Investigating the mechanisms of peroxisome homeostasis
研究过氧化物酶体稳态机制
基本信息
- 批准号:10808484
- 负责人:
- 金额:$ 1.36万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2022
- 资助国家:美国
- 起止时间:2022-09-01 至 2027-06-30
- 项目状态:未结题
- 来源:
- 关键词:ATP phosphohydrolaseATPase DomainAgingAllelesAspartic AcidAutophagocytosisBindingBiogenesisBiological AssayBlindnessBone DiseasesCellsCellular biologyDataDiseaseEnvironmentEnzymesFluorescenceFutureGeneticGlycineGoalsHealthHomeostasisHumanHuman Cell LineHydrophobicityKidney DiseasesKnowledgeLiver diseasesMaintenanceMembraneMetabolicMolecularMorphologyMutationNerve DegenerationNucleotidesOrangesOrganellesPHEX proteinProcessProtein BiochemistryReactionResearchSignal PathwayStressSystemTechniquesUbiquitinYeastsZellweger Syndromedisease-causing mutationexperiencehearing impairmentimprovedmulticatalytic endopeptidase complexmutantnoveloverexpressionparent grantperoxisomeperoxisome membranesmall moleculesummer research
项目摘要
R35 Parent Grant – Project Summary: Investigating the mechanisms of peroxisome
homeostasis
The overarching goal of my lab is to understand how cells make and maintain peroxisomes, a
ubiquitous membrane-bound organelle that harbors specialized metabolic reactions.
Peroxisomes are both versatile and dynamic: cells use them to adapt to their environment, and
thus can rapidly remodel their peroxisomes by altering enzyme content, morphology, and
number through peroxisome-specific autophagy and de novo biogenesis. Approximately 35 Pex
proteins are known to contribute to peroxisome formation and maintenance, yet the
mechanisms by which they act are not resolved at a molecular level. Furthermore, we are likely
missing many important players, especially in human cells, and this lack of basic mechanistic
knowledge hinders our understanding of how peroxisome contribute to human health, both in
rare, genetic Peroxisome Biogenesis Disorders (PBDs), and during the aging process. Our
approach is to use techniques in protein biochemistry and yeast cell biology to dissect the
mechanism of the Pex proteins, particularly focusing on the AAA-ATPase Pex1/Pex6. We aim
to identify the full repertoire of Pex1/Pex6’s endogenous substrates and the features that are
important for substrate selection. Since mutations in Pex1/Pex6 cause the majority of PBDs, we
are further focused on using disease-causing alleles to understand Pex1/Pex6 function in the
human cells and the cellular consequences of peroxisome stress induced by these alleles.
Finally, we have identified novel regulators of peroxisome homeostasis in human cells, and are
now exploring how peroxisome function integrates with the implicated canonical signaling
pathways. We anticipate that this research will improve our understanding of how peroxisomes
contribute to human health and disease.
R35家长资助-项目摘要:研究过氧化物酶体的机制
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)
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Brooke Meghan Gardner其他文献
Brooke Meghan Gardner的其他文献
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{{ truncateString('Brooke Meghan Gardner', 18)}}的其他基金
Investigating the mechanisms of peroxisome homeostasis
研究过氧化物酶体稳态机制
- 批准号:
10680467 - 财政年份:2022
- 资助金额:
$ 1.36万 - 项目类别:
Investigating the role of AAA+-ATPases in peroxisome biology
研究 AAA -ATP 酶在过氧化物酶体生物学中的作用
- 批准号:
10245266 - 财政年份:2017
- 资助金额:
$ 1.36万 - 项目类别:
Investigating the role of AAA+-ATPases in peroxisome biology
研究 AAA -ATP 酶在过氧化物酶体生物学中的作用
- 批准号:
10001560 - 财政年份:2017
- 资助金额:
$ 1.36万 - 项目类别:
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