about
Purinergic receptor-mediated rapid depletion of nuclear phosphorylated Akt depends on pleckstrin homology domain leucine-rich repeat phosphatase, calcineurin, protein phosphatase 2A, and PTEN phosphatasesPhosphatase and tensin homolog deleted on chromosome 10 (PTEN) and PH domain and leucine-rich repeat phosphatase cross-talk (PHLPP) in cancer cells and in transforming growth factor β-activated stem cellsCombined toxic exposures and human health: biomarkers of exposure and effectText mining for literature review and knowledge discovery in cancer risk assessment and researchExocrine pancreatic carcinogenesis and autotaxin expressionMEK-ERK-mediated phosphorylation of Mdm2 at Ser-166 in hepatocytes. Mdm2 is activated in response to inhibited Akt signalingA comparison and user-based evaluation of models of textual information structure in the context of cancer risk assessmentData and literature gathering in chemical cancer risk assessment.Phthalate diesters and their metabolites in human breast milk, blood or serum, and urine as biomarkers of exposure in vulnerable populations.Gender differences in chemical carcinogenesis in National Toxicology Program 2-year bioassays.Chemical induced alterations in p53 signaling.Automatic semantic classification of scientific literature according to the hallmarks of cancerExposure to polychlorinated biphenyls and prostate cancer: population-based prospective cohort and experimental studies.Toluene diisocyanate: Induction of the autotaxin-lysophosphatidic acid axis and its association with airways symptoms.Atorvastatin Decreases HBx-Induced Phospho-Akt in Hepatocytes via P2X Receptors.Silencing p110β prevents rapid depletion of nuclear pAkt.Statins exhibit anticancer effects through modifications of the pAkt signaling pathway.Emission of hexanal and carbon monoxide from storage of wood pellets, a potential occupational and domestic health hazard.Non-dioxin-like-PCBs phosphorylate Mdm2 at Ser166 and attenuate the p53 response in HepG2 cells.Mdm2 as a sensitive and mechanistically informative marker for genotoxicity induced by benzo[a]pyrene and dibenzo[a,l]pyrene.Statins and ATP regulate nuclear pAkt via the P2X7 purinergic receptor in epithelial cells.Dietary sphingolipids suppress a subset of preneoplastic rat liver lesions exhibiting high PTEN, low phospho-Akt and high levels of ceramide species.Grouping chemicals for health risk assessment: A text mining-based case study of polychlorinated biphenyls (PCBs).HMG-CoA reductase inhibitors, statins, induce phosphorylation of Mdm2 and attenuate the p53 response to DNA damage.Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) and PH domain and leucine-rich repeat phosphatase cross-talk (PHLPP) in cancer cells and in transforming growth factor β-activated stem cells.MEK-ERK-mediated phosphorylation of Mdm2 at Ser-166 in hepatocytes. Mdm2 IS ACTIVATED IN RESPONSE TO INHIBITED Akt SIGNALING.TCDD activates Mdm2 and attenuates the p53 response to DNA damaging agents.Hydroxyl metabolite of PCB 180 induces DNA damage signaling and enhances the DNA damaging effect of benzo[a]pyrene.PCB153, TCDD and estradiol compromise the benzo[a]pyrene-induced p53-response via FoxO3a.Non-dioxin-like PCBs interact with benzo[a]pyrene-induced p53-responses and inhibit apoptosis.Atorvastatin prevents ATP-driven invasiveness via P2X7 and EHBP1 signaling in PTEN-expressing prostate cancer cells.Sphingolipids suppress preneoplastic rat hepatocytes in vitro and in vivo.Characterizing the role of MDM2 in diethylnitrosamine induced acute liver damage and development of pre-neoplastic lesions.Heterozygous p53-deficient (+/-) mice develop fewer p53-negative preneoplastic focal liver lesions in response to treatment with diethylnitrosamine than do wild-type (+/+) mice.Induction of preneoplastic rat liver lesions with an attenuated p53 response by low doses of diethylnitrosamine.NAMPT (visfatin) and AKT1 genetic variants associate with myocardial infarction.ATM-activated autotaxin (ATX) propagates inflammation and DNA damage in lung epithelial cells: a new mode of action for silica-induced DNA damage?Cancer Hallmarks Analytics Tool (CHAT): a text mining approach to organize and evaluate scientific literature on cancer.Toluene diisocyanate exposure and autotaxin–lysophosphatidic acid signalling
P50
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P50
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Zweeds onderzoeker
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հետազոտող
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P106
P2038
Johan_Hoegberg