PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32660632-10 2020 Suppression of mTORC1/p70S6K pathway by either rapamycin or p70S6K knockdown promoted heterochromatin organization and ameliorated Dox- or H2O2-induced DNA damage and senescence. Doxorubicin 131-134 CREB regulated transcription coactivator 1 Mus musculus 15-21 34893642-8 2021 Silencing MSMO1 could significantly enhance the sensitivity of MDA-MB-231 cells to paclitaxel and doxorubicin through modulating mTORC1 signaling pathway. Doxorubicin 98-109 CREB regulated transcription coactivator 1 Mus musculus 129-135 34697389-3 2021 Low-dose doxorubicin (DOX) treatment induced REDD1 expression in cultured vascular and lymphatic endothelial cells and subsequently repressed the mRNA expression of mTORC1-dependent translation of vascular endothelial growth factor receptor (Vegfr)-2/3, resulting in the inhibition of VEGF-mediated angiogenesis and lymphangiogenesis. Doxorubicin 9-20 CREB regulated transcription coactivator 1 Mus musculus 165-171 34697389-3 2021 Low-dose doxorubicin (DOX) treatment induced REDD1 expression in cultured vascular and lymphatic endothelial cells and subsequently repressed the mRNA expression of mTORC1-dependent translation of vascular endothelial growth factor receptor (Vegfr)-2/3, resulting in the inhibition of VEGF-mediated angiogenesis and lymphangiogenesis. Doxorubicin 22-25 CREB regulated transcription coactivator 1 Mus musculus 165-171 33912444-11 2021 Moreover, rapamycin, an inhibitor of mTOR complex 1 (mTORC1), downregulated BCRP expression and enhanced the effects of particular drugs, including doxorubicin and paclitaxel. Doxorubicin 148-159 CREB regulated transcription coactivator 1 Mus musculus 53-59 34488932-3 2021 DOX treatment induced REDD1 expression in bone marrow mononuclear cells (BMMNCs) and subsequently reduced mTORC1-dependent translation of endothelial growth factor (VEGF) receptor (Vegfr)-2 mRNA, but not that of the mRNA transcripts for Vegfr-1, epidermal growth factor receptor, and insulin-like growth factor-1 receptor. Doxorubicin 0-3 CREB regulated transcription coactivator 1 Mus musculus 106-112 28767526-11 2017 CONCLUSION: These data suggest that DOX may inhibit mTORC1 activity and reduce MHCI and MHCIIa fiber size, potentially through elevated REDD1, and that exercise may provide a therapeutic strategy to preserve skeletal muscle size during chronic DOX treatment. Doxorubicin 36-39 CREB regulated transcription coactivator 1 Mus musculus 52-58 31973180-7 2020 Our results demonstrate that the 5 mixture prevents the DOX-dependent mitochondrial damage and oxidative stress better than the previous BCAAem, implying a KLF15/eNOS/mTORC1 signaling axis. Doxorubicin 56-59 CREB regulated transcription coactivator 1 Mus musculus 167-173 31377057-3 2019 Adriamycin administration elicited early activation of TGF-beta-ERK1/2-mTORC1 in podocytes, which persisted at later stages of albuminuria and glomerulosclerosis. Doxorubicin 0-10 CREB regulated transcription coactivator 1 Mus musculus 71-77 31026186-3 2019 Here, we show that sestrin 1 and sestrin 2, members of the sestrin family of proteins that are stress-inducible regulators of metabolism, are critical for suppressing doxorubicin cardiotoxicity and coordinating the AMPK-mammalian target of rapamycin complex 1 (mTORC1) autophagy signaling network for cardioprotection. Doxorubicin 167-178 CREB regulated transcription coactivator 1 Mus musculus 261-267 31377057-0 2019 Inhibition of the ERK1/2-mTORC1 axis ameliorates proteinuria and the fibrogenic action of transforming growth factor-beta in Adriamycin-induced glomerulosclerosis. Doxorubicin 125-135 CREB regulated transcription coactivator 1 Mus musculus 25-31 31377057-2 2019 Here, we identified the regulation of mammalian target of rapamycin complex1 (mTORC1) by TGF-beta via extracellular signal-regulated kinase-1/2 (ERK1/2) in the Adriamycin (ADR)-induced murine model of focal segmental glomerulosclerosis. Doxorubicin 160-170 CREB regulated transcription coactivator 1 Mus musculus 78-84 29475062-5 2018 DOX inhibited autophagy through activating E2F1/mammalian target of rapamycin complex 1 (mTORC1) pathway and further induced apoptosis by activating E2F1/AMP-activated protein kinase alpha2 (AMPKalpha2) pathway in starved H9C2 cells. Doxorubicin 0-3 CREB regulated transcription coactivator 1 Mus musculus 89-95 26271039-10 2015 Finally using pharmacological inhibitors of the PI3K pathway, we showed that insulin-mediated activation of the PI3K/Akt/mTORC1 pathway prevented doxorubicin-induced proteasome-mediated degradation of Sp1. Doxorubicin 146-157 CREB regulated transcription coactivator 1 Mus musculus 121-127 27488521-11 2016 Blocking of the mTORC1 kinase induces differentiation of tumor-initiating cells and allows their subsequent depletion using the chemotherapeutic drug doxorubicin. Doxorubicin 150-161 CREB regulated transcription coactivator 1 Mus musculus 16-22 25641920-4 2015 However, the synthetic selenadiazole derivatives effectively potentiated the cellular uptake of DOX and enhanced the antiproliferative activity of DOX on HepG2 cells by induction of apoptosis, via regulation of ROS-mediated AMPK activation, inhibition of mTORC1, and an increase in DNA damage. Doxorubicin 147-150 CREB regulated transcription coactivator 1 Mus musculus 255-261 26026051-4 2015 In this study, we examined the interaction between the dual mTORC1/2 inhibitor OSI-027 and doxorubicin in vitro and in vivo. Doxorubicin 91-102 CREB regulated transcription coactivator 1 Mus musculus 60-66 21274754-6 2011 Evidence in support of the activation of AMPK contributing to Doxorubicin-induced H9c2 cell death/apoptosis--probably by modulating multiple downstream signal targets, including regulating JNK, p53, and inhibiting mTORC1--is provided in this article. Doxorubicin 62-73 CREB regulated transcription coactivator 1 Mus musculus 214-220 22647622-6 2012 Simultaneous inhibition of class I PI3K and mTORC1 by ZSTK474 combined with Rapamycin additively or synergistically reduced cell viability whereas responses to the PI3K pathway inhibitors in combination with conventional drug Doxorubicin were cell line-dependent. Doxorubicin 226-237 CREB regulated transcription coactivator 1 Mus musculus 44-50 20802518-0 2010 Exogenous cell-permeable C6 ceramide sensitizes multiple cancer cell lines to Doxorubicin-induced apoptosis by promoting AMPK activation and mTORC1 inhibition. Doxorubicin 78-89 CREB regulated transcription coactivator 1 Mus musculus 141-147