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We chose the SC and liver because they are severely or scarcely affected, respectively, by Cbl deficiency in terms of histological damage. We found permanently increased NF\u2010\u03baB levels (particularly the p50 and p65 subunits) in the SCs and livers of both types of Cbl\u2010D rats, and Western blot analysis demonstrated increased p65 levels. NF\u2010\u03baB and p65 protein levels normalized when the totally gastrectomized (TGX) rats were treated with Cbl replacement. As we have previously demonstrated that Cbl deficiency increases tumor necrosis factor (TNF)\u2013\u03b1 and nerve growth factor (NGF) levels in the SC (each of which is a known NF\u2010\u03baB activator), we redetermined NF\u2010\u03baB levels in the SCs and livers of TGX rats treated with anti\u2010TNF\u2010\u03b1 or anti\u2010NGF antibodies and found that NF\u2010\u03baB levels normalized in both tissues after either treatment. These results demonstrate that: (1) Cbl physiologically and indirectly down\u2010regulates NF\u2010\u03baB levels in rat SC and liver, and (2) NF\u2010\u03baB is an important signaling molecule after Cbl deficiency injury. \u00a9 2008 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jnr.21599","type":"journal-article","created":{"date-parts":[[2008,1,8]],"date-time":"2008-01-08T23:16:50Z","timestamp":1199834210000},"page":"1380-1387","source":"Crossref","is-referenced-by-count":36,"title":["Indirect down\u2010regulation of nuclear NF\u2010\u03baB levels by cobalamin in the spinal cord and liver of the 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