PERK-dependent translationally regulated genes

FunctionFold change for induction in:Gene name and descriptionReference(s)
Perk+/+ cellsPerk−/− cells
Regulation of cell growth3.91.9NoneNoneIgfbp2: insulin-like growth factor binding protein 283 nephroblastoma overexpressed gene
Blood vessel formation4. VEGF and type I collagen inducible protein42
Cell adhesion2. poliovirus receptor
2.40.7NoneNoneThbs2: thrombospondin 210, 19
3.61.4NoneNonecspg2: chondroitin sulfate proteoglycan 2 (versican)13 procollagen, type VI, alpha 386
2.40.8NoneNonecol12a1: collagen, type XII, alpha 1 EGF-containing fibulin-like extracellular matrix protein 149
Collagen catabolism2.10.4NoneNonemmp13: matrix metalloproteinase 131 tissue inhibitor of metalloproteinase 378
Regulation of transcription2. AE binding protein 1
Ephrin receptor activityNoneNone2.60.7EphA4: ephrin receptor A499
Protein trasportation/folding2.51.5NoneNoneptprm: protein tyrosine phosphatase receptor type M ribosome binding protein 1 hypoxia up-regulated 1 (ORP150)73 slit-like 2 procollagen-lysine 1 2-oxoglutarate 5-dioxygenase 1 lysosomal membrane glycoprotein 2
Transporter activity2. aquaporin 1
Signal transduction2. growth factor receptor-bound protein 1068 platelet-derived growth factor receptor beta
2.40.8NoneNonestmn2: stathmin-like 2
Unknown4.6NoneNoneNonedcn: decorin zinc finger protein 503 tenascin C cytokine receptor-like factor 1
  • Results of microarray analyses to identify transcripts that were associated exclusively with high-molecular-weight polysomes in SV40-immortalized Perk+/+ MEFs following an acute response to hypoxic stress (4 h). Genespring 5.0 software was used to compare the relative expression of polysome-bound mRNAs from Perk+/+ and Perk−/− MEFs following acute normoxia (0 h poly) or hypoxia (4 h poly)-treated cells. Genes were exclusively induced >1.5-fold in the polysomes of Perk+/+ MEFs (4 h poly/0 h poly signal) and showed either a decrease or no significant change in their polysome association in Perk−/− MEFs (4 h poly/0 h poly signal). Candidates that demonstrated less than a twofold change in total cellular mRNA (4 h total/0 h total signal) were considered for further analysis. These genes were functionally clustered, and subsets of them are represented in this table. References are given for candidates with a described role in angiogenesis.