PML suppresses oncogenic transformation of NIH/3T3 cells by activated neu.
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The growth suppressor PML represses transcription by functionally and physically interacting with histone deacetylasesLeukemia-associated retinoic acid receptor alpha fusion partners, PML and PLZF, heterodimerize and colocalize to nuclear bodiesRING1 is associated with the polycomb group protein complex and acts as a transcriptional repressorMolecular cloning of a new interferon-induced PML nuclear body-associated proteinThe interferon (IFN)-stimulated gene Sp100 promoter contains an IFN-gamma activation site and an imperfect IFN-stimulated response element which mediate type I IFN inducibilityThe promyelocytic leukemia gene product (PML) forms stable complexes with the retinoblastoma proteinThe promyelocytic leukemia protein interacts with Sp1 and inhibits its transactivation of the epidermal growth factor receptor promoterResistance to virus infection conferred by the interferon-induced promyelocytic leukemia proteinPromyelocytic leukemia protein PML inhibits Nur77-mediated transcription through specific functional interactionsPML interaction with p53 and its role in apoptosis and replicative senescenceThe promyelocytic leukemia protein represses A20-mediated transcriptionCovalent modification of PML by the sentrin family of ubiquitin-like proteinsArsenic-induced PML targeting onto nuclear bodies: implications for the treatment of acute promyelocytic leukemiaPML interacts with Myc, and Myc target gene expression is altered in PML-null fibroblastsTransforming potential of the adenovirus type 5 E4orf3 protein.The pathogenesis of acute promyelocytic leukaemia: evaluation of the role of molecular diagnosis and monitoring in the management of the disease.Disruption of PML subnuclear domains by the acidic IE1 protein of human cytomegalovirus is mediated through interaction with PML and may modulate a RING finger-dependent cryptic transactivator function of PMLRegulation of cellular senescence by p53.Overexpression of promyelocytic leukemia protein precludes the dispersal of ND10 structures and has no effect on accumulation of infectious herpes simplex virus 1 or its proteinsSumoylation-promoted enterovirus 71 3C degradation correlates with a reduction in viral replication and cell apoptosis.Acute promyelocytic leukemia: PML/RARalpha and the leukemic stem cell.HO-1, RET and PML as possible markers for risk stratification of acute myelocytic leukemia and prognostic evaluation.Role of promyelocytic leukemia (PML) protein in tumor suppressionA highly amplified mouse gene is homologous to the human interferon-responsive Sp100 gene encoding an autoantigen associated with nuclear dots.Cell death induction by the acute promyelocytic leukemia-specific PML/RARalpha fusion protein.A bcr-3 isoform of RARalpha-PML potentiates the development of PML-RARalpha-driven acute promyelocytic leukemia.Regulation of apoptosis by PML and the PML-NBs.The nuclear bodies inside out: PML conquers the cytoplasm.PML mediates the interferon-induced antiviral state against a complex retrovirus via its association with the viral transactivatorPromyelocytic leukemia protein sensitizes tumor necrosis factor alpha-induced apoptosis by inhibiting the NF-kappaB survival pathway.PML-containing nuclear bodies: their spatial distribution in relation to other nuclear components.Altered expression of the suppressors PML and p53 in glioblastoma cells with the antisense-EGF-receptor.The biologic function of PML and its role in acute promyelocytic leukemia.Analysis of the growth and transformation suppressor domains of promyelocytic leukemia gene, PML.The retinoblastoma protein and PML collaborate to organize heterochromatin and silence E2F-responsive genes during senescence.Herpes virus induced proteasome-dependent degradation of the nuclear bodies-associated PML and Sp100 proteins.Formation of PML/RAR alpha high molecular weight nuclear complexes through the PML coiled-coil region is essential for the PML/RAR alpha-mediated retinoic acid response.Nuclear neighbours: the spatial and functional organization of genes and nuclear domains.Deregulation of NPM and PLZF in a variant t(5;17) case of acute promyelocytic leukemia.
P2860
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P2860
PML suppresses oncogenic transformation of NIH/3T3 cells by activated neu.
description
1995 nî lūn-bûn
@nan
1995年の論文
@ja
1995年学术文章
@wuu
1995年学术文章
@zh-cn
1995年学术文章
@zh-hans
1995年学术文章
@zh-my
1995年学术文章
@zh-sg
1995年學術文章
@yue
1995年學術文章
@zh
1995年學術文章
@zh-hant
name
PML suppresses oncogenic transformation of NIH/3T3 cells by activated neu.
@ast
PML suppresses oncogenic transformation of NIH/3T3 cells by activated neu.
@en
type
label
PML suppresses oncogenic transformation of NIH/3T3 cells by activated neu.
@ast
PML suppresses oncogenic transformation of NIH/3T3 cells by activated neu.
@en
prefLabel
PML suppresses oncogenic transformation of NIH/3T3 cells by activated neu.
@ast
PML suppresses oncogenic transformation of NIH/3T3 cells by activated neu.
@en
P2093
P2860
P356
P1476
PML suppresses oncogenic transformation of NIH/3T3 cells by activated neu.
@en
P2093
P2860
P304
P356
10.1084/JEM.181.6.1965
P407
P577
1995-06-01T00:00:00Z