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Signosis/IFN-a/ISRE Luciferase Reporter HeLa Stable Cell Line/SL-0052-NP/1 Ea
Description:
IFN-α/ISREResponsiveLuciferaseReporterHeLaCellLineisderivedhumancervicalcancer,andstablyexpressfireflyluciferasereportergeneunderthecontrolofIFN-α/ISREresponseelement.ThiscelllineisanidealcellularmodelformonitoringtheactivationofTYK2andJAK1responsePathwaytriggeredbystimulitreatment,enforcedgeneexpressionandgeneknockdown.Principle:
Interferon-alpha(IFN-α)bindstoreceptorsubunitsIFNαR1andIFNαR2onthecellsurface,whichinitiatethephosphorylationofTYK2andJAK1andtriggerdownstreamcascadeofJAK-Statsignaltransductionpathways.IFN-αcanalsoinducetheformationofInterferon-stimulatedgenefactor3(ISGF3),composedofSTAT1,STAT2,andIRF9.TheISGF3complexesbindISRE(IFN-stimulatedresponseelements)furtherinducingthetranscriptionofIFN-stimulatedgeneswhichcontainISREswithintheirpromotersthatleadstotranscriptionofselectedgenes.SignosisdevelopedtheIFN-α/ISREluciferasereporterstablecelllinetomonitorIFN-αassociatedJAK-Statpathway.
PrinciplebehindTFluciferasereporter. TFluciferasereporterstablecelllineutilizesartificialpromoterconstructstodriveluciferaseexpression. Thepromoterregioncanconsistsofmultiplerepeatsofacis-elementTFbindingsite,aDNAfragmentfromthepromoterregionofaknownTFdownstreamgene,oraDNAfragmentcontainingputative/knownTFbindingsites. ThereareseveralwaysthataTFcanbeactivated,suchasthroughextracellularstimuliorthroughintracellularsignalingpathways. Onceactivated,theTFtranslocatestothenucleusandofteninteractswithrelevantco-factorstodrivegeneexpression. Onceluciferaseisexpressed,itcangeneratelightinanenzymaticassayandtheamountoflightmeasuredispositivelycorrelatedwiththelevelofTFactivation. |
Data:
IFN-α/ISREDualResponsofLuciferaseReporterHeLacells. Cellsweretreatedwith20ng/mlIFN-α,20ng/mlIFN-γ,20ng/mlTNF-αand10ug/mlpoly(I:C)inDMEM/0.1%FBSmediumfor16hours.
