  Release of $Ca^{2+}$ from endoplasmatic retriculum (ER) $Ca^{2+}$ stores
causes stromal interaction molecules (STIM) in the ER membrane and ORAI
proteins in the plasma membrane (PM) to interact and form the $Ca^{2+}$ release
activated $Ca^{2+}$ (CRAC) channels, which represent a major $Ca^{2+}$ entry
route in non-excitable cells and thus control various cell functions. It is
experimentally possible to mutate ORAI1 proteins and therefore modify,
especially block, the $Ca^{2+}$ influx into the cell. On the basis of the model
of Hoover and Lewis (2011) [Hoover P J and Lewis R S, 2011], we formulate a
reaction-diffusion model to quantify the STIM1-ORAI1 interaction during CRAC
channel formation and analyze different ORAI1 channel stoichiometries and
different ratios of STIM1 and ORAI1 in comparison with experimental data. We
incorporate the inhibition of ORAI1 channels by ROS into our model and
calculate its contribution to the CRAC channel amplitude. We observe a large
decrease of the CRAC channel amplitude evoked by mutations of ORAI1 proteins.
