TCR-induced Ins(1,4,5)P3 production causes Ca2+ release from intracellular stores, which in turn relays a signal to the plasma membrane store-operated Ca2+ channel (ICRAC channel), causing it to open.
First-pass extracted concept
ICRAC channel
Aliases
Ca2+-release-activated Ca2+ current, SOC, store-operated Ca2+ channel
Evidence Snippets
Supporting Sources
Linked Claims
For B lymphocytes, calcium influx after BCR ligation is observed, but the review states that electrophysiological evidence for ICRAC in B cells was lacking and B-cell expression of this channel was unresolved.
In T cells, the TCR-activated calcium influx pathway is strongly supported to be identical to the store-operated ICRAC channel.
The initial antigen receptor-driven calcium signal in lymphocytes can involve multiple intracellular calcium channels, while the sustained phase depends on plasma membrane calcium entry together with intracellular channel contributions.
Antigen receptor ligation in lymphocytes induces a biphasic calcium response with an initial intracellular store-release phase followed by a prolonged extracellular calcium-dependent phase.