Attached is the final output. Should there be a need to review the work; I'm readily available. Thanks

Running head: ER STRESS AND ISCHEMIA/REPERFUSION INJURY

Er Stress and Ischemia/Reperfusion Injury

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Institutional Affiliation

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ER STRESS AND ISCHEMIA/REPERFUSION INJURY

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ER stress and ischemia/reperfusion injury
The ER/sarcoplasmic reticulum is an organelle involved in many cell functions, including
the folding of protein molecules, the transport of synthesized proteins to the Golgi apparatus, and
lipid metabolisms, etc. ER/sarcoplasmic reticulum is also a major storage site of Ca2+ in cells and
can contribute to cellular activities through Ca2+ signaling. Ca2+ concentrations within
ER/sarcoplasmic reticulum are regulated by RyRs and IP3 receptors which release Ca2+ from the
ER/sarcoplasmic reticulum to the cytosol, and the sarcoendoplasmic reticulum Ca2+ transport
ATPase, which transfers Ca2+ from the cytosol to the ER/sarcoplasmic reticulum.
Ca2+ homeostasis helps maintain normal ER function. Depletion of ER Ca2+ impairs the
processing and folding of newly synthesized proteins and thus, induces buildup of unfolded
proteins, resulting in ER stress. This stress triggers the unfolded protein response which activates
ER transmembrane sensors to initiate the adaptive responses. The three well-described ER
transmembrane sensors include protein kinase-like ER kinase (PERK), inositol-requiring kinase
1 (IRE1), and activating transcription factor 6 (ATF6). Activation of the PERK pathway leads to
phosphorylation of ...