Pathways of retinoic acid- or arsenic trioxide-induced PML/RARalpha catabolism, role of oncogene degradation in disease remission. - sprookjes - yvandenbroek - TriplyDB

Pathways of retinoic acid- or arsenic trioxide-induced PML/RARalpha catabolism, role of oncogene degradation in disease remission.

Pathways of retinoic acid- or arsenic trioxide-induced PML/RARalpha catabolism, role of oncogene degradation in disease remission.

http://www.wikidata.org/entity/Q34435558

about

PML nuclear bodies PML inhibits HIF-1alpha translation and neoangiogenesis through repression of mTOR The cell biology of disease: Acute promyelocytic leukemia, arsenic, and PML bodies In vivo activation of cAMP signaling induces growth arrest and differentiation in acute promyelocytic leukemia.Targeting iron homeostasis induces cellular differentiation and synergizes with differentiating agents in acute myeloid leukemia.Clastosome: a subtype of nuclear body enriched in 19S and 20S proteasomes, ubiquitin, and protein substrates of proteasome.Arsenic trioxide inhibits transforming growth factor-β1-induced fibroblast to myofibroblast differentiation in vitro and bleomycin induced lung fibrosis in vivo.SUMOylation substrates in neuronal intranuclear inclusion disease.All-trans retinoic acid/As2O3 combination yields a high quality remission and survival in newly diagnosed acute promyelocytic leukemia Targeting PML-RARα and Oncogenic Signaling Pathways by Chinese Herbal Mixture Tien-Hsien Liquid in Acute Promyelocytic Leukemia NB4 Cells Inhibition of Sp1 functions by its sequestration into PML nuclear bodies.Body language: the function of PML nuclear bodies in apoptosis regulation.Lysophosphatidic acid acyltransferase-beta: a novel target for induction of tumour cell apoptosis.Acute promyelocytic leukemia: where does it stem from?Speciation of arsenic trioxide metabolites in peripheral blood and bone marrow from an acute promyelocytic leukemia patient.Altered nuclear cofactor switching in retinoic-resistant variants of the PML-RARα oncoprotein of acute promyelocytic leukemia Nuclear structure in cancer cells.Proapoptotic regimes for HTLV-I-transformed cells: targeting Tax and the NF-kappaB pathway.Acute promyelocytic leukemia: a model of molecular target based therapy.Dose-dependent effects of selenite (Se(4+)) on arsenite (As(3+))-induced apoptosis and differentiation in acute promyelocytic leukemia cells.Development of Flow Cytometry-Fluorescent In Situ Hybridization (Flow-FISH) Method for Detection of PML/RARa Chromosomal Translocation in Acute Promyelocytic Leukemia Cell Line Treatment of acute promyelocytic leukaemia with all-trans retinoic acid and arsenic trioxide: a paradigm of synergistic molecular targeting therapy.Nuclear microenvironment in cancer diagnosis and treatment From dissection of disease pathogenesis to elucidation of mechanisms of targeted therapies: leukemia research in the genomic era.New strategies in acute promyelocytic leukemia: moving to an entirely oral, chemotherapy-free upfront management approach.PML, SUMOylation, and Senescence Immunohistochemical expression of promyelocytic leukemia body in soft tissue sarcomas Quality control of a transcriptional regulator by SUMO-targeted degradation Genome stability roles of SUMO-targeted ubiquitin ligases.All trans retinoic acid and cancer.The role of PML in the nervous system.Arsenic in the treatment of newly diagnosed acute promyelocytic leukemia: current status and future research direction.Arsenic trioxide for management of acute promyelocytic leukemia: current evidence on its role in front-line therapy and recurrent disease.Treatment of acute promyelocytic leukemia with arsenic trioxide: clinical results and open questions.The role of PML in hematopoietic and leukemic stem cell maintenance.Retinoic acid signaling in cancer: The parable of acute promyelocytic leukemia.Arsenic trioxide promotes histone H3 phosphoacetylation at the chromatin of CASPASE-10 in acute promyelocytic leukemia cells.Synergistic targeted therapy for acute promyelocytic leukaemia: a model of translational research in human cancer.p53 as an Effector or Inhibitor of Therapy Response.TRIM proteins and diseases.

P2860

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P2860

Pathways of retinoic acid- or arsenic trioxide-induced PML/RARalpha catabolism, role of oncogene degradation in disease remission.

http://www.wikidata.org/entity/Q34435558

description

2001 nî lūn-bûn

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Pathways of retinoic acid- or ...... radation in disease remission.

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Lallemand-Breitenbach V

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Zhu J

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de Thé H

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PML regulates p53 acetylation and premature senescence induced by oncogenic Ras

Leukemia-associated retinoic acid receptor alpha fusion partners, PML and PLZF, heterodimerize and colocalize to nuclear bodies

Interaction of thyroid-hormone receptor with a conserved transcriptional mediator

Ataxin-1 with an expanded glutamine tract alters nuclear matrix-associated structures

Conjugation with the ubiquitin-related modifier SUMO-1 regulates the partitioning of PML within the nucleus.

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

Coordinate regulation of RARgamma2, TBP, and TAFII135 by targeted proteolysis during retinoic acid-induced differentiation of F9 embryonal carcinoma cells

Role of the histone deacetylase complex in acute promyelocytic leukaemia

p300/MDM2 complexes participate in MDM2-mediated p53 degradation

Retinoic acid (RA) and As2O3 treatment in transgenic models of acute promyelocytic leukemia (APL) unravel the distinct nature of the leukemogenic process induced by the PML-RARalpha and PLZF-RARalpha oncoproteins

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10.1038/SJ.ONC.1204852

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49

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20

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1046166173

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