Ontology highlight
ABSTRACT:
SUBMITTER: Tong BC
PROVIDER: S-EPMC5384262 | biostudies-literature | 2016 Sep
REPOSITORIES: biostudies-literature
Tong Benjamin Chun-Kit BC Lee Claire Shuk-Kwan CS Cheng Wing-Hei WH Lai Kwok-On KO Foskett J Kevin JK Cheung King-Ho KH
Science signaling 20160906 444
Some forms of familial Alzheimer's disease (FAD) are caused by mutations in presenilins (PSs), catalytic components of a γ-secretase complex that cleaves target proteins, including amyloid precursor protein (APP). Calcium (Ca(2+)) dysregulation in cells with these FAD-causing PS mutants has been attributed to attenuated store-operated Ca(2+) entry [SOCE; also called capacitative Ca(2+) entry (CCE)]. CCE occurs when STIM1 detects decreases in Ca(2+) in the endoplasmic reticulum (ER) and activates ...[more]