Uncoupling RARA transcriptional activation and degradation clarifies the bases for APL response to therapies.
about
Targeting of leukemia-initiating cells in acute promyelocytic leukemiaRetinoic acid synergizes ATO-mediated cytotoxicity by precluding Nrf2 activity in AML cellsPin1-Targeted Therapy for Systemic Lupus ErythematosusActive Pin1 is a key target of all-trans retinoic acid in acute promyelocytic leukemia and breast cancerTargeting Transcription Factors in CancerBCL-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 modulationSynergy 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
P2860
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P2860
Uncoupling RARA transcriptional activation and degradation clarifies the bases for APL response to therapies.
description
2013 nî lūn-bûn
@nan
2013年の論文
@ja
2013年論文
@yue
2013年論文
@zh-hant
2013年論文
@zh-hk
2013年論文
@zh-mo
2013年論文
@zh-tw
2013年论文
@wuu
2013年论文
@zh
2013年论文
@zh-cn
name
Uncoupling RARA transcriptiona ...... for APL response to therapies.
@en
type
label
Uncoupling RARA transcriptiona ...... for APL response to therapies.
@en
prefLabel
Uncoupling RARA transcriptiona ...... for APL response to therapies.
@en
P2093
P2860
P356
P1476
Uncoupling RARA transcriptiona ...... for APL response to therapies.
@en
P2093
Elodie Anthony
Julien Ablain
Julien Fonsart
Laurent Peres
Magdalena Leiva
P2860
P304
P356
10.1084/JEM.20122337
P407
P577
2013-03-18T00:00:00Z