| Abstrakt: |
Ca2+ ions are signaling molecules responsible for controlling developmental processes, including fertilization, differentiation, proliferation, and transcription factor activation. Various cellular functions are regulated by changes in cytoplasmic Ca2+, including gene transcription and expression, protein synthesis, modification, folding and secretion, cell motility, cytoplasmic and mitochondrial energy metabolism, cell cycle progression, and apoptosis. Endoplasmic reticulum is an important Ca2+ storage organelle involved in virtually every aspect of Ca2+ homeostasis. Endoplasmic reticulum luminal Ca2+-binding chaperones such as calreticulin are critical for buffering endoplasmic reticulum Ca2+. In mice, calreticulin deficiency is lethal in utero because of the compromised Ca2+ storage capacity in the endoplasmic reticulum and disrupted InsP3 receptor-mediated Ca2+ release. A disturbance in Ca2+ release results in impaired cardiac development due to inhibited Ca2+-dependent transcriptional pathways. Calreticulin and the endoplasmic reticulum are the key upstream elements for calcineurin in Ca2+-signaling pathways. In contrast upregulation of calreticulin and overloading endoplasmic reticulum with Ca2+ leads to cardiac arrhythmias and impaired development of the cardiac conductive system. [ABSTRACT FROM AUTHOR] |
