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JCI early table of contents for Nov. 8, 2013

Ion channel inhibition limits injury-induced loss of kidney filtration

The kidney is responsible for retaining essential proteins and removing waste products from the blood stream. Injury to the kidney results in loss of kidney filter function, which if not treated promptly, can induce kidney failure. In this issue of the Journal of Clinical Investigation, Anna Greka and colleagues at Massachusetts General Hospital determined that mice lacking the ion channel TRPC5 were protected from losing kidney filter function following kidney injury. In the absence of TRPC5, kidney podocytes did not undergo any cytoskeletal remodeling, which kept the filtration barrier in tact. Furthermore, the authors demonstrated that pharmacological inhibition of TRPC5 protects animals from protein loss in the urine following kidney injury. This study indicates that activation of ion channel TRPC5 following kidney injury promotes loss of kidney filter function, and inhibition of this ion channel may have therapeutic potential.

TITLE: Inhibition of the TRPC5 ion channel protects the kidney filter

Massachusetts General Hospital, Charlestown, MA, USA
Phone: (617) 726-9363; Fax: (617) 726-5669; E-mail:

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Researchers identify a histone demethylase associated with non-small cell lung cancer

Non-small cell lung cancer (NSCLC) is one of the leading causes of cancer deaths worldwide. Current therapies that target cellular kinases have been effective for some patients: however, many individuals with NSCLS do not respond. Recent studies of other cancers indicate that the global changes in DNA methylation patterns may drive tumor formation. In this issue of the Journal of Clinical Investigation, MinGyu Lee and colleagues at MD Anderson Cancer Center evaluated histone methylation modifications in NSCLS cell lines and determined that the histone demethylase KDM2A was upregulated in NSCLC cell lines. Furthermore, induced KDM2A expression increased cell proliferation and invasiveness through activation of the ERK1/2 signaling pathway. Evaluation of tumors from NSCLS patients uncovered a correlation between increased levels of KDM2A and poor prognosis. This study suggests that therapies targeting KDM2A may benefit a subset of NSCLS patients.

TITLE: KDM2A promotes lung tumorigenesis by epigenetically enhancing ERK1/2 signaling

MD Anderson Cancer Center, Houston, TX, USA
Phone: 713-792-3678; E-mail:

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TITLE: Antibodies against low-density lipoprotein receptorrelated protein 4 induce myasthenia gravis

Institute of Molecular Medicine and Genetics, Augusta, , USA
Phone: 7065138002; E-mail:

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TITLE: Inhibition of Coxsackievirus-associated dystrophin cleavage prevents cardiomyopathy

UCSD, La Jolla, CA, USA
Phone: 858-822-1364; Fax: 858-822-3027; E-mail:

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TITLE: Differential AKT dependency displayed by mouse models of BRAFV600E-initiated melanoma

U.C. San Francisco, San Francisco, CA, USA
Phone: 415 502 5829; Fax: 415 502 3179; E-mail:

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TITLE: Histone deacetylase 6mediated selective autophagy regulates COPD-associated cilia dysfunction

AUTHOR CONTACT: Augustine M. K. Choi
New York Presbyterian/Weill Cornell Medical Center, New York, NY, USA
Phone: 212-746-4720; Fax: 212-746-8793; E-mail:

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TITLE: JUNB/AP-1 controls IFN-γ during inflammatory liver disease

Spanish National Cancer Research Centre (CNIO), Madrid, UNK, ESP
Phone: +34912246913; E-mail:

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TITLE: Germinal center dysregulation by histone methyltransferase EZH2 promotes lymphomagenesis

AUTHOR CONTACT: Stefano Casola
IFOM, FIRC Institute for Molecular Oncology Foundation, Milano, UNK, ITA
Phone: 003902574303714; E-mail:

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Contact: Corinne Williams
Journal of Clinical Investigation

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