Regulation of Lipotoxicity by the non-coding RNA gadd7
非编码 RNA gadd7 的脂毒性调节
基本信息
- 批准号:7294862
- 负责人:
- 金额:$ 2.16万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2006
- 资助国家:美国
- 起止时间:2006-09-21 至 2008-06-20
- 项目状态:已结题
- 来源:
- 关键词:Adipose tissueApoptosisCardiomyopathiesCell DeathCellsChinese Hamster Ovary CellConditionCultured CellsDiseaseDisruptionEndoplasmic ReticulumExposure toFamily memberFatty AcidsFatty acid glycerol estersFunctional RNAFunctional disorderGene ExpressionGene FamilyGenerationsGenesGenetic ScreeningHeartHeart failureHuman DevelopmentHydrogen PeroxideMetabolic DiseasesMolecularNon-Insulin-Dependent Diabetes MellitusOnset of illnessOrganOxidative StressPalmitatesPalmitic AcidsPancreasPathogenesisPathway interactionsPersonal SatisfactionPhenotypePredispositionProcessRNAReactive Oxygen SpeciesRegulationResearchResistanceRoleSmall Interfering RNAStressSupplementationTestingbiological adaptation to stressmutantprogramsresponseuptake
项目摘要
DESCRIPTION (provided by applicant): Lipotoxicity is the process by which non-adipose tissues, such as the heart and pancreas, accumulate an excess of fatty acids leading to cellular dysfunction and cell death. Lipotoxic-cell death is implicated in the development of human metabolic diseases such as cardiomyopathy and type 2 diabetes. The generation of reactive oxygen species (ROS) and activation of the ER stress response are central to lipotoxic-cell death. However, the exact molecular pathways involved in this process have not been well characterized. To elucidate the key players in the lipotoxic-response, a genetic screen in Chinese hamster ovary cells was carried out by our lab. The screen led to the identification of the non-coding RNA gadd7, which has no known function. Gadd7 expression is induced by the ROS precussor H2O2 and several of its gene family members are associated with the ER stress response. These results and the isolation of gadd7 in our screen suggest a role for gadd7 in the lipotoxic-response. This proposal will test the hypothesis that gadd7 is regulated by lipotoxic-conditions and functions to regulate a program of gene expression in the lipotoxic- response. My aims are to: 1. Confirm the role of gadd7 in lipotoxicity, 2. Characterize the step in the lipotoxic-response where gadd7 disruption inhibits lipotoxic-cell death, 3. Determine the function of gadd7 in the lipotoxic-response by assessing if gadd7 functions as a regulatory RNA. The excess accumulation of fat is implicated in the pathogenesis of diseases like heart failure and type 2 diabetes. The proposed research will increase our understanding of how excess fat disrupts organ function, contributing to the onset of these diseases, and may provide new avenues of treatment and therapy.
描述(由申请人提供):脂毒性是心脏和胰腺等非脂肪组织积累过量脂肪酸导致细胞功能障碍和细胞死亡的过程。脂毒性细胞死亡与人类代谢疾病如心肌病和2型糖尿病的发展有关。活性氧(ROS)的产生和ER应激反应的激活是脂毒性细胞死亡的核心。然而,参与这一过程的确切分子途径尚未得到很好的表征。为了阐明脂毒性反应的关键参与者,我们实验室在中国仓鼠卵巢细胞中进行了遗传筛选。筛选导致鉴定出非编码RNA gadd7,其没有已知的功能。Gadd7表达由ROS前体H2O2诱导,其几个基因家族成员与ER应激反应相关。这些结果和我们筛选中gadd7的分离表明gadd7在脂毒反应中的作用。该提议将检验gadd7受脂毒性条件调节并在脂毒性反应中起调节基因表达程序的作用的假设。我的目标是:1。证实gadd7在脂毒性中的作用。表征脂毒性反应中gadd7破坏抑制脂毒性细胞死亡的步骤,3.通过评估gadd7是否作为调节RNA发挥功能,确定gadd7在脂毒反应中的功能。脂肪的过度积累与心力衰竭和2型糖尿病等疾病的发病机制有关。这项拟议中的研究将增加我们对过量脂肪如何破坏器官功能的理解,有助于这些疾病的发生,并可能提供新的治疗和治疗途径。
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
数据更新时间:{{ journalArticles.updateTime }}
{{
item.title }}
{{ item.translation_title }}
- DOI:
{{ item.doi }} - 发表时间:
{{ item.publish_year }} - 期刊:
- 影响因子:{{ item.factor }}
- 作者:
{{ item.authors }} - 通讯作者:
{{ item.author }}
数据更新时间:{{ journalArticles.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ monograph.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ sciAawards.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ conferencePapers.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ patent.updateTime }}
Rita Thomas Brookheart其他文献
Rita Thomas Brookheart的其他文献
{{
item.title }}
{{ item.translation_title }}
- DOI:
{{ item.doi }} - 发表时间:
{{ item.publish_year }} - 期刊:
- 影响因子:{{ item.factor }}
- 作者:
{{ item.authors }} - 通讯作者:
{{ item.author }}
{{ truncateString('Rita Thomas Brookheart', 18)}}的其他基金
Site-1 Protease in the regulation of skeletal muscle metabolism and exercise endurance
位点 1 蛋白酶在骨骼肌代谢和运动耐力调节中的作用
- 批准号:
10421052 - 财政年份:2019
- 资助金额:
$ 2.16万 - 项目类别:
Site-1 Protease in the regulation of skeletal muscle metabolism and exercise endurance
位点 1 蛋白酶在骨骼肌代谢和运动耐力调节中的作用
- 批准号:
10186796 - 财政年份:2019
- 资助金额:
$ 2.16万 - 项目类别:
Site-1 Protease in the regulation of skeletal muscle metabolism and exercise endurance
Site-1 蛋白酶在骨骼肌代谢和运动耐力调节中的作用
- 批准号:
10630296 - 财政年份:2019
- 资助金额:
$ 2.16万 - 项目类别:
The role of PGRMC1 in hepatic cholesterol homeostasis
PGRMC1 在肝脏胆固醇稳态中的作用
- 批准号:
8402604 - 财政年份:2011
- 资助金额:
$ 2.16万 - 项目类别:
The role of PGRMC1 in hepatic cholesterol homeostasis
PGRMC1 在肝脏胆固醇稳态中的作用
- 批准号:
8210363 - 财政年份:2011
- 资助金额:
$ 2.16万 - 项目类别:
The role of PGRMC1 in hepatic cholesterol homeostasis
PGRMC1 在肝脏胆固醇稳态中的作用
- 批准号:
8060758 - 财政年份:2011
- 资助金额:
$ 2.16万 - 项目类别:
Regulation of Lipotoxicity by the non-coding RNA gadd7
非编码 RNA gadd7 的脂毒性调节
- 批准号:
7231127 - 财政年份:2006
- 资助金额:
$ 2.16万 - 项目类别:
相似国自然基金
Epac1/2通过蛋白酶体调控中性粒细胞NETosis和Apoptosis在急性肺损伤中的作用研究
- 批准号:LBY21H010001
- 批准年份:2020
- 资助金额:0.0 万元
- 项目类别:省市级项目
基于Apoptosis/Ferroptosis双重激活效应的天然产物AlbiziabiosideA的抗肿瘤作用机制研究及其结构改造
- 批准号:81703335
- 批准年份:2017
- 资助金额:20.0 万元
- 项目类别:青年科学基金项目
双肝移植后Apoptosis和pyroptosis在移植物萎缩差异中的作用和供受者免疫微环境变化研究
- 批准号:81670594
- 批准年份:2016
- 资助金额:58.0 万元
- 项目类别:面上项目
Serp-2 调控apoptosis和pyroptosis 对肝脏缺血再灌注损伤的保护作用研究
- 批准号:81470791
- 批准年份:2014
- 资助金额:73.0 万元
- 项目类别:面上项目
Apoptosis signal-regulating kinase 1是七氟烷抑制小胶质细胞活化的关键分子靶点?
- 批准号:81301123
- 批准年份:2013
- 资助金额:23.0 万元
- 项目类别:青年科学基金项目
APO-miR(multi-targeting apoptosis-regulatory miRNA)在前列腺癌中的表达和作用
- 批准号:81101529
- 批准年份:2011
- 资助金额:22.0 万元
- 项目类别:青年科学基金项目
放疗与细胞程序性死亡(APOPTOSIS)相关性及其应用研究
- 批准号:39500043
- 批准年份:1995
- 资助金额:9.0 万元
- 项目类别:青年科学基金项目
相似海外基金
Development of an apoptosis biosensor for monitoring of breast cancer
开发用于监测乳腺癌的细胞凋亡生物传感器
- 批准号:
10719415 - 财政年份:2023
- 资助金额:
$ 2.16万 - 项目类别:
Milk fat globule-EGF factor 8 and hepatocyte apoptosis-induced liver wound healing response
乳脂肪球-EGF因子8与肝细胞凋亡诱导的肝脏创面愈合反应
- 批准号:
10585802 - 财政年份:2023
- 资助金额:
$ 2.16万 - 项目类别:
Interrogating the Fgl2-FcγRIIB axis on CD8+ T cells: A novel mechanism mediating apoptosis of tumor-specific memory CD8+ T cells
询问 CD8 T 细胞上的 Fgl2-FcγRIIB 轴:介导肿瘤特异性记忆 CD8 T 细胞凋亡的新机制
- 批准号:
10605856 - 财政年份:2023
- 资助金额:
$ 2.16万 - 项目类别:
Mechanistic analysis of apoptosis induction by HDAC inhibitors in head and neck cancer
HDAC抑制剂诱导头颈癌凋亡的机制分析
- 批准号:
23K15866 - 财政年份:2023
- 资助金额:
$ 2.16万 - 项目类别:
Grant-in-Aid for Early-Career Scientists
Novel targeted therapy for FGFR inhibitor-resistant urothelial cancer and apoptosis based therapy for urothelial cancer
FGFR抑制剂耐药性尿路上皮癌的新型靶向治疗和基于细胞凋亡的尿路上皮癌治疗
- 批准号:
23K08773 - 财政年份:2023
- 资助金额:
$ 2.16万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Interrogating the Fgl2-FcgRIIB axis: A novel mechanism mediating apoptosis of tumor-specific memory CD8+ T cells
探究 Fgl2-FcgRIIB 轴:介导肿瘤特异性记忆 CD8 T 细胞凋亡的新机制
- 批准号:
10743485 - 财政年份:2023
- 资助金额:
$ 2.16万 - 项目类别:
Investigating the role of apoptosis-resistance and the tumor environment on development and maintenance of sacrococcygeal teratomas
研究细胞凋亡抗性和肿瘤环境对骶尾部畸胎瘤发生和维持的作用
- 批准号:
10749797 - 财政年份:2023
- 资助金额:
$ 2.16万 - 项目类别:
The effects of glucose on immune cell apoptosis and mitochondrial membrane potential and the analysis of its mechanism by which glucose might modulate the immune functions.
葡萄糖对免疫细胞凋亡和线粒体膜电位的影响及其调节免疫功能的机制分析。
- 批准号:
22K09076 - 财政年份:2022
- 资助金额:
$ 2.16万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
XAF1 IN P53 SIGNALING, APOPTOSIS AND TUMOR SUPPRESSION
P53 信号传导、细胞凋亡和肿瘤抑制中的 XAF1
- 批准号:
10583516 - 财政年份:2022
- 资助金额:
$ 2.16万 - 项目类别:
Role of Thioredoxin system in regulation of autophagy-apoptosis cross talk in neurons: Uncovering Novel Molecular Interactions.
硫氧还蛋白系统在神经元自噬-凋亡串扰调节中的作用:揭示新的分子相互作用。
- 批准号:
RGPIN-2019-05371 - 财政年份:2022
- 资助金额:
$ 2.16万 - 项目类别:
Discovery Grants Program - Individual