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JCI online early table of contents: May 17, 2010
Date:5/10/2010

Keeping blood cells in check with the protein Lnk

Genetic mutations that lead to aberrant activation of the signaling protein JAK2 have been linked to several myeloproliferative diseases, a group of diseases of the bone marrow that includes chronic myeloid leukemia. Wei Tong and colleagues, at the University of Pennsylvania School of Medicine, Philadelphia, have now generated several lines of evidence in mice indicating that the protein Lnk acts as a suppressor of the development of JAK2-induced myeloproliferative diseases. For example, loss of Lnk accelerated and exacerbated JAK2-induced myeloproliferative diseases in mice. Furthermore, as old mice lacking Lnk spontaneously developed a myeloproliferative disease resembling chronic myeloid leukemia, the authors suggest that Lnk dysfunction might contribute to the development of cancers of the blood and bone marrow in humans.

TITLE: Lnk constrains myeloproliferative diseases in mice

AUTHOR CONTACT:
Wei Tong
University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA.
Phone: 267.426.0930; Fax: 267.426.5476; E-mail: tongw@email.chop.edu.

View this article at: http://www.jci.org/articles/view/42032?key=344a892df66bb135b5fd


NEUROBIOLOGY: Cellular help to activate thyroid hormone in the brain

Hypothyroidism is a medical condition caused by insufficient production of thyroid hormone. Although iodine deficiency is the most common cause of hypothyroidism, it can be inherited. In neonates, this form of hypothyroidism is accompanied by severe neurological consequences, indicating a role for thyroid hormone in the brain. However, little is known about the mechanisms regulating thyroid hormone action in the brain.

A team of researchers, led by Antonio Bianoc, at the University of Miami Mi
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Contact: Karen Honey
press_releases@the-jci.org
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Journal of Clinical Investigation
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