iron transport through blood

Jron in blood Apotrans feuotransferin H2O2 2011 jessin fe2t Bindsto Trans jevin receptor fe3t Toxic Phylojevillin (plonts) export CSS -store 6,000 iron molecules Clathrin Animals - 3,000 Receptor & Invagination transported back to PM2 without iron iron transfeuin released toblood vesicle endosome irononly (fe3t) (acidicpHD) dissociate Fe2t regulate transfering reduced & felittin translation fe2t (toxic) fe2t transfering failfin 1/xc) feuitin fender reaction protein wheniron is high few receptors needed bothigh store fe2t jevitin in needer. avoid radical Fauilin mRNA (x) formation Iron responce element (IRE) High iron 5' Coding region (Ribose can translate with the Ap help of helicase CIFHA) YOTR IREBP inactive how iron IREBP high iron, iron bindsto active IREEP and make it inactive IREBPhoondon IRE active inactive codinarmin no translation

(b) Transfelin (1/2) investment 30TR IRE highiron 5' 3' An Degradation hight Q inactive P howiron conc active high iron active IP (REBP Lowiron AD Little degradation 5 3 more transferin Nitrogen Staivation produced GCN - General Control of Nitrogen metabolism in years NT , Transcriptionof some factors GCN-4- Hat AMAT Tf available when NI recruite GCN - 5 - HAT acetylation Gene activation Nitrogen starvation GCN2 an cIr2kinase Transcription of GCN4. actual GINNORF GENYORE MRNAbas Ashort ORFC code 10 residue peptide

if CIF2 inpfillenty. sbort ORF will be translated and ribosome detach,the GCN4 ORE will not be translated @ loweIf2 the short ORE will be skipped by the available eIf2. and the GGCNH ORF will be translated and this protein requite HAT (watson Innormal sbort ORF prevents translation of GCN4 560) In nitrogen starvation eIf2+ by ac tivity of GICN? kinase allow translation of GCNH ORF, since the chance of skippin the first 4 short ORE in high