50 research outputs found
ΠΠ΅ΡΠΎΠ΄ΠΈ ΡΠΏΡΠ°Π²Π»ΡΠ½Π½Ρ Π΅ΠΊΠΎΠ»ΠΎΠ³ΡΡΠ½ΠΈΠΌΠΈ ΡΠΈΠ·ΠΈΠΊΠ°ΠΌΠΈ Π² ΡΠΈΡΡΠ΅ΠΌΡ Π·Π°Π±Π΅Π·ΠΏΠ΅ΡΠ΅Π½Π½Ρ Π΅ΠΊΠΎΠ½ΠΎΠΌΡΡΠ½ΠΎΠ³ΠΎ ΡΠΎΠ·Π²ΠΈΡΠΊΡ ΡΠ΅Π³ΡΠΎΠ½Ρ
ΠΠ΅ΡΠΎΡ ΡΡΠ°ΡΡΡ Ρ Π΄ΠΎΡΠ»ΡΠ΄ΠΆΠ΅Π½Π½Ρ ΠΌΠ΅ΡΠΎΠ΄ΡΠ² ΡΠΏΡΠ°Π²Π»ΡΠ½Π½Ρ Π΅ΠΊΠΎΠ»ΠΎΠ³ΡΡΠ½ΠΈΠΌΠΈ ΡΠΈΠ·ΠΈΠΊΠ°ΠΌΠΈ Π² ΡΠΈΡΡΠ΅ΠΌΡ Π·Π°Π±Π΅Π·ΠΏΠ΅ΡΠ΅Π½Π½Ρ Π΅ΠΊΠΎΠ½ΠΎΠΌΡΡΠ½ΠΎΠ³ΠΎ ΡΠΎΠ·Π²ΠΈΡΠΊΡ ΡΠ΅Π³ΡΠΎΠ½Ρ
PCV18 Relative Efficacy of Bivalirudin vs. Heparin Alone in STEMI Patients Treated with Primary PCI β an Indirect Treatment Comparison
Hippocalcin functions as a calcium sensor in hippocampal LTD.
It is not fully understood how NMDAR-dependent LTD causes Ca2+-dependent endocytosis of AMPARs. Here we show that the neuronal Ca2+ sensor hippocalcin binds the ?2-adaptin subunit of the AP2 adaptor complex and that along with GluR2 these coimmunoprecipitate in a Ca2+-sensitive manner. Infusion of a truncated mutant of hippocalcin (HIP2-72) that lacks the Ca2+ binding domains prevents synaptically evoked LTD but has no effect on LTP. These data indicate that the AP2-hippocalcin complex acts as a Ca2+ sensor that couples NMDAR-dependent activation to regulated endocytosis of AMPARs during LTD