Uncoupling RARA transcriptional activation and degradation clarifies the bases for APL response to therapies. - Wikidata - awgldk - TriplyDB

Uncoupling RARA transcriptional activation and degradation clarifies the bases for APL response to therapies.

Uncoupling RARA transcriptional activation and degradation clarifies the bases for APL response to therapies.

http://www.wikidata.org/entity/Q36750049

about

Targeting of leukemia-initiating cells in acute promyelocytic leukemia Retinoic acid synergizes ATO-mediated cytotoxicity by precluding Nrf2 activity in AML cells Pin1-Targeted Therapy for Systemic Lupus Erythematosus Active Pin1 is a key target of all-trans retinoic acid in acute promyelocytic leukemia and breast cancer Targeting Transcription Factors in Cancer BCL-xL/MCL-1 inhibition and RARγ antagonism work cooperatively in human HL60 leukemia cells.A Novel Glycogen Synthase Kinase-3 Inhibitor Optimized for Acute Myeloid Leukemia Differentiation Activity.Induction of autophagy is a key component of all-trans-retinoic acid-induced differentiation in leukemia cells and a potential target for pharmacologic modulation Synergy against PML-RARa: targeting transcription, proteolysis, differentiation, and self-renewal in acute promyelocytic leukemia.Chemical or genetic Pin1 inhibition exerts potent anticancer activity against hepatocellular carcinoma by blocking multiple cancer-driving pathways.PML/RARa inhibits PTEN expression in hematopoietic cells by competing with PU.1 transcriptional activity.C/EBPα: critical at the origin of leukemic transformation.Retinoid receptor signaling and autophagy in acute promyelocytic leukemia.Retinoic acid signaling in cancer: The parable of acute promyelocytic leukemia.p53 as an Effector or Inhibitor of Therapy Response.PML-RAR alpha induces the downmodulation of HHEX: a key event responsible for the induction of an angiogenetic response.The isomerase PIN1 controls numerous cancer-driving pathways and is a unique drug target.All-trans retinoic acid and arsenic trioxide fail to derepress the monocytic differentiation driver Irf8 in acute promyelocytic leukemia cells.Comparative study of autophagy inhibition by 3MA and CQ on Cytarabine‑induced death of leukaemia cells.The autophagy scaffold protein ALFY is critical for the granulocytic differentiation of AML cells.Pml nuclear body disruption cooperates in APL pathogenesis and impairs DNA damage repair pathways in mice.The acute promyelocytic leukaemia success story: curing leukaemia through targeted therapies.Retinoic acid and arsenic trioxide sensitize acute promyelocytic leukemia cells to ER stress.Pin1 inhibition exerts potent activity against acute myeloid leukemia through blocking multiple cancer-driving pathways.Arsenic targets Pin1 and cooperates with retinoic acid to inhibit cancer-driving pathways and tumor-initiating cells

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P2860

Uncoupling RARA transcriptional activation and degradation clarifies the bases for APL response to therapies.

http://www.wikidata.org/entity/Q36750049

description

2013 nî lūn-bûn

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2013年论文

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2013年论文

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name

Uncoupling RARA transcriptiona ...... for APL response to therapies.

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type

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Uncoupling RARA transcriptiona ...... for APL response to therapies.

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Uncoupling RARA transcriptiona ...... for APL response to therapies.

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Uncoupling RARA transcriptiona ...... for APL response to therapies.

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P2093

Elodie Anthony

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Julien Ablain

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Julien Fonsart

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Laurent Peres

http://www.w3.org/2001/XMLSchema#string

Magdalena Leiva

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P2860

PML nuclear bodies

Identification of a retinoic acid responsive element in the retinoic acid receptor beta gene

Deconstructing a disease: RARalpha, its fusion partners, and their roles in the pathogenesis of acute promyelocytic leukemia

Use of all-trans retinoic acid in the treatment of acute promyelocytic leukemia

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

Positive and negative regulation of granulopoiesis by endogenous RARalpha

Eradication of acute promyelocytic leukemia-initiating cells through PML-RARA degradation

Retinoic acid and arsenic synergize to eradicate leukemic cells in a mouse model of acute promyelocytic leukemia

In vivo activation of cAMP signaling induces growth arrest and differentiation in acute promyelocytic leukemia.

Valproic acid induces differentiation and transient tumor regression, but spares leukemia-initiating activity in mouse models of APL.

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647-653

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10.1084/JEM.20122337

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3620357

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