This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Our goal is to understand the mechanisms underlying observed alterations in calcium homeostasis and the oxidation and nitration of intracellular proteins that occur under a range of biological pathologies, including biological aging. In this work we will focus on stress-response signaling pathways in mouse macrophages involving the critical calcium regulatory protein calmodulin (CaM). The mass spectrometry tools available to us will be used to 1) identify CaM binding partners and their involvement in signaling pathways 2) investigate the role of nitrated tyrosine in the regulatory processes, using CaM as a model protein and 3) explore the use of CaM as a biosensor to differentiate between types of oxidative stress.
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