ReliaTech/Rabbit AntiHuman PlGF (Peptide)/102PA01S/100 µg

Antibodygeneration:

ProducedfromseraofrabbitsimmunizedwithahighlypurifiedN-terminalpeptideofhumanPlGF(placentagrowthfactor).Anti-PlGFwaspurifiedbyaffinitychromatographywithimmobilizedProteinA.

Antigen:

N-terminalpeptide(20aa)ofnativehumanPlGF

Stability:

Thelyophilizedantibodyisstableatroomtemperatureforupto1month.Thereconstitutedantibodyisstableforatleasttwoweeksat2-8°C.Frozenaliquotsarestableforatleast6monthswhenstoredat-20°C

Reconstitution:

Centrifugevialpriortoopening.Reconstituteinsterilewatertoaconcentrationof0.1-1.0mg/ml.

Description:

Placentagrowthfactor(PlGF)isamemberofthePDGF/VEGFfamilyofgrowthfactorsthatshareaconservedpatternofeightcysteines.AlternatesplicingresultsinatleastthreehumanmaturePlGFformscontaining131(PlGF1),152(PlGF2),and203(PlGF3)aminoacids(aa)respectively.OnlyPlGF2containsahighlybasicheparinbinding21aainsertattheC-terminus.Inthemouse,onlyonePlGFthatistheequivalentofhumanPlGF2hasbeenidentified.HumanPlGF1shares56%,55%,74%and95%aaidentitywiththeappropriateisoformofmouse,rat,canineandequinePlGF.PlGFismainlyfoundasvariablyglycosylated,secreted,55-60kDadisulfidelinkedhomodimers.MammaliancellsexpressingPlGFincludevilloustrophoblasts,decidualcells,erythroblasts,keratinocytesandsomeendothelialcells.CirculatingPlGFincreasesduringpregnancy,reachingapeakinmid-gestation;thisincreaseisattenuatedinpreeclampsia.However,deletionofPlGFinthemousedoesnotaffectdevelopmentorreproduction.Postnatally,micelackingPlGFshowimpairedangiogenesisinresponsetoischemia.PlGFbindsandsignalsthroughVEGFR1/Flt1,butnotVEGFR2/Flk-1/KDR,whileVEGFbindsbothbutsignalsonlythroughtheangiogenicreceptor,VEGFR2.PlGFandVEGFthereforecompeteforbindingtoVEGFR1,allowinghighPlGFtodiscourageVEGF/VEGFR1bindingandpromoteVEGF/VEGFR2mediatedangiogenesis.However,PlGF(especiallyPlGF1)andsomeformsofVEGFcanformdimersthatdecreasetheangiogeniceffectofVEGFonVEGFR2.PlGF2,butnotPLGF-1,showsheparindependentbindingofneuropilin(Npn)-1andNpn2.PlGFinducesmonocyteactivation,migration,andproductionofinflammatorycytokinesandVEGF.Theseactivitiesfacilitatewoundandbonefracturehealing,butalsocontributetoinflammationinactivesicklecelldiseaseandatherosclerosis.