ATF6alpha-Rheb-mTOR signaling promotes survival of dormant tumor cells in vivo. - Wikidata - wikimedia - TriplyDB

ATF6alpha-Rheb-mTOR signaling promotes survival of dormant tumor cells in vivo.

ATF6alpha-Rheb-mTOR signaling promotes survival of dormant tumor cells in vivo.

http://www.wikidata.org/entity/Q36802449

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ERp29 induces breast cancer cell growth arrest and survival through modulation of activation of p38 and upregulation of ER stress protein p58IPK Recapitulating the Tumor Ecosystem Along the Metastatic Cascade Using 3D Culture Models Glioblastoma Circulating Cells: Reality, Trap or Illusion?DangER: protein ovERload. Targeting protein degradation to treat myeloma Mechanisms of disseminated cancer cell dormancy: an awakening field Tumor cell dormancy PDK4 protein promotes tumorigenesis through activation of cAMP-response element-binding protein (CREB)-Ras homolog enriched in brain (RHEB)-mTORC1 signaling cascade 6-Shogaol induces apoptosis in human leukemia cells through a process involving caspase-mediated cleavage of eIF2α PERK Integrates Oncogenic Signaling and Cell Survival During Cancer Development Mfn2 modulates the UPR and mitochondrial function via repression of PERK Tumorigenic and Immunosuppressive Effects of Endoplasmic Reticulum Stress in Cancer Development of an anti-angiogenic therapeutic model combining scAAV2-delivered siRNAs and noninvasive photoacoustic imaging of tumor vasculature development Endoplasmic reticulum stress-activated transcription factor ATF6α requires the disulfide isomerase PDIA5 to modulate chemoresistance New Insights into the Pathogenesis of Alcohol-Induced ER Stress and Liver Diseases Dormancy of metastatic melanoma Regulation of basal cellular physiology by the homeostatic unfolded protein response mTOR signaling in lymphangioleiomyomatosis The best of both worlds - managing the cancer, saving the bone.Transient mTOR inhibition facilitates continuous growth of liver tumors by modulating the maintenance of CD133+ cell populations.The Unfolded Protein Response, Degradation from Endoplasmic Reticulum and Cancer NR2F1 controls tumour cell dormancy via SOX9- and RARβ-driven quiescence programmes.Mechanisms governing metastatic dormancy and reactivation.ERK1/2 and p38α/β signaling in tumor cell quiescence: opportunities to control dormant residual disease.Curcumin differentially regulates endoplasmic reticulum stress through transcriptional corepressor SMILE (small heterodimer partner-interacting leucine zipper protein)-mediated inhibition of CREBH (cAMP responsive element-binding protein H)Identification of markers that functionally define a quiescent multiple myeloma cell sub-population surviving bortezomib treatment p38α mediates cell survival in response to oxidative stress via induction of antioxidant genes: effect on the p70S6K pathway Cell intrinsic and extrinsic activators of the unfolded protein response in cancer: Mechanisms and targets for therapy The specialized unfolded protein response of B lymphocytes: ATF6α-independent development of antibody-secreting B cells.PERK utilizes intrinsic lipid kinase activity to generate phosphatidic acid, mediate Akt activation, and promote adipocyte differentiation Staying alive: metabolic adaptations to quiescence Cancer drug pan-resistance: pumps, cancer stem cells, quiescence, epithelial to mesenchymal transition, blocked cell death pathways, persisters or what?The impact of the unfolded protein response on human disease Interplay between unfolded protein response and autophagy promotes tumor drug resistance Quiescent fibroblasts are protected from proteasome inhibition-mediated toxicity Suppression of the GTPase-activating protein RGS10 increases Rheb-GTP and mTOR signaling in ovarian cancer cells.Regulation of tumor cell dormancy by tissue microenvironments and autophagy.Tumour dormancy and clinical implications in breast cancer.Computational identification of a p38SAPK-regulated transcription factor network required for tumor cell quiescence Inhibition of eIF2alpha dephosphorylation maximizes bortezomib efficiency and eliminates quiescent multiple myeloma cells surviving proteasome inhibitor therapy Mirk regulates the exit of colon cancer cells from quiescence.

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P2860

ATF6alpha-Rheb-mTOR signaling promotes survival of dormant tumor cells in vivo.

http://www.wikidata.org/entity/Q36802449

description

2008 nî lūn-bûn

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2008年の論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年论文

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2008年论文

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2008年论文

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name

ATF6alpha-Rheb-mTOR signaling promotes survival of dormant tumor cells in vivo.

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ATF6alpha-Rheb-mTOR signaling promotes survival of dormant tumor cells in vivo.

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type

label

ATF6alpha-Rheb-mTOR signaling promotes survival of dormant tumor cells in vivo.

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ATF6alpha-Rheb-mTOR signaling promotes survival of dormant tumor cells in vivo.

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prefLabel

ATF6alpha-Rheb-mTOR signaling promotes survival of dormant tumor cells in vivo.

@ast

ATF6alpha-Rheb-mTOR signaling promotes survival of dormant tumor cells in vivo.

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PNAS.0800939105

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Proceedings of the National Academy of Sciences of the United States of America

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ATF6alpha-Rheb-mTOR signaling promotes survival of dormant tumor cells in vivo.

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Denis M Schewe

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Julio A Aguirre-Ghiso

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P2860

XBP1 mRNA is induced by ATF6 and spliced by IRE1 in response to ER stress to produce a highly active transcription factor

Requirement of the p38 mitogen-activated protein kinase signalling pathway for the induction of the 78 kDa glucose-regulated protein/immunoglobulin heavy-chain binding protein by azetidine stress: activating transcription factor 6 as a target for st

ONCOMINE: a cancer microarray database and integrated data-mining platform

Multiclass cancer diagnosis using tumor gene expression signatures

Growing roles for the mTOR pathway

Systemic spread is an early step in breast cancer

Inhibition of proliferation by PERK regulates mammary acinar morphogenesis and tumor formation.

Active mutants of the human p38alpha mitogen-activated protein kinase.

Urokinase receptor and fibronectin regulate the ERK(MAPK) to p38(MAPK) activity ratios that determine carcinoma cell proliferation or dormancy in vivo.

Mechanism of p38 MAP kinase activation in vivo.

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10519-10524

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105

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2492459

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