Promyelocytic leukemia protein PML inhibits Nur77-mediated transcription through specific functional interactions (Q28200940)

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Ruixiang Ran

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Feng Meng

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Kun-Sang Chang

Costimulatory signals are required for induction of transcription factor Nur77 during negative selection of CD4(+)CD8(+) thymocytes

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language of work or name

English

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publication date

30 May 2002

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published in

Oncogene

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volume

21

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issue

24

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page(s)

3925-33

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cites work

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Promyelocytic leukemia (PML) nuclear bodies are protein structures that do not accumulate RNA

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The transcription coactivator CBP is a dynamic component of the promyelocytic leukemia nuclear body

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A role for the orphan steroid receptor Nur77 in apoptosis accompanying antigen-induced negative selection

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Human T-cell leukemia retrovirus-Tax protein is a repressor of nuclear receptor signaling

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Modulation of CREB binding protein function by the promyelocytic (PML) oncoprotein suggests a role for nuclear bodies in hormone signaling

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DNA viruses and viral proteins that interact with PML nuclear bodies

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The function of PML in p53-dependent apoptosis

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A gene inducible by serum growth factors encodes a member of the steroid and thyroid hormone receptor superfamily

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Primary response genes induced by growth factors and tumor promoters

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PML is critical for ND10 formation and recruits the PML-interacting protein daxx to this nuclear structure when modified by SUMO-1

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Identification of three major sentrinization sites in PML

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Role of PML and PML-RARalpha in Mad-mediated transcriptional repression

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Localization of nascent RNA and CREB binding protein with the PML-containing nuclear body.

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Analysis of the growth and transformation suppressor domains of promyelocytic leukemia gene, PML.

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Recombinant PML adenovirus suppresses growth and tumorigenicity of human breast cancer cells by inducing G1 cell cycle arrest and apoptosis

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Cytochrome c release and apoptosis induced by mitochondrial targeting of nuclear orphan receptor TR3.

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Sequestration and inhibition of Daxx-mediated transcriptional repression by PML

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Transcriptional regulation in acute promyelocytic leukemia.

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PML suppresses oncogenic transformation of NIH/3T3 cells by activated neu.

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Apoptotic signals delivered through the T-cell receptor of a T-cell hybrid require the immediate-early gene nur77.

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Nuclear domain 10, the site of DNA virus transcription and replication

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Nerve growth factor induces a gene homologous to the glucocorticoid receptor gene.

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DNA damage-dependent nuclear dynamics of the Mre11 complex

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PML, a growth suppressor disrupted in acute promyelocytic leukemia

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Stable overexpression of PML alters regulation of cell cycle progression in HeLa cells

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A human early response gene homologous to murine nur77 and rat NGFI-B, and related to the nuclear receptor superfamily

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Atmospheric carbon dioxide concentrations over the past 60 million years

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PML induces a novel caspase-independent death process

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SUMO: of branched proteins and nuclear bodies

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Potentiation of GATA-2 activity through interactions with the promyelocytic leukemia protein (PML) and the t(15;17)-generated PML-retinoic acid receptor alpha oncoprotein

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Transcriptional repression by the promyelocytic leukemia protein, PML.

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The promyelocytic leukemia protein interacts with Sp1 and inhibits its transactivation of the epidermal growth factor receptor promoter

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Role of PML in cell growth and the retinoic acid pathway

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Apoptosis of nur77/N10-transgenic thymocytes involves the Fas/Fas ligand pathway

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The orphan nuclear receptor NGFI-B regulates expression of the gene encoding steroid 21-hydroxylase.

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Requirement for the orphan steroid receptor Nur77 in apoptosis of T-cell hybridomas

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The growth suppressor PML represses transcription by functionally and physically interacting with histone deacetylases

21 January 2018

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A RA-dependent, tumour-growth suppressive transcription complex is the target of the PML-RARalpha and T18 oncoproteins

21 January 2018

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PML regulates p53 acetylation and premature senescence induced by oncogenic Ras

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inferred from DOI database lookup

7 January 2021

based on heuristic

Antisense TR3 orphan receptor can increase prostate cancer cell viability with etoposide treatment

1 reference

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