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These results suggest that different DDB1-CUL4 associated factors play distinct roles in human lung adenocarcinoma development.
The DDB1 is acetylated and acetylation promotes DDB1 binding to CUL4.
Results revealed a function independent of its transcriptional activity, as TTF-1 (显示 NKX2-1 蛋白) was found to interact with DDB1 and block its binding to CHK1 (显示 CHEK1 蛋白), which in turn attenuated ubiquitylation and subsequent degradation of CHK1 (显示 CHEK1 蛋白).
SIRT7 inhibits TR4 degradation by deacetylation of DDB1.
the c-Abl (显示 ABL1 蛋白) non-receptor kinase phosphorylates DDB1 at residue Tyr (显示 TYR 蛋白)-316 to recruit a small regulatory protein, DDA1 (显示 DDA1 蛋白), leading to increased substrate ubiquitination
knockdown of DCAF7 (显示 DCAF7 蛋白) reduced the degradation of DNA ligase I (显示 LIG1 蛋白) in response to inhibition of proliferation and replacement of ubiquitylated lysine residues reduced the in vitro ubiquitylation of DNA ligase I (显示 LIG1 蛋白) by Cul4-DDB1 and DCAF7 (显示 DCAF7 蛋白). In contrast, a different E3 ubiquitin ligase (显示 MUL1 蛋白) regulates FEN-1 (显示 FEN1 蛋白) turnover.
This study presents the crystal structure of the DDB1-DCAF1-HIV-1-Vpr-uracil-DNA glycosylase (显示 UNG 蛋白) (cyclin U (显示 CCNO 蛋白)) complex.
Our data are consistent with the idea that the CUL4A (显示 CUL4A 蛋白)/B-DDB1-CRBN (显示 CRBN 蛋白) complex catalyses the polyubiquitination and thus controls the degradation of CLC-1 (显示 CLCN1 蛋白) channels.
These results revealed a novel role of DDB in H3K56Ac deacetylation during early step of NER (显示 NR1H2 蛋白) and the existence of active functional cross-talk between DDB-mediated damage recognition and H3K56Ac deacetylation.
The identification of Vpr mutants which associate with DCAF1 but only poorly with DDB1 suggests that DCAF1 is necessary but is not sufficient for the Vpr association with DDB1-containing E3 ligase complex.
Bovine herpesvirus-1 VP8 interacts with DDB1 and is monoubiquitinated during infection.
These studies identify CUL4-DDB1 complex as a novel post-translational regulator of stem and progenitor maintenance and differentiation.
uncovered a novel biological role for CUL4A (显示 CUL4A 蛋白)-DDB1-CDT2 E3 ligase that regulates molecular circadian behaviors via promoting ubiquitination-dependent degradation of CRY1 (显示 CRY1 蛋白)
UCH-L1 disrupts a complex between the DDB1-CUL4 ubiquitin ligase complex.
In a constructive process, pM27 recruits DDB1 to exploit ubiquitin ligase (显示 RNF123 蛋白) complexes catalyzing the obstruction of the STAT2 (显示 STAT2 蛋白)-dependent antiviral state of cells to permit viral replication.
Hepatocyte-specific deletion of DDB1 induces liver regeneration and tumorigenesis.
These results indicate that DDB1 plays an essential role in maintaining viability and genomic integrity of dividing cells.
DDB1 plays an important role in development by controlling levels of cell cycle regulators and thereby maintaining genomic stability.
Caenorhabditis elegans DDB-1 is required for the degradation of CDT-1 during S phase. DDB-1 interacts specifically with CUL-4 but not with other C. elegans cullins.
Data show that SKN-1 protein levels, nuclear accumulation, and activity are repressed by the WD40 repeat protein WDR-23, which interacts with the CUL-4/DDB-1 ubiquitin ligase to presumably target the transcription factor for proteasomal degradation.
The protein encoded by this gene is the large subunit (p127) of the heterodimeric DNA damage-binding (DDB) complex while another protein (p48) forms the small subunit. This protein complex functions in nucleotide-excision repair and binds to DNA following UV damage. Defective activity of this complex causes the repair defect in patients with xeroderma pigmentosum complementation group E (XPE) - an autosomal recessive disorder characterized by photosensitivity and early onset of carcinomas. However, it remains for mutation analysis to demonstrate whether the defect in XPE patients is in this gene or the gene encoding the small subunit. In addition, Best vitelliform mascular dystrophy is mapped to the same region as this gene on 11q, but no sequence alternations of this gene are demonstrated in Best disease patients. The protein encoded by this gene also functions as an adaptor molecule for the cullin 4 (CUL4) ubiquitin E3 ligase complex by facilitating the binding of substrates to this complex and the ubiquitination of proteins.
DDB p127 subunit
, DNA damage-binding protein 1
, DNA damage-binding protein a
, HBV X-associated protein 1
, UV-DDB 1
, UV-damaged DNA-binding factor
, UV-damaged DNA-binding protein 1
, XPE-binding factor
, xeroderma pigmentosum group E-complementing protein
, damage-specific DNA-binding protein 1
, damage-specific DNA binding protein 1, 127kDa
, DNA damage-binding protein 1-like
, DNA repair protein
, damage-specific DNA-binding protein, DNA repair
, damaged-DNA recognition protein 1
, damage specific DNA binding protein 1