( Zhou et al . 2007 ). Normally, p53 protein levels are very low due to its rapid degradation via the ubiquitin-proteasome pathway (see review Brooks & Gu (2011) ). The ubiquitination of p53 is mainly mediated by MDM2, an E3 ubiquitin ligase ( Haupt et
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Kenichi Kanai, Shinsaku Aramata, Sayo Katakami, Kunio Yasuda, and Kohsuke Kataoka
LF Chi Y Clurman BE Roberts JM 2007 Ubiquitin-independent degradation of cell-cycle inhibitors by the REGgamma proteasome . Molecular Cell 26 843 – 852 . doi:10.1016/j.molcel.2007.05.022 . Docherty HM Hay CW Ferguson LA Barrow J
Elin Swedenborg, Joëlle Rüegg, Sari Mäkelä, and Ingemar Pongratz
endogenous hormones. Interference with hormone receptor activity through direct protein degradation Targeted degradation via the ubiquitin–proteasome pathway is one way by which the levels of nuclear hormone receptors are regulated. Recent findings indicate
Pablo Pánico, Marcia Hiriart, Patricia Ostrosky-Wegman, and Ana María Salazar
_001017575.1) is shown adjacent to the predicted cleavage sites 3, 4 and 5. Conserved residues are shown in bold. The TUG domains are indicated as UBL1 for ubiquitin-like domain 1, UBL2 for ubiquitin-like domain 2 and Ubx for ubiquitin-like domain 3. (C) In
A R Rodrigues, D Sousa, H Almeida, and A M Gouveia
accessory proteins ( Cooray et al . 2009 , Cooray & Clark 2011 , Meimaridou et al . 2011 ). Misfolded polypeptides are retained in the ER and later degraded by the ubiquitin–proteasome system. MCRs that correctly reach the cell surface are able to bind
Andrea Weckman, Antonio Di Ieva, Fabio Rotondo, Luis V Syro, Leon D Ortiz, Kalman Kovacs, and Michael D Cusimano
ubiquitin-proteosome system, build-ups of protein aggregates ( Mathew et al . 2007 ). Autophagy involves several steps beginning with induction – it is most commonly triggered by nutrient deprivation ( Mizushima 2007 ) – and continuing with the engulfment
Suzuka Onishi and Kohsuke Kataoka
. Previous reports suggested that PIASy, a member of PIAS family of small ubiquitin-like modifier (SUMO) E3 ligases, affects the activities of the Islet1 and Glis3 transcription factors ( Yan et al. 2016 , Hoard et al. 2018 ). SUMO is covalently
H Santti, L Mikkonen, A Anand, S Hirvonen-Santti, J Toppari, M Panhuysen, F Vauti, M Perera, G Corte, W Wurst, O A Jänne, and J J Palvimo
a posttranslational modification resembling ubiquitination, where a SUMO (small ubiquitin-related modifier) protein is attached to a lysine residue of a target protein. Several consequences for sumoylation have been found. Sumoylation may block
Cristina L Esteves, Val Kelly, Valérie Bégay, Simon G Lillico, Achim Leutz, Jonathan R Seckl, and Karen E Chapman
allows for GFP expression. Constitutive expression of the reverse Tet transactivator (rtTA3) and the neomycin resistance gene (Neo) is driven by the ubiquitin-c (Ubi-c) promoter ( Fig. 1A ). In order to express C/EBPβ-LIP in mature adipocytes, we first
H Watanabe, A Suzuki, M Goto, S Ohsako, C Tohyama, H Handa, and T Iguchi
) AGCTGGTTCGCAGCCAAA, CAGAGCGACCTCCCCATCT NM_009455 (ubiquitin-conjugating enzyme E2E 1; Ube2e1 ) GCTATGTCGGATGAC GATTCG, TCTCGGTCTGCTGGTTGGA NM_007479 (ADP-ribosylation factor 4
