Disease relevance of Trim63

• MuSK antibody positive myasthenia gravis plasma modifies MURF-1 expression in C2C12 cultures and mouse muscle in vivo [1].
• MuSK-MG plasma and purified IgG from a patient with marked muscle atrophy modestly increased MURF-1 expression in C2C12 cells in culture, and MURF-1 expression in mouse masseter (facial) muscle, but not in gastrocnemius (leg) [1].
• Muscle ring finger protein-1 inhibits PKC{epsilon} activation and prevents cardiomyocyte hypertrophy [2].
• Additionally, peritonitis produced by cecal ligation and puncture increased atrogin-1 and MuRF1 mRNA in gastrocnemius (but not soleus or heart) by 8 h, which was sustained for 72 and 24 h, respectively [3].

High impact information on Trim63

• Thus, violation of the conserved preference for tyrosine and glycine in D(H) RF1 alters CDR-H3 content and impairs B cell development and antibody production [4].
• Coincident with this agonist-stimulated interaction, MURF1 blocks PKCepsilon translocation to focal adhesions, which is a critical event in the hypertrophic signaling cascade [2].
• MURF1 inhibits phenylephrine-induced (but not IGF-1-induced) increases in cell size [2].
• We define a novel anti-hypertrophic signaling pathway regulated by muscle ring finger protein-1 (MURF1) that inhibits the agonist-stimulated PKC-mediated signaling response in neonatal rat ventricular myocytes [2].
• Similarly, whereas dexamethasone increased atrogene expression, pretreatment with the glucocorticoid receptor antagonist RU-486 failed to ameliorate the sepsis-induced increase in atrogin-1 and MuRF1 [3].

Biological context of Trim63

• We found that the loss of titin's kinase domain and binding sites for myomesin and MURF-1 causes structural changes in the sarcomere that proceed from the M-line to the Z-disc and ultimately result in disassembly of the sarcomere [5].

Anatomical context of Trim63

• Hormone, cytokine, and nutritional regulation of sepsis-induced increases in atrogin-1 and MuRF1 in skeletal muscle [3].
• RAW264.7 cells and J774 cells of murine macrophage cell lines were cultured with chrysotile B (CH) asbestos, crocidolite (CR) asbestos, or MMMFs comprised of glass wool (GW), rock wool (RW), or ceramic (RF1) [6].

Associations of Trim63 with chemical compounds

• Dex had a more marked effect on MURF-1 expression in C2C12 cells, but did not affect MURF-1 expression in either muscle [1].
• Thus, under in vivo conditions in mature adult rats, the sepsis-induced increase in muscle atrogin-1 and MuRF1 mRNA appears both glucocorticoid and TNF independent and is unresponsive to leucine [3].
• To assess the role of D(H) RF1-encoded tyrosine and glycine in regulating CDR-H3 content and potentially influencing B cell function, we created mice limited to a single D(H) encoding asparagine, histidine, and arginines in RF1 [4].

Analytical, diagnostic and therapeutic context of Trim63

• Here we investigated the effects of MuSK antibodies or Dex on MURF-1 expression in C2C12 cultures and in mouse muscles after treatment in vivo, using quantitative Western blotting [1].

References