This is an abbreviated version! For detailed information about phosphogluconate dehydrogenase (NADP+-dependent, decarboxylating), go to the full flat file.
fragment. Its is proposed that plastid-lacking excavata acquire cyanobacterial gnd genes via eukaryote-to-eukaryote lateral gene transfer or primary endosymbiotic gene transfer early in eukaryotic evolution, and then lose either their pre-existing or cyanobacterial gene
fragment. Its is proposed that plastid-lacking excavata acquire cyanobacterial gnd genes via eukaryote-to-eukaryote lateral gene transfer or primary endosymbiotic gene transfer early in eukaryotic evolution, and then lose either their pre-existing or cyanobacterial gene
fragment. Its is proposed that plastid-lacking excavata acquire cyanobacterial gnd genes via eukaryote-to-eukaryote lateral gene transfer or primary endosymbiotic gene transfer early in eukaryotic evolution, and then lose either their pre-existing or cyanobacterial gene
fragment. Its is proposed that plastid-lacking excavata acquire cyanobacterial gnd genes via eukaryote-to-eukaryote lateral gene transfer or primary endosymbiotic gene transfer early in eukaryotic evolution, and then lose either their pre-existing or cyanobacterial gene
fragment. Its is proposed that plastid-lacking excavata acquire cyanobacterial gnd genes via eukaryote-to-eukaryote lateral gene transfer or primary endosymbiotic gene transfer early in eukaryotic evolution, and then lose either their pre-existing or cyanobacterial gene
fragment. Its is proposed that plastid-lacking excavata acquire cyanobacterial gnd genes via eukaryote-to-eukaryote lateral gene transfer or primary endosymbiotic gene transfer early in eukaryotic evolution, and then lose either their pre-existing or cyanobacterial gene
the strain is lacking the zinc-responsive transcriptional repressor Loz1 with the goal of identifying metabolic pathways that are altered by cellular zinc status
the strain is lacking the zinc-responsive transcriptional repressor Loz1 with the goal of identifying metabolic pathways that are altered by cellular zinc status