The nucleoporin RanBP2 tethers the cAMP effector Epac1 and inhibits its catalytic activity.

Cyclic adenosine monophosphate (cAMP) is a second messenger that relays a wide range of hormone responses. In this paper, we demonstrate that the nuclear pore component RanBP2 acts as a negative regulator of cAMP signaling through Epac1, a cAMP-regulated guanine nucleotide exchange factor for Rap. We show that Epac1 directly interacts with the zinc fingers (ZNFs) of RanBP2, tethering Epac1 to the nuclear pore complex (NPC).

Possible role of the innate immunity in temporal lobe epilepsy.

Purpose: Temporal lobe epilepsy (TLE) is a multifactorial disease often involving the hippocampus. So far the etiology of the disease has remained elusive. In some pharmacoresistant TLE patients the hippocampus is surgically resected as treatment.