1. Home
2. Flashcards
3. Preview

PHRD5015 Mechanisms of Disease - Module 3 (Cellular Responses to Stress)

Home Get App Take Quiz Create how mitochondria are a source of oxidative stress electrons are lost during ATP synthesis sources of ROS -exogenous: pollutants, tobacco, drugs -endogenous: NADPH oxidase, ETC types of ROS 1) superoxide anions 2) H2O2 3) hydroxy/peroxy radicals forms of oxidative damage (4) 1) DNA damage 2) lipid peroxidation 3) AA oxidation 4) cofactor oxidation enzyme family that converts molecules into more water soluble forms that are more efficiently excreted cytochrome P450 xenobiotic compound did not originate from the body glutathione peroxidase reduces ROS to nonreactive molecule glutathione reductase reduces glutathione and creates NADP+ from NADPH + H+ catalyzes the conversion of hydrogen peroxide to water catalase coverts superoxide to water superoxide dismutase 3 ER stress sensors 1) PERK 2) ATF6 3) IRE1 cells that fuse such that many nuclei share 1 cytoplasm syncytia stem cells of muscle myoblasts create myoblasts satellite cells protein that functions as a negative regulator or muscle mass mystatin 3 caspase targets 1) actin 2) laminin 3) ICAD organelle that initiates apoptotic signal mitochondria mitochondrial apoptotic pathway cyt c -> Apaf-1 aggregation -> caspase 9 pro-apoptotic Bcl protein Bax anti-apoptotic protein Bcl-2 binds Bax to inhibit apoptosis Bcl-2 stress sensor doman in Bcl-2 BH3 "eat me" signal phosphatidyl serine (PS) activated by Ca2+ to activate apoptosis calcineurin promotes creation of autophagosome, negatively regulated by mTOR ULK complex proteins playing role in formation/fusion of autophagosomes; activated by SIRT1 ATG proteins response in autophagy with decrease in mTOR increase in autophagy Fas activators Fas ligand TNFR1

Author daynuhmay ID 235150 Card Set PHRD5015 Mechanisms of Disease - Module 3 (Cellular Responses to Stress) Description Cellular Responses to Stress Updated 2013-09-16T19:38:58Z Show Answers