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Human HeLa cell isonicotinylation proteomic

ABSTRACT: Qualitative proteomic research by isonicoacylation enrichment technique and high resolution liquid chromatography-mass spectrometry.In this project, a qualitative study of isonicotinylation proteomics was carried out. A total of 2792 were identified in this study 11,442 isonicotinylation sites on individual proteins. We conducted a systematic bioinformatics analysis of the modified proteins,It includes Motif analysis, annotation of modified proteins, functional classification and functional enrichment analysis

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ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture

SUBMITTER: li yixiao

LAB HEAD: Yixiao Li

PROVIDER: PXD050143 | Pride | 2024-08-08

REPOSITORIES: Pride

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Project description:Backgroud Alzheimer's disease (AD) is a progressive and irreversible neurodegenerative disorder for which there is currently no cure, representing a serious clinical challenge. Lysine 2-hydroxyisobutyrylation (Khib) is a newly discovered post-translational modification that has been found to be widespread in a variety of organisms in recent years and is involved in important biometabolic processes that regulate protein function. However, it is unclear whether and how protein Khib modifications are involved in AD. This study aimed to explore the involvement of Khib in AD and its underlying mechanisms. Methods We compared a series of lysine acylation modification patterns between 9-month-old APP/PS1 mice and wild-type (WT) control mice by Western blot assays. Quantitative Khib proteomic analysis identified Khib modification proteins and key sites associated with AD. Using stereotactic brain injection, we delivered adeno- associated viruse (AAV) overexpressing Clusterin (CLU) K436R (lysine to arginine mutation at site 436, mimicking Khib deficiency) into the bilateral lateral ventricles of 9-month-old WT and APP/PS1 mice. Additionally, C8-D1A cells were infected with lentivirus carrying CLU K436 mutation. These approaches enabled functional assessment of CLU K436 khib modification in AD pathogenesis. Furthermore, co-immunoprecipitation analyses revealed that CLU K436 khib modification modulates the interaction between CLU and Aβ. Results The level of Khib was significantly increased in 9-month-old APP/PS1 mice. Quantitative Khib analysis identified Clusterin (CLU) as a differentially modified protein, with K436 serving as its primary Khib modification site. Further investigation revealed that CLU K436 Khib levels was upregulated in APP/PS1 AD model mice. Loss of K436 Khib in CLU K436R mutant APP/PS1 mice notably ameliorated β-amyloid plaque, gliosis, and neuroinflammation, consequently mitigating memory deficits in vivo. The lentiviral vector carrying CLU K436R mutant in C8-D1A astrocyte cell enhanced glial cell activation and cell survival in vitro. Mechanistically, CLU K436 Khib modification may affect Aβ metabolism by impacting the interaction between CLU and Aβ. Conclusions Our results indicated the role of Khib in AD, elucidating the function and potential molecular mechanism of CLU K436 Khib modification in AD. These findings offer novel perspectives on therapeutic approaches for AD.

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	HD231PI_INH_Hela_1_1.raw	Raw
	HD231PI_INH_Hela_1_2.raw	Raw
	HD231PI_INH_Hela_1_3.raw	Raw
	HD231PI_INH_Hela_1_4.raw	Raw
	HD231PI_INH_Hela_2_1.raw	Raw

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Human HeLa cell isonicotinylation proteomic

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