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JCI online early table of contents: Jan. 10 2008
Date:1/10/2008

tment alone, was shown to increase expression of the AE2 alternative isoforms AE2b1 and AE2b2 and this was associated with enhanced AE2 activity in the liver. Further analysis revealed that the combination treatment led to upregulation of AE2b1 and AE2b2 expression by promoting HNF1, glucocorticoid receptor, and p300 binding to the AE2 alternate promoter, from which AE2b1 and AE2b2 are expressed.

TITLE: Combination of ursodeoxycholic acid and glucocorticoids upregulates the AE2 alternate promoter in human liver cells

AUTHOR CONTACT:
Juan F. Medina
University of Navarra School of Medicine, Pamplona, Spain.
Phone: 34-948-194700, Ext. 4001; Fax: 34-948-194717; E-mail: jfmedina@unav.es.

View the PDF of this article at: https://www.the-jci.org/article.php?id=33156


HEMATOLOGY: PIP5KI-gamma ensures the cytoskeleton makes a firm attachment to the cell membrane

Many features of a cell, including its ability to move, rely on the normal functioning of the cytoskeleton that is attached to the membrane of the cell. The molecule PIP2 has an important role in regulating the function of the cytoskeleton. There are 3 forms of the protein PIP5KI, which synthesizes PIP2, and many cell types express more than one form of PIP5KI, leading to the suggestion that different forms of PIP5KI have different functions. Support for this hypothesis has now been provided by Charles Abrams and colleagues at the University of Pennsylvania, Philadelphia, who have shown that PIP5KI-gamma has a unique role in anchoring the cell membrane to the cytoskeleton of mouse megakaryocytes. Indeed, in the study, mouse megakaryocytes lacking PIP5KI-gamma were shown to exhibit defects in cytoskeleton attachment to the cell membrane and this defect could be reversed by PIP5KI-gamma but not PIP5K-beta.

TITLE: Loss of PIP5KI-gamma, unlike ot
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Contact: Karen Honey
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Journal of Clinical Investigation
Source:Eurekalert

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