0000000000481909

AUTHOR

Gerd Klock

showing 4 related works from this author

Nerve growth factor and epidermal growth factor stimulate clusterin gene expression in PC12 cells

1999

Clusterin (apolipoprotein J) is an extracellular glycoprotein that might exert functions in development, cell death and lipid transport. Clusterin gene expression is elevated at sites of tissue remodelling, such as differentiation and apoptosis; however, the signals responsible for this regulation have not been identified. We use here the clusterin gene as a model system to examine expression in PC12 cells under the control of differentiation and proliferation signals produced by nerve growth factor (NGF) and by epidermal growth factor (EGF) respectively. NGF induced clusterin mRNA, which preceded neurite outgrowth typical of neuronal differentiation. EGF also activated the clusterin mRNA, …

Transcriptional ActivationProgrammed cell deathNeuriteMolecular Sequence DataResponse ElementsTransfectionBinding CompetitivePC12 CellsBiochemistryEpidermal growth factorConsensus SequenceNeuritesAnimalsNerve Growth FactorsRNA MessengerCloning MolecularPromoter Regions GeneticMolecular BiologyGlycoproteinsSequence DeletionNeuronsRegulation of gene expressionMessenger RNABase SequenceEpidermal Growth FactorClusterinbiologyKinaseCell DifferentiationDNACell BiologyMolecular biologyeye diseasesRatsTranscription Factor AP-1ClusterinNerve growth factorbiology.proteinsense organsCell DivisionMolecular ChaperonesSignal TransductionResearch ArticleBiochemical Journal
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Chapter 7 Cell Protective Functions of Secretory Clusterin (sCLU)

2009

Secretory clusterin (sCLU) is found as an 80-kDa glycoprotein in virtually all body fluids, in serum it is associated with high-density lipoprotein (HDL). Here, we discuss demonstrated and proposed mechanisms of the cytoprotective functions of sCLU in instances of apoptosis, necrosis, and disease. These include prevention from cell damage by lipid oxidation in blood vessels, removal of dead cell remnants in tissues undergoing various forms of cell death, and clearance of harmful extracellular molecules such as amyloid beta (Aβ) by endocytosis or transcytosis. All these functions may reflect the propensity of sCLU to bind to a wide spectrum of hydrophobic molecules on one hand and to specifi…

Cell signalingTranscytosisClusterinbiologyLipid oxidationLDL receptorbiology.proteinSignal transductionReceptorEndocytosisCell biology
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Apoptotic Cell Debris and Phosphatidylserine-Containing Lipid Vesicles Induce Apolipoprotein J (Clusterin) Gene Expression in Vital Fibroblasts

2001

The molecular events in cells undergoing programmed cell death (apoptosis) are well studied; however, the response of the surviving neighbor cells to local cell death is largely uncharacterized. Apolipoprotein J (clusterin) is an 80-kDa glycoprotein that has been implied in cytoprotection of the vital cells, presumably by assisting in the clearance of apoptotic vesicles and membrane remnants. Its mRNA is specifically up-regulated in the vital cells of apoptotic tissues. The molecular mechanisms, however, leading to this response are not known. We here show that exposure of vital fibroblasts to apoptotic vesicles, disrupted vital cells, and trypsin-treated membrane remnants induces apoJ mRNA…

Programmed cell deathEndocytic cycleGene ExpressionApoptosisPhosphatidylserinesCell Linechemistry.chemical_compoundCricetinaeAnimalsTrypsinGlycoproteinsClusterinbiologyVesicleCell BiologyPhosphatidylserinePhosphatidic acidFibroblastsLipid MetabolismMolecular biologyCytoprotectionRatsCell biologyClusterinchemistryApoptosisbiology.proteinMolecular ChaperonesExperimental Cell Research
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Differential regulation of the clusterin gene by Ha-ras and c-myc oncogenes and during apoptosis

1998

Clusterin (ApoJ) is an extracellular glycoprotein expressed during processes of tissue differentiation and regression that involve programmed cell death (apoptosis). Increased clusterin expression has also been found in tumors, however, the mechanism underlying this induction is not known. Apoptotic processes in tumors could be responsible for clusterin gene activation. Alternatively, oncogenic mutations could modulate signal transduction, thereby inducing the gene. We examined the response of the rat clusterin gene to two oncogenes, Ha-ras and c-myc, in transfected Rat1 fibroblasts. While c-myc overexpression did not modify clusterin gene activity, the Ha-ras oncogene produced a seven to t…

Cell signalingProgrammed cell deathUltraviolet RaysPhysiologyRecombinant Fusion ProteinsClinical BiochemistryGenes mycApoptosisDNA FragmentationBiologyTransfectionProto-Oncogene Proteins c-mycProto-Oncogene Proteins p21(ras)AnimalsRNA MessengerCell Line TransformedGlycoproteinsOncogeneClusterinCell CycleCell BiologyTransfectionFibroblastsCell cycleeye diseasesRatsClusterinGenes rasApoptosisMutationCancer researchbiology.proteinsense organsSignal transductionMolecular ChaperonesSignal TransductionJournal of Cellular Physiology
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