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JCI early table of contents for April 1, 2013

Promoting muscle regeneration in a mouse model of muscular dystrophy

Duchenne muscular dystrophy (DMD) is a degenerative skeletal muscle disease caused by mutations in the protein dystrophin. Dystrophin functions to protect muscle cells from injury and loss of functional dystrophin results in break down and loss of muscle cells. A cellular signal relay system, known as a MAP kinase cascade, regulates the function of muscle stem cells, serving as a source of the new cells that are required for muscle regeneration. In this issue of the Journal of Clinical Investigation, researchers led by Anton Bennett at Yale University identified the protein MKP-5 as a negative regulator of MAP kinase cascades in muscle stem cells. Loss of MKP-5 in a mouse model of DMD enhanced the development of new muscle cells (myogenesis) and helped prevent muscle degeneration. These results identify MKP-5 as an important suppressor of myogenesis and suggest that therapeutics that inhibit MKP-5 could be useful in the treatment of degenerative muscle diseases.

Improved regenerative myogenesis and muscular dystrophy in mice lacking MKP-5

Anton Bennett
Yale University School of Medicine, New Haven, CT, USA
Phone: 203-737-2441; Fax: 203-737-2738; E-mail:

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Alternative fuel for your brain

Tight control of blood glucose levels is critical to mitigating the long-term complications of diabetes; however, the intensive insulin therapy required for this control is frequently accompanied by recurrent episodes of low blood sugar (hypoglycemia). Hypoglycemic episodes have been implicated in brain damage and cognitive impairment. Though the brain depends predominantly on glucose as an energy source, it can also use alternative fuels, such as lactate, to satisfy its energy requirements. In this issue of the Journal of Clinical Investigation, Raimund Herzog and colleagues at Yale University used magnetic resonance spectroscopy (MRS) to measure the concentrations and enrichment of different energy substrates and their metabolites in a rat model of recurrent hypoglycemia. They found that recurrent hypoglycemia enhances neuronal uptake of lactate which allows the brain to retain normal neural activity during hypoglycemia. These observations suggest that lactate supports neuronal function and indicate that supplementation of alternative fuels could protect the brain during hypoglycemia.

Lactate preserves neuronal metabolism and function following antecedent recurrent hypoglycemia

Raimund I. Herzog
Yale School of Medicine, New Haven, CT, USA
Phone: 203-737-4773; E-mail:

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MicroRNA-26 governs profibrillatory inward-rectifier potassium current changes in atrial fibrillation

Stanley Nattel
Montreal Heart Institute, Montreal, PQ, CAN
Phone: (514) 376-3330 ext. 3990; Fax: (514) 376-1355; E-mail:

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Melanoma adapts to RAF/MEK inhibitors through FOXD3-mediated upregulation of ERBB3

Andrew Aplin
Thomas Jefferson University, Philadelphia, PA, USA
Phone: 215 503 7296; E-mail: Andrew.Aplin@KimmelCancerCenter.Org

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SLITRK6 mutations cause myopia and deafness in humans and mice

Mustafa Tekin
University of Miami, Miami, FL, USA
Phone: 305-243-2381; Fax: 305-243-2703; E-mail:

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Co-operativity of imprinted genes inactivated by acquired chromosome 20q deletions

Anthony Green
University of Cambridge, Cambridge, , GBR
Phone: +44-1223-336829; E-mail:

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The phosphatase CD148 promotes airway hyperresponsiveness through SRC family kinases

Arthur Weiss
Dept. Of Medicine, San Francisco, CA, USA
Phone: 415/476-8983; Fax: 415-502-5081; E-mail:

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Discovering naturally processed antigenic determinants that confer protective T-cell immunity

Sebastian Joyce
Vanderbilt Univ. School of Medicine, Nashville, TN, USA
Phone: 615-322-1472; E-mail:

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Contact: Jillian Hurst
Journal of Clinical Investigation

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