Endoplasmic reticulum (ER) stress-induced inflammation plays an important role in the progression of many diseases, such as type II diabetes, insulin resistance, cancers, and so on. NF-κB is believed to be a central regulator of ER stress-induced inflammation. However, studies on how ER stress induces NF-κB activation are limited and, in some cases, controversial. In the present study, we utilized two commonly used ER stress inducers, thapsigargin and tunicamycin, to study the mechanism. We found that two caspase-recruitment domain (CARD)-containing proteins, CARMA3 and BCL10, play a crucial roles on ER stress-induced NF-κB activation by regulating IκBα kinase activity. Consistently, we observed that a physiological ER stress inducer, hypoxia, could activate NF-κB in a CARMA3-dependent manner. Additionally, we showed that the activation of the UPR signaling pathways were intact in both CARMA3- and BCL10-deficient cells under ER stress. Together, this study provides insight into the mechanism of how ER stress induces NF-κB activation. It allows us to better understand ER stress-induced inflammation and develop the corresponding therapeutic interference to treat diseases
","abstract_html":"<p>Endoplasmic reticulum (ER) stress-induced inflammation plays an important role in the progression of many diseases, such as type II diabetes, insulin resistance, cancers, and so on. NF-κB is believed to be a central regulator of ER stress-induced inflammation. However, studies on how ER stress induces NF-κB activation are limited and, in some cases, controversial. In the present study, we utilized two commonly used ER stress inducers, thapsigargin and tunicamycin, to study the mechanism. We found that two caspase-recruitment domain (CARD)-containing proteins, CARMA3 and BCL10, play a crucial roles on ER stress-induced NF-κB activation by regulating IκBα kinase activity. Consistently, we observed that a physiological ER stress inducer, hypoxia, could activate NF-κB in a CARMA3-dependent manner. Additionally, we showed that the activation of the UPR signaling pathways were intact in both CARMA3- and BCL10-deficient cells under ER stress. Together, this study provides insight into the mechanism of how ER stress induces NF-κB activation. It allows us to better understand ER stress-induced inflammation and develop the corresponding therapeutic interference to treat diseases</p>","abstract_has_math":false,"creators":["Zhou, Zhicheng, Mr"],"institution":null,"degree_name":"Masters of Science (MS)","degree_level":"Thesis (MS)","degree_discipline":null,"degree_department":null,"school":null,"contributors":["XIN LIN","HUI-KUAN LIN","PAUL J. CHIAO"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2013,"date_issued":"2013-05-01T07:00:00Z","date_published":"2013-05-01T07:00:00Z","updated_at":"2026-07-24T05:49:30Z","subjects":["NF-KB","Endoplasmic reticulum","inflammation","Medicine and Health Sciences"],"languages":[],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://digitalcommons.library.tmc.edu/utgsbs_dissertations/349","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["XIN LIN","HUI-KUAN LIN","PAUL J. CHIAO"]},{"key":"dc:creator","label":"Author","values":["Zhou, Zhicheng, Mr"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.available","label":"Dc Date Available","values":["2014-05-07T07:00:00Z"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Thesis (MS)"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Masters of Science (MS)"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["NF-KB","Endoplasmic reticulum","inflammation","Medicine and Health Sciences"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://digitalcommons.library.tmc.edu/utgsbs_dissertations/349"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Endoplasmic reticulum (ER) stress-induced inflammation plays an important role in the progression of many diseases, such as type II diabetes, insulin resistance, cancers, and so on. NF-κB is believed to be a central regulator of ER stress-induced inflammation. However, studies on how ER stress induces NF-κB activation are limited and, in some cases, controversial. In the present study, we utilized two commonly used ER stress inducers, thapsigargin and tunicamycin, to study the mechanism. We found that two caspase-recruitment domain (CARD)-containing proteins, CARMA3 and BCL10, play a crucial roles on ER stress-induced NF-κB activation by regulating IκBα kinase activity. Consistently, we observed that a physiological ER stress inducer, hypoxia, could activate NF-κB in a CARMA3-dependent manner. Additionally, we showed that the activation of the UPR signaling pathways were intact in both CARMA3- and BCL10-deficient cells under ER stress. Together, this study provides insight into the mechanism of how ER stress induces NF-κB activation. It allows us to better understand ER stress-induced inflammation and develop the corresponding therapeutic interference to treat diseases
"]},{"key":"dc:title","label":"Title","values":["Characterization of The Role of Carma3 In Endoplasmic Reticulum Stress-Induced Nf-Κb Activation"]}]}],"canonical_facts":{"dc:contributor":["XIN LIN","HUI-KUAN LIN","PAUL J. CHIAO"],"dc:creator":["Zhou, Zhicheng, Mr"],"dc:date.available":["2014-05-07T07:00:00Z"],"dc:description.abstract":["Endoplasmic reticulum (ER) stress-induced inflammation plays an important role in the progression of many diseases, such as type II diabetes, insulin resistance, cancers, and so on. NF-κB is believed to be a central regulator of ER stress-induced inflammation. However, studies on how ER stress induces NF-κB activation are limited and, in some cases, controversial. In the present study, we utilized two commonly used ER stress inducers, thapsigargin and tunicamycin, to study the mechanism. We found that two caspase-recruitment domain (CARD)-containing proteins, CARMA3 and BCL10, play a crucial roles on ER stress-induced NF-κB activation by regulating IκBα kinase activity. Consistently, we observed that a physiological ER stress inducer, hypoxia, could activate NF-κB in a CARMA3-dependent manner. Additionally, we showed that the activation of the UPR signaling pathways were intact in both CARMA3- and BCL10-deficient cells under ER stress. Together, this study provides insight into the mechanism of how ER stress induces NF-κB activation. It allows us to better understand ER stress-induced inflammation and develop the corresponding therapeutic interference to treat diseases
"],"dc:identifier":["https://digitalcommons.library.tmc.edu/utgsbs_dissertations/349"],"dc:subject":["NF-KB","Endoplasmic reticulum","inflammation","Medicine and Health Sciences"],"dc:title":["Characterization of The Role of Carma3 In Endoplasmic Reticulum Stress-Induced Nf-Κb Activation"],"thesis:degree_level":["Thesis (MS)"],"thesis:degree_name":["Masters of Science (MS)"]},"updated_at":"2026-07-24T05:49:30Z"}