against Parkinson's Disease

Researchers report that a chemical called thioredoxin helps prevent loss of neurons in a fruit fly model of Parkinson's disease and improve their locomotor activity.

Parkinson's disease is a neurodegenerative disorder in which neurons that produce the chemical dopamine die, resulting in loss of motor control in affected people. Although the disease cannot yet be cured, affected individuals can take drugs that stimulate the release of more dopamine in the brain or they can undergo surgery.

Toshiro Aigaki and colleagues showed that a chemical called thioredoxin, which has not yet been used to treat Parkinson's disease, suppresses the toxicity of a protein called Pael-R in fruit flies, resulting in an increase of dopaminergic neurons and improved locomotor activity.

Article: "Thioredoxin Suppresses Pael-R-Induced Neurotoxicity and Extends Longevity in Drosophila" by Yumi Umeda-Kameyama, Manabu Tsuda, Chiaki Ohkura, Takashi Matsuo, Yoshio Namba, Yasuyoshi Ohuchi, and Toshiro Aigaki

MEDIA CONTACT: Toshiro Aigaki, Department of Biological Sciences, Tokyo Metropolitan University, Japan; tel: +81-426-77-2560; e-mail: aigaki-toshiro@c.metro-u.ac.jp


Mechanisms of Mitochondrial Fission Revealed

Researchers report new details about how mitochondria divide during cell division, providing new insight into a phenomenon still not well documented.

When a cell divides, some of its constituents are distributed between the two daughter cells while others divide into two parts, which are distributed between the two cells. Mitochondria, discrete structure that generate energy within a cell, frequently divide and fuse with each other. During cell division, mitochondria divide as well, but how this happens is not well understood.

Katsuyoshi Mihara and colleagues showed that when mammalian cells divide, the mitochondria break apart and then segregate randomly between the two daughter cells. The scientists also determined that a protein called Dynamin-related protein 1 (Drp1) -- known to divide and fuse other cellular structures -- was key to mitochondrial fragmentation.

Article: "Mitotic Phosphorylation of Dynamin-Related GTPase Drp1 Participates in Mitochondrial Fission" by Naoko Taguchi, Naotada Ishihara, Akihiro Jofuku, Toshihiko Oka, and Katsuyoshi Mihara

MEDIA CONTACT: Katsuyoshi Mihara, Department of Molecular Biology, Graduate School of Medical Science, Kyushu University, Fukuoka, Japan; tel: +81-92-642-4709; e-mail: mihara@cell.med.kyushu-u.ac.jp
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