JCI table of contents, November 15 2004

racting fibers in Nfkb1- and Bcl3-deficient mice appeared to be resistant to atrophy. The results demonstrate that muscular inactivity triggers the activation of P50 and Bcl3, which in turn may activate genes necessary for the development of atrophy.

TITLE: Disruption of either the Nfkb1 or Bcl3 gene inhibits skeletal muscle atrophy.

AUTHOR CONTACT: Susan C. Kandarian
Department of Health Sciences, Boston University, Boston, Massachusetts, USA.
Phone: 617-353-5169; Fax: 617-353-7567; E-mail: skandar@bu.edu.

View the PDF of this article at: https://www.the-jci.org/press/21696.pdf


New structure described for kidney filter: the slit diaphragm

One of the main functions of the kidney is the formation of urine by filtration of the plasma. The size-selective kidney filter, known as the slit diaphragm (SD), prevents plasma proteins from leaking into the urine. This filtration barrier consists of layers of specialized cells, including podocytes, which are connected by the interdigitating zipper-like structure of the SD, and defects in the SD are associated with a number of kidney diseases. In 1974, the zipper-like SD structure was first described, however this model was later questioned and the molecular nature of the SD has since remained obscure.

In the November 15 issue of the Journal of Clinical Investigation, Karl Tryggvason and colleagues from the Karolinska Institute used electron tomography to obtain detailed images of the SD that were previously impossible to obtain. They found that some elements of the proposed zipper-like structure hold true but the pores of this filtration structure appear to be more irregularly shaped that previously proposed. The authors also demonstrated a crucial role for the protein

Contact: Brooke Grindlinger
Journal of Clinical Investigation

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