Connection

WILLIAM MITCH to Ubiquitin

This is a "connection" page, showing publications WILLIAM MITCH has written about Ubiquitin.
Connection Strength

2.890
  1. Inhibition of Stat3 activation suppresses caspase-3 and the ubiquitin-proteasome system, leading to preservation of muscle mass in cancer cachexia. J Biol Chem. 2015 Apr 24; 290(17):11177-87.
    View in: PubMed
    Score: 0.421
  2. Mechanisms stimulating muscle wasting in chronic kidney disease: the roles of the ubiquitin-proteasome system and myostatin. Clin Exp Nephrol. 2013 Apr; 17(2):174-82.
    View in: PubMed
    Score: 0.362
  3. Proteolysis by the ubiquitin-proteasome system and kidney disease. J Am Soc Nephrol. 2011 May; 22(5):821-4.
    View in: PubMed
    Score: 0.320
  4. Ubiquitin, proteasomes and proteolytic mechanisms activated by kidney disease. Biochim Biophys Acta. 2008 Dec; 1782(12):795-9.
    View in: PubMed
    Score: 0.266
  5. Muscle wasting in chronic kidney disease: the role of the ubiquitin proteasome system and its clinical impact. Pediatr Nephrol. 2008 Apr; 23(4):527-35.
    View in: PubMed
    Score: 0.253
  6. Insulin resistance accelerates muscle protein degradation: Activation of the ubiquitin-proteasome pathway by defects in muscle cell signaling. Endocrinology. 2006 Sep; 147(9):4160-8.
    View in: PubMed
    Score: 0.230
  7. Protein degradation by the ubiquitin-proteasome pathway in normal and disease states. J Am Soc Nephrol. 2006 Jul; 17(7):1807-19.
    View in: PubMed
    Score: 0.229
  8. Regulation of muscle protein degradation: coordinated control of apoptotic and ubiquitin-proteasome systems by phosphatidylinositol 3 kinase. J Am Soc Nephrol. 2004 Jun; 15(6):1537-45.
    View in: PubMed
    Score: 0.199
  9. Review of muscle wasting associated with chronic kidney disease. Am J Clin Nutr. 2010 Apr; 91(4):1128S-1132S.
    View in: PubMed
    Score: 0.074
  10. Malnutrition is an unusual cause of decreased muscle mass in chronic kidney disease. J Ren Nutr. 2007 Jan; 17(1):66-9.
    View in: PubMed
    Score: 0.060
  11. Tissue-specific regulation of ubiquitin (UbC) transcription by glucocorticoids: in vivo and in vitro analyses. Am J Physiol Renal Physiol. 2007 Feb; 292(2):F660-6.
    View in: PubMed
    Score: 0.058
  12. Proteolytic mechanisms, not malnutrition, cause loss of muscle mass in kidney failure. J Ren Nutr. 2006 Jul; 16(3):208-11.
    View in: PubMed
    Score: 0.058
  13. Cellular signals activating muscle proteolysis in chronic kidney disease: a two-stage process. Int J Biochem Cell Biol. 2005 Oct; 37(10):2147-55.
    View in: PubMed
    Score: 0.055
  14. Strategies for suppressing muscle atrophy in chronic kidney disease: mechanisms activating distinct proteolytic systems. J Ren Nutr. 2005 Jan; 15(1):23-7.
    View in: PubMed
    Score: 0.052
  15. Cellular mechanisms causing loss of muscle mass in kidney disease. Semin Nephrol. 2004 Sep; 24(5):484-7.
    View in: PubMed
    Score: 0.051
  16. Activation of caspase-3 is an initial step triggering accelerated muscle proteolysis in catabolic conditions. J Clin Invest. 2004 Jan; 113(1):115-23.
    View in: PubMed
    Score: 0.048
  17. Mechanisms activating proteolysis to cause muscle atrophy in catabolic conditions. J Ren Nutr. 2003 Apr; 13(2):149-52.
    View in: PubMed
    Score: 0.046
  18. Nutrition in CAPD: serum bicarbonate and the ubiquitin-proteasome system in muscle. Kidney Int. 2002 Apr; 61(4):1286-92.
    View in: PubMed
    Score: 0.043
  19. Ubiquitin (UbC) expression in muscle cells is increased by glucocorticoids through a mechanism involving Sp1 and MEK1. J Biol Chem. 2002 May 10; 277(19):16673-81.
    View in: PubMed
    Score: 0.043
  20. Myostatin/activin pathway antagonism: molecular basis and therapeutic potential. Int J Biochem Cell Biol. 2013 Oct; 45(10):2333-47.
    View in: PubMed
    Score: 0.023
Connection Strength

The connection strength for concepts is the sum of the scores for each matching publication.

Publication scores are based on many factors, including how long ago they were written and whether the person is a first or senior author.