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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Deleted in bladder cancer 1

DBC1, DBCCR1, deleted in breast cancer 1, BRINP1
This gene is located within a chromosomal region that shows loss of heterozygosity in some bladder cancers. It contains a 5' CpG island that may be a frequent target of hypermethylation, and it may undergo hypermethylation-based silencing in some bladder cancers. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Sir2, p53, CAN, Histone, V1a
Papers on DBC1
High-definition CpG methylation of novel genes in gastric carcinogenesis identified by next-generation sequencing.
Sepulveda et al., New York City, United States. In Mod Pathol, Feb 2016
Overall, 13 genes had significantly increased CpG methylation in gastric cancer vs non-metaplastic mucosa (BRINP1, CDH11, CHFR, EPHA5, EPHA7, FGF2, FLI1, GALR1, HS3ST2, PDGFRA, SEZ6L, SGCE, and SNRPN).
Cancer-predisposition gene KLLN maintains pericentric H3K9 trimethylation protecting genomic stability.
Eng et al., Cleveland, United States. In Nucleic Acids Res, Jan 2016
Interestingly, we show that KLLN interacts with DBC1, with consequent abrogation of DBC1 inhibition of SUV39H1, a H3K9 methyltransferase, suggesting the mode of KLLN regulating H3K9me3.
SIRT1 activating compounds (STACs) negatively regulate pancreatic cancer cell growth and viability through a SIRT1-lysosomal-dependent pathway.
Chini et al., In Clin Cancer Res, Jan 2016
Furthermore, the effect of STACs on cell viability was also dependent on the expression of the endogenous SIRT1 inhibitor DBC1.
The proteomic profile of deleted in breast cancer 1 (DBC1) interactions points to a multi-faceted regulation of gene expression.
Cristea et al., Princeton, United States. In Mol Cell Proteomics, Jan 2016
UNASSIGNED: Deleted in breast cancer 1 (DBC1) has emerged as an important regulator of multiple cellular processes, ranging from gene expression to cell cycle progression.
Potential Modulation of Sirtuins by Oxidative Stress.
Denicola et al., Montevideo, Uruguay. In Oxid Med Cell Longev, Dec 2015
In addition, oxidative stress can alter the interaction with other proteins, like SIRT1 with its protein inhibitor DBC1 resulting in a net increase of deacetylase activity.
High DBC1 (CCAR2) expression in gallbladder carcinoma is associated with favorable clinicopathological factors.
Lee et al., Seoul, South Korea. In Int J Clin Exp Pathol, 2014
The DBC1 gene (deleted in breast cancer 1) was initially cloned from region 8p21, which was homozygously deleted in breast cancer.
Relationships between Circulating Urea Concentrations and Endometrial Function in Postpartum Dairy Cows.
Wathes et al., United Kingdom. In Animals (basel), 2014
These were predominantly associated with tissue turnover (e.g., BRINP1, FOXG1), immune function (e.g., IL17RB, CRISPLD2), inflammation (e.g., C3, SERPINF1, SERPINF2) and lipid metabolism (e.g., SCAP, ACBD5, SLC10A).
Deleted in breast cancer-1 (DBC-1) in the interface between metabolism, aging and cancer.
Escande et al., Rochester, United States. In Biosci Rep, 2012
DBC1 (deleted in breast cancer-1) is a nuclear protein that regulates cellular metabolism.
Brown remodeling of white adipose tissue by SirT1-dependent deacetylation of Pparγ.
Accili et al., New York City, United States. In Cell, 2012
Here we report that gain of function of the NAD-dependent deacetylase SirT1 or loss of function of its endogenous inhibitor Deleted in breast cancer-1 (Dbc1) promote "browning" of WAT by deacetylating peroxisome proliferator-activated receptor (Ppar)-γ on Lys268 and Lys293.
Role of deleted in breast cancer 1 (DBC1) protein in SIRT1 deacetylase activation induced by protein kinase A and AMP-activated protein kinase.
Chini et al., Rochester, United States. In J Biol Chem, 2012
Data indicate that an increase in cAMP/PKA activity resulted in the dissociation of SIRT1 and DBC1 in an AMP-activated protein kinase (AMPK)-dependent manner.
DBIRD complex integrates alternative mRNA splicing with RNA polymerase II transcript elongation.
Svejstrup et al., London, United Kingdom. In Nature, 2012
data indicate that the DBIRD complex (consisting of DBC1 and ZNF326) acts at the interface between mRNP particles and RNAPII, integrating transcript elongation with the regulation of alternative splicing
Regulation of SIRT1 activity by genotoxic stress.
Lou et al., Shanghai, China. In Genes Dev, 2012
the stress-induced DBC1-SIRT1 interaction is important for cell fate determination following genotoxic stress.
The overexpression of DBC1 in esophageal squamous cell carcinoma correlates with poor prognosis.
Park et al., Seoul, South Korea. In Histol Histopathol, 2012
Suggest that DBC1 may promote tumor progression, and DBC1 could be a prognostic biomarker in esophageal squamous cell carcinoma.
Protected from the inside: endogenous histone deacetylase inhibitors and the road to cancer.
Gulino et al., Roma, Italy. In Biochim Biophys Acta, 2011
Recent evidence has demonstrated that the tumor suppressors HIC1 and DBC1 induce direct repression of Sirt1 function, whereas Chfr and REN(KCTD11/KASH family) downregulate HDAC1, by inducing its ubiquitin-dependent degradation.
Expression of DBC1 and SIRT1 is associated with poor prognosis for breast carcinoma.
Jang et al., Chŏnju, South Korea. In Hum Pathol, 2011
Rxpression of DBC1 and SIRT1 is a significant prognostic indicator for breast carcinoma patients.
Molecular genesis of non-muscle-invasive urothelial carcinoma (NMIUC).
Theodorescu et al., Charlottesville, United States. In Expert Rev Mol Med, 2009
The regions of chromosome 9 that harbour CDKN2A, CDKN2B, TSC1, PTCH1 and DBC1 are frequently mutated in NMIUC, resulting in functional loss; in addition, HRAS and FGFR3, which are both proto-oncogenes encoding components of the Ras-MAPK signalling pathway, have been found to harbour activating mutations in a large number of NMIUCs.
p30 DBC is a potential regulator of tumorigenesis.
Lou et al., Seoul, South Korea. In Cell Cycle, 2009
[review] summarizes the current understandings on p30 DBC functions, with a focus on the proposed roles of p30 DBC in tumorigenesis
Negative regulation of the deacetylase SIRT1 by DBC1.
Gu et al., New York City, United States. In Nature, 2008
DBC1 (deleted in breast cancer 1) acts as a native inhibitor of SIRT1 in human cells
DBC1 is a negative regulator of SIRT1.
Lou et al., New Haven, United States. In Nature, 2008
DBC1 directly interacts with SIRT1 and inhibits SIRT1 activity in vitro and in vivo
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