about
Guidelines for the use and interpretation of assays for monitoring autophagyCritical role for Daxx in regulating Mdm2CARPs enhance p53 turnover by degrading 14-3-3sigma and stabilizing MDM2Suppression of caspase-8- and -10-associated RING proteins results in sensitization to death ligands and inhibition of tumor cell growthhADA3 is required for p53 activitySilencing of the novel p53 target gene Snk/Plk2 leads to mitotic catastrophe in paclitaxel (taxol)-exposed cellsWAF1, a potential mediator of p53 tumor suppressionThe antiapoptotic decoy receptor TRID/TRAIL-R3 is a p53-regulated DNA damage-inducible gene that is overexpressed in primary tumors of the gastrointestinal tractTat-binding protein-1, a component of the 26S proteasome, contributes to the E3 ubiquitin ligase function of the von Hippel-Lindau proteinBID regulation by p53 contributes to chemosensitivityTransactivation of repair genes by BRCA1KILLER/DR5 is a DNA damage-inducible p53-regulated death receptor geneFADD: essential for embryo development and signaling from some, but not all, inducers of apoptosisEGF-mediated regulation of IGFBP-3 determines esophageal epithelial cellular response to IGF-IER stress regulates myeloid-derived suppressor cell fate through TRAIL-R-mediated apoptosisCaspase 10 levels are increased following DNA damage in a p53-dependent mannerMolecular definitions of cell death subroutines: recommendations of the Nomenclature Committee on Cell Death 2012Circulating Tumor Cells Versus Circulating Tumor DNA in Colorectal Cancer: Pros and Cons.Essential versus accessory aspects of cell death: recommendations of the NCCD 2015.Acoustic separation of circulating tumor cells.Yeast two-hybrid screening as a means of deciphering tumor suppressor pathways.Identification of inhibitors of TRAIL-induced death (ITIDs) in the TRAIL-sensitive colon carcinoma cell line SW480 using a genetic approach.Differentiation of vascular and non-vascular skin spectral signatures using in vivo hyperspectral radiometric imaging: implications for monitoring angiogenesis.Hyperspectral image analysis of live cells in various cell cycle stages.Visualization and enrichment of live putative cancer stem cell populations following p53 inactivation or Bax deletion using non-toxic fluorescent dyes.Regulation of p53 downstream genes.The NFκB inhibitor, SN50, induces differentiation of glioma stem cells and suppresses their oncogenic phenotypeApoptotic circulating tumor cells (CTCs) in the peripheral blood of metastatic colorectal cancer patients are associated with liver metastasis but not CTCsDetection of circulating tumor cells in the cerebrospinal fluid of a patient with a solitary metastasis from breast cancer: A case reportPIGN gene expression aberration is associated with genomic instability and leukemic progression in acute myeloid leukemia with myelodysplastic features.Deoxycholic acid (DCA) causes ligand-independent activation of epidermal growth factor receptor (EGFR) and FAS receptor in primary hepatocytes: inhibition of EGFR/mitogen-activated protein kinase-signaling module enhances DCA-induced apoptosis.Induction of p21(WAF1/CIP1) and inhibition of Cdk2 mediated by the tumor suppressor p16(INK4a)Apoptotic threshold is lowered by p53 transactivation of caspase-6Epidermal growth factor receptor regulates aberrant expression of insulin-like growth factor-binding protein 3Tissue specific expression of p53 target genes suggests a key role for KILLER/DR5 in p53-dependent apoptosis in vivo.p53-Dependent and p53-independent induction of insulin-like growth factor binding protein-3 by deoxyribonucleic acid damage and hypoxia.DNA replication blockade impairs p53-transactivationCheckpoint genes in cancer.Targeting TRAIL death receptor 4 with trivalent DR4 Atrimer complexes.IGFBP-3 regulates esophageal tumor growth through IGF-dependent and independent mechanisms.
P50
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P50
description
Forscher
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investigador
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ricercatore
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wetenschapper
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研究者
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Wafik S. El-Deiry
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el-Deiry WS
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type
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Wafik S. El-Deiry
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el-Deiry WS
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el-Deiry WS
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Wafik S. El-Deiry
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el-Deiry WS
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el-Deiry WS
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el-Deiry WS
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P31
P496
0000-0002-9577-8266