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transcription (PIAS) family of proteins (PIAS1, PIAS x β and Ubc9 as MR coregulators. Both PIAS1 and PIAS x β behave as small ubiquitin-related modifier-3 (SUMO-E3) ligases able to sumoylate MR both in vitro and in vivo ( Metivier et al . 2000

ongoing conformational changes ( Manin et al. 2000 ) may explain the reduction of functionally competent p53 through an ubiquitin-mediated proteolysis, since β-catenin can no longer interact with p53 and interfere with the normal proteasomal degradation

). The same group have since shown that E7 from HR-HPV types can stabilize A3A protein by blocking its polyubiquitination by cullin-RING-based E3 ubiquitin ligase complexes ( Fig. 3 ); thus, HPVs appear to modulate A3 expression at multiple levels

to be fully elucidated, the rapamycin-mediated decrease in ERRα protein levels was shown to be triggered by the proteasome upon ubiquitination of ERRα by the ubiquitin ligase STUB1, a genomic target of nuclear mTOR ( Chaveroux et al. 2013

& Wrana 2000 ). In contrast, the inhibitory SMAD (I-SMAD), SMAD7, binds to TβRI and prevents the phosphorylation of R-SMADs, resulting in the inhibition of TGFβ signaling ( Imamura et al . 1997 , Nakao et al . 1997 ). A SMAD ubiquitin regulatory factor

degradation. Indeed, two ubiquitin ligases, AMSH and dorfin, which reduce CaSR expression by increasing receptor degradation, have been demonstrated to bind to this region of the C-terminus ( McCullough et al. 2004 , Huang et al. 2006 ), and the ADH1

, member 1 −0.13 −0.66 0.47 Transport AA817792 EST −0.01 −0.48 0.42 Unclassified AA924091 Leprecan-like protein 2 −0.02 −0.31 0.83 Oxidoreductase/metabolism AA996896 Ubiquitin-conjugating enzyme UBC7 0.39 −0.08 −0.12 ubiquitin-conjugating AA859043 Triadin 1

SCF ubiquitin ligase complex that regulates the entry into S phase ( Reed 2003 ) and (4) SURVIVIN, is a member of the inhibitor of apoptosis (IAP) family that is involved in the regulation of cell division ( Kobayashi et al. 1999 ). Importantly

. 2015 ) which, if not checked, can lead to cell death. Experiments in transgenic mice have suggested that overexpression of hIAPP, but not the rodent peptide, generates ER stress and activation of the ubiquitin pathway targeting degradation ( Huang et

study demonstrated that TSH induces association between IRS-2 and Nedd4, one of the E3 ubiquitin ligases and IRS-2 monoubiquitination in cultured thyroid FRTL-5 cells, thereby enhancing IGF signaling and mitogenic activity ( Fukushima et al . 2015 ). We