ArticleThe Journal of biological chemistry2011
The stability of histone acetyltransferase general control non-derepressible (Gcn) 5 is regulated by Cullin4-RING E3 ubiquitin ligase.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 26 citations in OpenAlex.
- Ubiquitin proteasome system (UPS): a crucial determinant of the epigenetic landscape in cancer.Epigenomics · 2025Review
- Article
- WD Repeat and HMG Box DNA Binding Protein 1: An Oncoprotein at the Hub of Tumorigenesis and a Novel Therapeutic Target.International journal of molecular sciences · 2023Review
- Posttranslational regulation of the GCN5 and PCAF acetyltransferases.PLoS genetics · 2022Review
- Leukemia inhibitory factor receptor homodimerization mediated by acetylation of extracellular lysine promotes prostate cancer progression through the PDPK1/AKT/GCN5 axis.Clinical and translational medicine · 2022Article
- The CRL4DTL E3 ligase induces degradation of the DNA replication initiation factor TICRR/TRESLIN specifically during S phase.Nucleic acids research · 2021Article
- WDHD1 facilitates G1 checkpoint abrogation in HPV E7 expressing cells by modulating GCN5.BMC cancer · 2020Article
- The emerging role for Cullin 4 family of E3 ligases in tumorigenesis.Biochimica et biophysica acta. Reviews on cancer · 2019Review
- The structure and polymerase-recognition mechanism of the crucial adaptor protein AND-1 in the human replisome.The Journal of biological chemistry · 2017Article
- And-1 is required for homologous recombination repair by regulating DNA end resection.Nucleic acids research · 2017Article
- MMSET is dynamically regulated during cell-cycle progression and promotes normal DNA replication.Cell cycle (Georgetown, Tex.) · 2016Article
- Overexpression of denticleless E3 ubiquitin protein ligase homolog (DTL) is related to poor outcome in gastric carcinoma.Oncotarget · 2015Article
- And-1 coordinates with Claspin for efficient Chk1 activation in response to replication stress.The EMBO journal · 2015Article
- Replisome function during replicative stress is modulated by histone h3 lysine 56 acetylation through Ctf4.Genetics · 2015Article
- The stress phenotype makes cancer cells addicted to CDT2, a substrate receptor of the CRL4 ubiquitin ligase.Oncotarget · 2014Article
- The p38-interacting protein (p38IP) regulates G2/M progression by promoting α-tubulin acetylation via inhibiting ubiquitination-induced degradation of the acetyltransferase GCN5.The Journal of biological chemistry · 2013Article
- SCF(Fbxw15) mediates histone acetyltransferase binding to origin recognition complex (HBO1) ubiquitin-proteasomal degradation to regulate cell proliferation.The Journal of biological chemistry · 2013Article
- CRL4(CDT2) targets CHK1 for PCNA-independent destruction.Molecular and cellular biology · 2013Article
- The involvement of acidic nucleoplasmic DNA-binding protein (And-1) in the regulation of prereplicative complex (pre-RC) assembly in human cells.The Journal of biological chemistry · 2012Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Histone acetyltransferases play important roles in the regulation of chromatin structure and gene transcription. As one of the most important histone acetyltransferases, general control non-derepressible (Gcn) 5 has been linked to diverse cellular processes and tumorigenesis as well. We have recently identified a functional link between Gcn5 and acidic nucleoplasmic DNA-binding protein 1 (And-1) that is elevated in multiple cancer cells and is essential for Gcn5 protein stability. However, the mechanism by which And-1 regulates Gcn5 protein stability remains unknown. Here we show that the ablation of Cullin4-RING E3 ubiquitin ligase (CRL4) leads to the stabilization of Gcn5 in cells with depleted And-1, and Cdc10-dependent transcript 2 (Cdt2) serves as a substrate receptor protein of CRL4. Overexpression of Cdt2 reduces the Gcn5 protein levels, and CRL(Cdt2) is sufficient to ubiquitinate Gcn5 both in vivo and in vitro. And-1 stabilizes Gcn5 by impairing the interaction between Gcn5 and CRL(Cdt2) and thereby preventing Gcn5 ubiquitination and degradation. The degradation of Gcn5 is not dependent on proliferating cell nuclear antigen, an important player involved in CRL(Cdt2)-mediated protein degradation. Thus, CRL(Cdt2) and And-1 play an essential role in the regulation of Gcn5 protein stability. This study provides us with the mechanistic basis to develop alternative approaches to inhibit Gcn5 activity for cancer therapy.
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