Kim, G M <br/><br/>
Tumor necrosis factor receptor deletion reduces nuclear factor-kappaB activation, cellular inhibitor of apoptosis protein 2 expression, and functional recovery after traumatic spinal cord injury.  [electronic resource] 

 -  The Journal of neuroscience : the official journal of the Society for Neuroscience  Sep 2001 
 - 6617-25 p.  digital 
<br/><br/> Publication Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S. 
<br/><br/><label>ISSN: </label>1529-2401 
<br/><br/><label>Subjects--Topical Terms: </label><br/>Animals<br/>Antigens, CD--genetics<br/>Apoptosis<br/>Axons--pathology<br/>Baculoviral IAP Repeat-Containing 3 Protein<br/>Caspase 3<br/>Caspases--metabolism<br/>Female<br/>In Situ Nick-End Labeling<br/>Inhibitor of Apoptosis Proteins<br/>Magnetic Resonance Imaging<br/>Mice<br/>Mice, Inbred C57BL<br/>Mice, Knockout<br/>Mice, Transgenic<br/>Motor Activity<br/>Myelin Sheath--metabolism<br/>NF-kappa B--metabolism<br/>Proteins--metabolism<br/>Receptors, Tumor Necrosis Factor--deficiency<br/>Receptors, Tumor Necrosis Factor, Type I<br/>Receptors, Tumor Necrosis Factor, Type II<br/>Recovery of Function<br/>Signal Transduction--physiology<br/>Spinal Cord--metabolism<br/>Spinal Cord Injuries--genetics<br/>Ubiquitin-Protein Ligases<br/>Wounds, Nonpenetrating