List of protein phosphosites in Jurkat cells that are increased by different combinations of PDE inhibitors

Jurkat Cell Data - PGE2 + PDE inhibitorsFold increase over control
GeneDescriptionSite#SequencePGE2 1 nMCIL 5 µMRol 10 µMIC BRL PF8CIL & ROLIBMXPF8 50 µMIBMX PF8 200 µM
RANBP2E3 Sumo-prot lig RanBP21509PRKQSLPA1.
MAGED2Melanoma-assoc antig D2200ARRASRG1.
SEC22BVesicle-traffic prot SEC22b137RNLGSINT1.
PWP1Periodic trypt prot 1 homolog485ARNSSISGP1.
HIST1H1EHistone H1.437KRKASGP1.
NUMA1Nucl mitotic apparatus pro11955LRRASMQ1.
NFRKBNuc factor rel to kappa-B BP310GRKGSLA1.
CADCAD protein - Dihydroorotase1343GRRLSSFV1.
MKI6Antigen KI-67538TKRKSLV1.
DGK2Diacylglycerol kinase zeta163LRRASSHL1.
  • The fold response of different inhibitors or combinations of inhibitors on the same site in each protein is shown. All but one protein has a good consensus PKA site. Each PDE inhibitor has an isozyme selectivity of at least 30–200-fold if used at appropriate concentrations. From (Beltejar et al., 2017).

  • BRL, BRL50481, a PDE7-selective inhibitor; Cil, cilostamide, a PDE3-selective inhibitor; IBMX, isobutyl-methyl-xanthine, a nonselective inhibitor that targets all PDEs except PDE8; IC, ITI-078, a PDE1-selective inhibitor; PF8, PF-04957325, a selective PDE8 inhibitor; PGE2, prostaglandin E2; Rol, rolipram, a PDE4 selective inhibitor.