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MS analysis of anti-Senp7 pulldown in adipocytes

ABSTRACT: To identify the function of Senp7 in adipocytes, we conducted a pulldown aasay and mass spectrometry analysis to identify proteins that interacted with Senp7.

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): White Adipose Tissue

SUBMITTER: Zhaoyu Lin

LAB HEAD: Zhaoyu Lin

PROVIDER: PXD043479 | Pride | 2024-06-16

REPOSITORIES: Pride

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			Action	DRS
	1_IgG.wiff	Wiff
	1_IgG.wiff.scan	Wiff
	1_IgG_FDR.xlsx	Xlsx
	1_IgG_PeptideSummary.txt	Txt
	1_IgG_ProteinSummary.txt	Txt

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Publications

Senp7 deficiency impairs lipid droplets maturation in white adipose tissues via Plin4 deSUMOylation.

Pei Jingwen J Zou Dayuan D Li Lu L Kang Lulu L Sun Minli M Li Xu X Chen Qianyue Q Chen Danning D Qu Bin B Gao Xiang X Lin Zhaoyu Z

The Journal of biological chemistry 20240425 6

Lipid metabolism is important for the maintenance of physiological homeostasis. Several members of the small ubiquitin-like modifier (SUMO)-specific protease (SENP) family have been reported as the regulators of lipid homeostasis. However, the function of Senp7 in lipid metabolism remains unclear. In this study, we generated both conventional and adipocyte-specific Senp7 KO mice to characterize the role of Senp7 in lipid metabolism homeostasis. Both Senp7-deficient mice displayed reduced white a ...[more]

PMID: 38677512

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Expression data of human coronary artery perivascular adipocytes and subcutaneous adipocytes

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Effects of bisphenol A on gene expression in adipocytes from lean children: association to metabolic disorders

Project description:Bisphenol A (BPA) is a xenobiotic endocrine disrupting chemical. In vitro and in vivo studies indicated that BPA alters endocrine-metabolic pathways in adipose tissue increasing the risk of developing metabolic disorders. BPA effects on human adipocytes, specifically in children, are poorly investigated. To investigate in childhood the effect of exposure to BPA on metabolic disorders we analyzed in vitro the effects of environmentally relevant doses of BPA on gene expression of mature human adipocytes from pre-pubertal lean patients and on related physiological outcomes. Adipocytes from children were treated in vitro with BPA and gene expression was evaluated by qRT-PCR. Genome wide analyses were performed using GeneChip Human Gene 1.0 ST array. Lipid content in adipocytes was estimated by ORO staining and Triglyceride Quantification Kit. Secreted IL-1beta, in adipocytes culture medium, and insulin, in PANC-1 culture medium, were performed using ELISA assays. BPA was found to promote up-regulation of ER? and ERR?, and down-regulation of GPR30 expression modulating estrogen signaling and following a non-linear dose-response. Microarray data analysis demonstrated that BPA increases the gene expression of pro-inflammatory cytokines and lipid metabolism-related FABP4 and CD36 in adipocytes. PCSK1 resulted the most interesting gene being down-regulated by BPA thus impairing insulin production in pancreas. BPA promotes inflammation and lipid metabolism dysregulation in adipocytes from lean children. Moreover, PCSK1 can be a key gene in BPA action modulating insulin production. Exposure to BPA in childhood may be an important risk factor in developing obesity and metabolic disorders. Three prototypic situations were analyzed (5 replication each): untreated cells (C), 10 nM BPA treated cells (BPA), 1 nM 17-beta Estradiol treated cells (ES).

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SENP2 is an important regulator of energy metabolism in adipocytes and knockdown increases markers of browning

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