PPARδ induces estrogen receptor-positive mammary neoplasia through an inflammatory and metabolic phenotype linked to mTOR activation.
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Lipid-sensors, enigmatic-orphan and orphan nuclear receptors as therapeutic targets in breast-cancerTherapeutic targeting of replicative immortalityDisruptive environmental chemicals and cellular mechanisms that confer resistance to cell deathNCOA3 is a selective co-activator of estrogen receptor α-mediated transactivation of PLAC1 in MCF-7 breast cancer cells.Integrative and systemic approaches for evaluating PPARβ/δ (PPARD) function.Quantitative proteomic analysis reveals that anti-cancer effects of selenium-binding protein 1 in vivo are associated with metabolic pathwaysPPARδ and PGE2 signaling pathways communicate and connect inflammation to colorectal cancerPeroxisome proliferator-activated receptorβ/δ activation is essential for modulating p-Foxo1/Foxo1 status in functional insulin-positive cell differentiation.PPAR-delta promotes survival of breast cancer cells in harsh metabolic conditionsPPARδ as a Metabolic Initiator of Mammary Neoplasia and Immune ToleranceActivation of peroxisome proliferator-activated receptor-β/δ (PPAR-β/δ) inhibits human breast cancer cell line tumorigenicity.Suppression of PPARβ, and DHA treatment, inhibit NaV1.5 and NHE-1 pro-invasive activities.PPARs as determinants of the estrogen receptor lineage: use of synthetic lethality for the treatment of estrogen receptor-negative breast cancer.Targeting Peroxisome Proliferator-Activated Receptor-β/δ (PPARβ/δ) for Cancer Chemoprevention.ADAMTS1-mediated targeting of TSP-1 by PPARδ suppresses migration and invasion of breast cancer cells.PLAC1 as a serum biomarker for breast cancer.MMTV-NeuT/ATTAC mice: a new model for studying the stromal tumor microenvironment.PPARδ promotes tumor progression via activation of Glut1 and SLC1-A5 transcription.Transcriptomic response of breast cancer cells to anacardic acid.Plac1 Is a Key Regulator of the Inflammatory Response and Immune Tolerance In Mammary Tumorigenesis.Low-fat diet, and medium-fat diets containing coconut oil and soybean oil exert different metabolic effects in untrained and treadmill-trained mice.
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PPARδ induces estrogen receptor-positive mammary neoplasia through an inflammatory and metabolic phenotype linked to mTOR activation.
description
article científic
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article scientifique
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articolo scientifico
@it
artigo científico
@pt
bilimsel makale
@tr
scientific article published on 27 June 2013
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vedecký článok
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vetenskaplig artikel
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videnskabelig artikel
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vědecký článek
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name
PPARδ induces estrogen recepto ...... ype linked to mTOR activation.
@en
PPARδ induces estrogen recepto ...... ype linked to mTOR activation.
@nl
type
label
PPARδ induces estrogen recepto ...... ype linked to mTOR activation.
@en
PPARδ induces estrogen recepto ...... ype linked to mTOR activation.
@nl
prefLabel
PPARδ induces estrogen recepto ...... ype linked to mTOR activation.
@en
PPARδ induces estrogen recepto ...... ype linked to mTOR activation.
@nl
P2093
P2860
P1433
P1476
PPARδ induces estrogen recepto ...... ype linked to mTOR activation.
@en
P2093
Bhaskar Kallakury
Geeta Upadhyay
Hongyan Yuan
Junfeng Xiao
Levy Kopelovich
Michael E Fant
Rachel Umans
Robert I Glazer
P2860
P304
P356
10.1158/0008-5472.CAN-13-0322
P407
P577
2013-06-27T00:00:00Z