0000000000373155

AUTHOR

Michael Kracht

0000-0002-8501-043x

showing 2 related works from this author

Activation of NF-kappaB and IL-8 by yersinia enterocolitica invasin protein is conferred by engagement of rac1 and MAP kinase cascades.

2003

International audience; Yersinia enterocolitica triggers activation of the nuclear factor (NF)-kappaB and production of the proinflammatory chemokine interleukin (IL)-8 in intestinal epithelial cells. This activation is due to adhesion of the bacteria via their outer membrane protein invasin to the host cells. Using Clostridium difficile toxins that specifically inactivate small GTPases, and transfection of inhibitory proteins of the Rho-GTPases, we demonstrate that Rac1, but not Cdc42 or Rho, is required for activation of NF-kappaB by invasin. Invasin activated the mitogen activated protein kinases (MAPK) p38 and c-Jun N-terminal protein kinase (JNK) but not extracellular signal regulated …

rac1 GTP-Binding ProteinMAP Kinase Kinase 4MAP Kinase Signaling SystemRNA Stability[SDV]Life Sciences [q-bio]ImmunologyMitogen-activated protein kinase kinasep38 Mitogen-Activated Protein KinasesMicrobiologyBacterial AdhesionMAP2K703 medical and health sciencesBacterial ProteinsVirologyHumansASK1RNA Messengerc-RafAdhesins Bacterialcdc42 GTP-Binding ProteinrhoB GTP-Binding ProteinYersinia enterocolitica030304 developmental biologyMitogen-Activated Protein Kinase Kinases0303 health sciencesbiologyMAP kinase kinase kinase030306 microbiologyInterleukin-8Cyclin-dependent kinase 2JNK Mitogen-Activated Protein KinasesNF-kappa BProtein kinase RMolecular biologyCell biologybiology.proteinCyclin-dependent kinase 9Mitogen-Activated Protein KinasesrhoA GTP-Binding ProteinHeLa CellsSignal Transduction
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PHD3 Controls Lung Cancer Metastasis and Resistance to EGFR Inhibitors through TGFα.

2018

Abstract Lung cancer is the leading cause of cancer-related death worldwide, in large part due to its high propensity to metastasize and to develop therapy resistance. Adaptive responses to hypoxia and epithelial–mesenchymal transition (EMT) are linked to tumor metastasis and drug resistance, but little is known about how oxygen sensing and EMT intersect to control these hallmarks of cancer. Here, we show that the oxygen sensor PHD3 links hypoxic signaling and EMT regulation in the lung tumor microenvironment. PHD3 was repressed by signals that induce EMT and acted as a negative regulator of EMT, metastasis, and therapeutic resistance. PHD3 depletion in tumors, which can be caused by the EM…

0301 basic medicineCancer ResearchEpithelial-Mesenchymal TransitionLung NeoplasmsMice NudeAntineoplastic AgentsSMADDrug resistanceMetastasisHypoxia-Inducible Factor-Proline DioxygenasesMitochondrial Proteins03 medical and health sciencesErlotinib HydrochlorideMice0302 clinical medicineDownregulation and upregulationCell Line TumorTumor MicroenvironmentMedicineAnimalsHumansNeoplasm MetastasisLung cancerProtein Kinase InhibitorsEGFR inhibitorsbusiness.industryIntracellular Signaling Peptides and ProteinsCancerTransforming Growth Factor alphamedicine.diseaseHCT116 CellsXenograft Model Antitumor AssaysCell HypoxiaErbB Receptors030104 developmental biologyOncologyA549 CellsDrug Resistance Neoplasm030220 oncology & carcinogenesisembryonic structuresCancer researchFemaleErlotinibbusinessApoptosis Regulatory Proteinsmedicine.drugCancer research
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