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JCI early table of contents for Nov. 8, 2013
Date:11/8/2013

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

AUTHOR CONTACT: Anna Greka
Massachusetts General Hospital, Charlestown, MA, USA
Phone: (617) 726-9363; Fax: (617) 726-5669; E-mail: greka.anna@mgh.harvard.edu

View this article at: http://www.jci.org/articles/view/71165?key=e26e1234395ef52d73c5


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

AUTHOR CONTACT: MinGyu Lee
MD Anderson Cancer Center, Houston, TX, USA
Phone: 713-792-3678; E-mail: mglee@mdanderson.org

View this article at: http://www.jci.org/articles/view/68642?key=c85b37ed02f837ee5ede


ALSO IN THIS ISSUE

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

AUTHOR CONTACT: Lin Mei
Institute of Molecular Medicine and Genetics, Augusta, , USA
Phone: 7065138002; E-mail: lmei@georgiahealth.edu

View this article at: http://www.jci.org/articles/view/66039?key=c1820c1751a31705f85c

TITLE: Inhibition of Coxsackievirus-associated dystrophin cleavage prevents cardiomyopathy

AUTHOR CONTACT: Kirk Knowlton
UCSD, La Jolla, CA, USA
Phone: 858-822-1364; Fax: 858-822-3027; E-mail: kknowlton@ucsd.edu

View this article at: http://www.jci.org/articles/view/66271?key=088944a6b78b042482eb

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

AUTHOR CONTACT: Martin McMahon
U.C. San Francisco, San Francisco, CA, USA
Phone: 415 502 5829; Fax: 415 502 3179; E-mail: mcmahon@cc.ucsf.edu

View this article at: http://www.jci.org/articles/view/69619?key=c234e15768a4df8180ba

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: amc2056@med.cornell.edu

View this article at: http://www.jci.org/articles/view/69636?key=864ee0280dbf58dbfbb8

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

AUTHOR CONTACT: Erwin F. Wagner
Spanish National Cancer Research Centre (CNIO), Madrid, UNK, ESP
Phone: +34912246913; E-mail: ewagner@cnio.es

View this article at: http://www.jci.org/articles/view/70405?key=836a51da9c7c85166739

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: stefano.casola@ifom.eu

View this article at: http://www.jci.org/articles/view/70626?key=70ad9bd4b95f662511c0


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Contact: Corinne Williams
press_releases@the-jci.org
Journal of Clinical Investigation
Source:Eurekalert

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