The ubiquitin–proteasome system and signal transduction pathways regulating epithelial mesenchymal transition of cancer

IA Voutsadakis - Journal of biomedical science, 2012 - Springer
Epithelial to Mesenchymal transition (EMT) in cancer, a process permitting cancer cells to
become mobile and metastatic, has a signaling hardwire forged from development. Multiple …

Regulation of p53 by E3s

M Pan, C Blattner - Cancers, 2021 - mdpi.com
Simple Summary The p53 protein is a transcription factor that initiates cell cycle arrest and
apoptosis and by this counteracts tumorigenesis. Because of its anti-proliferative activity …

The CUL7 E3 ubiquitin ligase targets insulin receptor substrate 1 for ubiquitin-dependent degradation

X Xu, A Sarikas, DC Dias-Santagata, G Dolios… - Molecular cell, 2008 - cell.com
Recent genetic studies have documented a pivotal growth-regulatory role played by the
Cullin 7 (CUL7) E3 ubiquitin ligase complex containing the Fbw8-substrate-targeting …

AP4 encodes a c-MYC-inducible repressor of p21

P Jung, A Menssen, D Mayr… - Proceedings of the …, 2008 - National Acad Sciences
In the majority of human tumors, expression of the c-MYC oncogene becomes constitutive.
Here, we report that c-MYC directly regulates the expression of AP4 via CACGTG motifs in …

The CUL7/F-box and WD repeat domain containing 8 (CUL7/Fbxw8) ubiquitin ligase promotes degradation of hematopoietic progenitor kinase 1

H Wang, Y Chen, P Lin, L Li, G Zhou, G Liu… - Journal of Biological …, 2014 - ASBMB
HPK1, a member of mammalian Ste20-like serine/threonine kinases, is lost in> 95%
pancreatic cancer through proteasome-mediated degradation. However, the mechanism of …

Exome sequencing identifies CCDC8 mutations in 3-M syndrome, suggesting that CCDC8 contributes in a pathway with CUL7 and OBSL1 to control human growth

D Hanson, PG Murray, J O'Sullivan, J Urquhart… - The American Journal of …, 2011 - cell.com
3-M syndrome, a primordial growth disorder, is associated with mutations in CUL7 and
OBSL1. Exome sequencing now identifies mutations in CCDC8 as a cause of 3-M …

The primordial growth disorder 3-M syndrome connects ubiquitination to the cytoskeletal adaptor OBSL1

D Hanson, PG Murray, A Sud, SA Temtamy… - The American Journal of …, 2009 - cell.com
3-M syndrome is an autosomal-recessive primordial growth disorder characterized by
significant intrauterine and postnatal growth restriction. Mutations in the CUL7 gene are …

[HTML][HTML] Cullin family proteins and tumorigenesis: genetic association and molecular mechanisms

Z Chen, J Sui, F Zhang, C Zhang - Journal of Cancer, 2015 - ncbi.nlm.nih.gov
Cullin family proteins function as scaffolds to form numerous E3 ubiquitin ligases with RING
proteins, adaptor proteins and substrate recognition receptors. These E3 ligases further …

Small compound inhibitors of basal glucose transport inhibit cell proliferation and induce apoptosis in cancer cells via glucose-deprivation-like mechanisms

Y Liu, W Zhang, Y Cao, Y Liu, S Bergmeier, X Chen - Cancer letters, 2010 - Elsevier
Cancer cells depend heavily on glucose as both energy and biosynthesis sources and are
found to upregulate glucose transport and switch their main energy supply pathway from …

Quantitative proteomic analysis of cellular protein modulation upon inhibition of the NEDD8-activating enzyme by MLN4924

H Liao, XJ Liu, JL Blank, DC Bouck, H Bernard… - Molecular & Cellular …, 2011 - ASBMB
Cullin-RING ubiquitin ligases (CRLs) are responsible for the ubiquitination of many cellular
proteins, thereby targeting them for proteasomal degradation. In most cases the substrates …