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Integrating transcriptome, proteome, and phosphoproteome analysis reveals loss function of IQGAP2 promotes cell proliferation through the mTOR pathway

ABSTRACT: Integrating transcriptome, proteome, and phosphoproteome analysis reveals loss function of IQGAP2 promotes cell proliferation through the mTOR pathway

PROVIDER: PRJNA882099 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21629261_1.fastq.gz	Fastqsanger.gz
	SRR21629261_2.fastq.gz	Fastqsanger.gz
	SRR21629262_1.fastq.gz	Fastqsanger.gz
	SRR21629262_2.fastq.gz	Fastqsanger.gz
	SRR21629263_1.fastq.gz	Fastqsanger.gz

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Integrating transcriptome, proteome, and phosphoproteome analysis reveals loss function of IQGAP2 promotes cell proliferation through the mTOR pathway

Project description:Tuberous sclerosis complex (TSC) is a rare genetic disease caused by abnormal of TSC1 or TSC2 gene. Our previous data deduced that IQGAP2 can be one of the genes potentially responsible for non-TSC1 or TSC2 mutation TSC patients. To investigate the pathogenesis of IQGAP2 in TSC, we performed global transcriptome, proteome, and phosphoproteome analyses and found the alter of genes related to mTOR signaling pathway in IQGAP2 knockdown cells. In addition, we found that knockdown of IQGAP2 resulted in increased cell proliferation and enhanced the phosphorylation level of AKT and S6K by functional analysis, meanwhile, the AKT and mTOR inhibitors can partially rescue cell abnormal proliferation by decreasing hyperphosphorylation. Our data revealed a potential connection between mTOR signaling pathway and aberrant cell proliferation in IQGAP2 knockdown cells, and provide a new latent therapeutic strategy for non-TSC1 or TSC2 mutation patients.

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