ATAD2 is a novel cofactor for MYC, overexpressed and amplified in aggressive tumors.
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Histone recognition and large-scale structural analysis of the human bromodomain familyObserved bromodomain flexibility reveals histone peptide- and small molecule ligand-compatible forms of ATAD2Atad2 is a generalist facilitator of chromatin dynamics in embryonic stem cellsA Chemical Probe for the ATAD2 BromodomainBET domain co-regulators in obesity, inflammation and cancerGenome-wide transcriptional reorganization associated with senescence-to-immortality switch during human hepatocellular carcinogenesisIdentification of tumor suppressors and oncogenes from genomic and epigenetic features in ovarian cancerIdentifying in-trans process associated genes in breast cancer by integrated analysis of copy number and expression dataIdentification of candidate growth promoting genes in ovarian cancer through integrated copy number and expression analysis.miR-372 down-regulates the oncogene ATAD2 to influence hepatocellular carcinoma proliferation and metastasis.HIF-1α promoted vasculogenic mimicry formation in hepatocellular carcinoma through LOXL2 up-regulation in hypoxic tumor microenvironment.Direct cooperation between androgen receptor and E2F1 reveals a common regulation mechanism for androgen-responsive genes in prostate cells.High-resolution comparative genomic hybridization of inflammatory breast cancer and identification of candidate genes.RNA-Seq analyses generate comprehensive transcriptomic landscape and reveal complex transcript patterns in hepatocellular carcinoma.Kinesin family deregulation coordinated by bromodomain protein ANCCA and histone methyltransferase MLL for breast cancer cell growth, survival, and tamoxifen resistance.MYC cofactors: molecular switches controlling diverse biological outcomes.ANCCA/ATAD2 overexpression identifies breast cancer patients with poor prognosis, acting to drive proliferation and survival of triple-negative cells through control of B-Myb and EZH2.Molecular insights into the recognition of N-terminal histone modifications by the BRPF1 bromodomain.Bromodomain coactivators in cancer, obesity, type 2 diabetes, and inflammationIntegrated genomic analysis of the 8q24 amplification in endometrial cancers identifies ATAD2 as essential to MYC-dependent cancers.Small-molecular modulators of cancer-associated epigenetic mechanisms.Fragment-based screening of the bromodomain of ATAD2.Inflammatory breast cancer (IBC): clues for targeted therapiesLessons from yeast on emerging roles of the ATAD2 protein family in gene regulation and genome organization.Screen identifies bromodomain protein ZMYND8 in chromatin recognition of transcription-associated DNA damage that promotes homologous recombination.Low mir-372 expression correlates with poor prognosis and tumor metastasis in hepatocellular carcinomaTranscriptional Dynamics of Immortalized Human Mesenchymal Stem Cells during Transformation.Bioinformatics analysis of thousands of TCGA tumors to determine the involvement of epigenetic regulators in human cancer.ATAD2 as a Poor Prognostic Marker for Hepatocellular Carcinoma after Curative ResectionATAD2 overexpression links to enrichment of B-MYB-translational signatures and development of aggressive endometrial carcinoma.Abo1, a conserved bromodomain AAA-ATPase, maintains global nucleosome occupancy and organisation.Suppression of ATAD2 inhibits hepatocellular carcinoma progression through activation of p53- and p38-mediated apoptotic signalingDifferential gene expression between skin and cervix induced by the E7 oncoprotein in a transgenic mouse modelThe Arabidopsis acetylated histone-binding protein BRAT1 forms a complex with BRP1 and prevents transcriptional silencing.Nuclear receptor coregulators as a new paradigm for therapeutic targeting.Gene expression profiling of the 8q22-24 position in human breast cancer: TSPYL5, MTDH, ATAD2 and CCNE2 genes are implicated in oncogenesis, while WISP1 and EXT1 genes may predict a risk of metastasis.Integrated genomic and epigenomic analysis of breast cancer brain metastasisChemical synthesis of the ATAD2 bromodomain.Significance of PRO2000/ANCCA expression, a novel proliferation-associated protein in hepatocellular carcinoma.Bromodomains as therapeutic targets.
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P2860
ATAD2 is a novel cofactor for MYC, overexpressed and amplified in aggressive tumors.
description
2009 nî lūn-bûn
@nan
2009年の論文
@ja
2009年学术文章
@wuu
2009年学术文章
@zh
2009年学术文章
@zh-cn
2009年学术文章
@zh-hans
2009年学术文章
@zh-my
2009年学术文章
@zh-sg
2009年學術文章
@yue
2009年學術文章
@zh-hant
name
ATAD2 is a novel cofactor for MYC, overexpressed and amplified in aggressive tumors.
@en
ATAD2 is a novel cofactor for MYC, overexpressed and amplified in aggressive tumors.
@nl
type
label
ATAD2 is a novel cofactor for MYC, overexpressed and amplified in aggressive tumors.
@en
ATAD2 is a novel cofactor for MYC, overexpressed and amplified in aggressive tumors.
@nl
prefLabel
ATAD2 is a novel cofactor for MYC, overexpressed and amplified in aggressive tumors.
@en
ATAD2 is a novel cofactor for MYC, overexpressed and amplified in aggressive tumors.
@nl
P2093
P1433
P1476
ATAD2 is a novel cofactor for MYC, overexpressed and amplified in aggressive tumors.
@en
P2093
Elena Prosperini
Fraser McBlane
Giovanni Pacchiana
Jesper Christensen
Julian Walfridsson
Marco Ciró
Maria Capra
Micaela Quarto
Paolo Nucifero
Ursula Grazini
P304
P356
10.1158/0008-5472.CAN-09-2131
P407
P577
2009-10-20T00:00:00Z