GoPubMed Proteins lists recent and important papers and reviews for
proteins. Page last changed on 14 Mar 2013.
Death-domain associated protein
Daxx, hDaxx
This gene encodes a multifunctional protein that resides in multiple locations in the nucleus and in the cytoplasm. It interacts with a wide variety of proteins, such as apoptosis antigen Fas, centromere protein C, and transcription factor erythroblastosis virus E26 oncogene homolog 1. In the nucleus, the encoded protein functions as a potent transcription repressor that binds to sumoylated transcription factors. Its repression can be relieved by the sequestration of this protein into promyelocytic leukemia nuclear bodies or nucleoli. This protein also associates with centromeres in G2 phase. In the cytoplasm, the encoded protein may function to regulate apoptosis. The subcellular localization and function of this protein are modulated by post-translational modifications, including sumoylation, phosphorylation and polyubiquitination. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Nov 2008] (from
NCBI)
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Papers on
Daxx
[Effects of SUMOylation on the subcellular localization and function of DAXX].
New
Hengyang, China. In Sheng Li Xue Bao, 25 Mar 2013
Death domain-associated protein (DAXX) as a multifunctional nuclear protein widely resides in nucleolus, nucleoplasm, chromatin, promyelocytic leukaemia nuclear bodies (PML-NBs) and cytoplasm.
Neuroendocrine tumours: cracking the epigenetic code.
New
London, United Kingdom. In Endocr Relat Cancer, 21 Mar 2013
Recent progress has been facilitated by development of high throughput tools including second generation sequencing and arrays for analysis of the 'epigenome' of tumour and normal tissue, permitting unbiased approaches such as exome sequencing which identified mutations of chromatin remodelling genes ATRX/DAXX in 44% of pancreatic NETs.
Ubiquitin-independent proteasomal degradation of tumor suppressors by human cytomegalovirus pp71 requires the 19S regulatory particle.
New
Madison, United States. In J Virol, 13 Mar 2013
For example, the human cytomegalovirus (HCMV) pp71 protein induces the proteasome-dependent, ubiquitin-independent degradation of the retinoblastoma (Rb) and Daxx proteins.
Control of human adenovirus type 5 gene expression by cellular Daxx/ATRX chromatin-associated complexes.
New
Glasgow, United Kingdom. In Nucleic Acids Res, 08 Mar 2013
Death domain-associated protein (Daxx) cooperates with X-linked α-thalassaemia retardation syndrome protein (ATRX), a putative member of the sucrose non-fermentable 2 family of ATP-dependent chromatin-remodelling proteins, acting as the core ATPase subunit in this complex, whereas Daxx is the targeting factor, leading to histone deacetylase recruitment, H3.3 deposition and transcriptional repression of cellular promoters.
Phosphorylation of Daxx by ATM Contributes to DNA Damage-Induced p53 Activation.
New
Philadelphia, United States. In Plos One, Dec 2012
The optimal function of Mdm2 requires Daxx, which stabilizes Mdm2 through the deubiquitinase Hausp/USP7 and also directly promotes Mdm2's ubiquitin ligase activity towards p53.
DAXX envelops a histone H3.3-H4 dimer for H3.3-specific recognition.
New
Impact
New York City, United States. In Nature, Dec 2012
DAXX is a metazoan histone chaperone specific to the evolutionarily conserved histone variant H3.3.
Molecular pathology and genetics of pancreatic endocrine tumours.
Review
New
Roma, Italy. In J Mol Endocrinol, Aug 2012
Mutations of DAXX and ATRX are common and related to altered telomeres but not to prognosis.
Driver mutations in histone H3.3 and chromatin remodelling genes in paediatric glioblastoma.
New
Impact
Montréal, Canada. In Nature, Mar 2012
Mutations in ATRX (α-thalassaemia/mental retardation syndrome X-linked) and DAXX (death-domain associated protein), encoding two subunits of a chromatin remodelling complex required for H3.3 incorporation at pericentric heterochromatin and telomeres, were identified in 31% of samples overall, and in 100% of tumours harbouring a G34R or G34V H3.3 mutation.
General blockade of human cytomegalovirus immediate-early mRNA expression in the S/G2 phase by a nuclear, Daxx- and PML-independent mechanism.
GeneRIF
Berlin, Germany. In J Gen Virol, 2011
Neither Daxx nor PML, the main players of ND10-based immunity, are required for the block to viral gene expression in the S/G2 phase.
Interplay between human cytomegalovirus and intrinsic/innate host responses: a complex bidirectional relationship.
Review
Bologna, Italy. In Mediators Inflamm, 2011
We review the viral and cellular partners that mediate early host responses to HCMV with regard to the interaction between structural components of virions (viral glycoproteins) and cellular receptors (attachment/entry receptors, toll-like receptors, and other nucleic acid sensors) or intrinsic factors (PML, hDaxx, Sp100, viperin, interferon inducible protein 16), the reactions of innate immune cells (antigen presenting cells and natural killer cells), the numerous mechanisms of viral immunoevasion, and the potential exploitation of events that are associated with early phases of virus-host interplay as a therapeutic strategy.
Adenovirus type 5 early region 1B 55K oncoprotein-dependent degradation of cellular factor Daxx is required for efficient transformation of primary rodent cells.
GeneRIF
Hamburg, Germany. In J Virol, 2011
These results provide evidence for the idea that SUMO-1-conjugated E1B-55K-mediated degradation of Daxx plays a key role in adenoviral oncogenic transformation.
Altered telomeres in tumors with ATRX and DAXX mutations.
Impact
GeneRIF
Baltimore, United States. In Science, 2011
study found 61% of pancreatic neuroendocrine tumors had abnormal telomeres; all of the tumors with abnormal telomeres had ATRX or DAXX mutations or loss of nuclear ATRX or DAXX protein
Daxx mediates activation-induced cell death in microglia by triggering MST1 signalling.
GeneRIF
Seoul, South Korea. In Embo J, 2011
Daxx and macrophage Ste20-like kinase (MST)1 mediate interferon (IFN)-gamma-induced apoptosis in microglia.
Intrinsic cellular defense mechanisms targeting human cytomegalovirus.
Review
Erlangen, Germany. In Virus Res, 2011
In recent studies we and others have identified the cellular proteins PML, hDaxx, Sp100 and ATRX, which form a subnuclear structure known as nuclear domain 10 (ND10) or PML nuclear bodies (PML-NBs), as host restriction factors that counteract cytomegalovirus infections by inhibiting the initiation of viral immediate-early (IE) gene expression.
DAXX/ATRX, MEN1, and mTOR pathway genes are frequently altered in pancreatic neuroendocrine tumors.
Impact
GeneRIF
Baltimore, United States. In Science, 2011
identification of mutations in pancreatic neuroendocrine tumors; 44% had somatic inactivating mutations in MEN1; 43% had mutations in genes encoding DAXX and ATRX; clinically, mutations in MEN1 and DAXX/ATRX genes were associated with better prognosis
Role of promyelocytic leukemia protein in host antiviral defense.
Review
Paris, France. In J Interferon Cytokine Res, 2011
PML is the organizer of the NBs that contains at least 2 permanent NB-associated proteins, the IFN-stimulated gene product Speckled protein of 100 kDa (Sp100) and death-associated dead protein (Daxx), as well as numerous other transient proteins recruited in these structures in response to different stimuli.
Assessment of the pathway of apoptosis involving PAR-4, DAXX and ZIPK proteins in CLL patients and its relationship with the principal prognostic factors.
GeneRIF
Lublin, Poland. In Folia Histochem Cytobiol, 2010
The results confirm the significance of apoptosis deregulation in CLL, and suggest a possible relationship between DAXX expression and the clinical course of the disease.
Distinct factors control histone variant H3.3 localization at specific genomic regions.
Impact
New York City, United States. In Cell, 2010
Immunoaffinity purification and mass spectrometry reveal that the proteins Atrx and Daxx associate with H3.3 in a Hira-independent manner.
Emerging roles of the EBF family of transcription factors in tumor suppression.
Review
Gainesville, United States. In Mol Cancer Res, 2009
Functional studies revealed that EBF3 represses the expression of genes required for cell proliferation [e.g., cyclins and cyclin-dependent kinases (CDK)] and survival (e.g., Mcl-1 and Daxx) but activates those involved in cell cycle arrest (e.g., p21 and p27), leading to growth suppression and apoptosis.
