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High-throughput mRNA-sequence of MCM7 and SHCBP1 knock down hepatocytes with IL-1β stimulation

ABSTRACT: High-throughput mRNA-sequence of MCM7 and SHCBP1 knock down hepatocytes with IL-1β stimulation

PROVIDER: PRJNA1149027 | ENA |

REPOSITORIES: ENA

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High-throughput mRNA-sequence of MCM7 and SHCBP1 knock down hepatocytes with IL-1β stimulation

Project description:Liver fibrosis, characterized by the excessive deposition of extracellular matrix, remains a formidable challenge due to its complex and poorly understood mechanisms. In this study, we aimed to elucidate the role of Minichromosome Maintenance Complex Component 7 (MCM7) and SHC SH2-Domain Binding Protein 1 (SHCBP1) in liver fibrosis, focusing on their regulatory network and interaction. Stable hepatocyte cell lines with knockdown of MCM7 and SHCBP1 were constructed and subsequently stimulated with IL-1β to mimic inflammatory conditions. RNA sequencing was conducted to identify differentially expressed genes and pathways affected by the knockdown. Our analysis revealed significant changes in gene expression profiles, particularly in pathways related to fibrosis and inflammation. We discovered that MCM7 interacts with SHCBP1, which in turn binds to RACGAP1. This interaction activates the SHCBP1-RACGAP1-STAT3 signaling axis, leading to increased IL11 expression. Elevated IL11 levels contribute to the activation of hepatic stellate cells and the progression of liver fibrosis. The findings demonstrate that MCM7 is an important regulatory factor in liver fibrosis and promotes IL11 expression through the SHCBP1-RACGAP1-STAT3 signaling pathway, driving hepatic stellate cell (HSC) activation and fibrosis progression. Overall, our findings highlight a mechanistic pathway where MCM7 and SHCBP1 collaborate to regulate IL11 expression, thereby influencing liver fibrosis progression.

2025-08-09 | GSE275059 | GEO

mRNA Sequencing Analysis of MCM7 Knockdown in Primary Hepatocytes Under IL-6 Stimulation

Project description:Liver fibrosis, marked by excessive extracellular matrix deposition, remains a significant challenge due to its complex and not fully understood mechanisms. This study explores the role of Minichromosome Maintenance Complex Component 7 (MCM7) in the development of liver fibrosis, with a focus on its regulatory network and interactions. We knocked down MCM7 in primary hepatocytes and exposed them to IL-6 to simulate inflammatory conditions. RNA sequencing was then utilized to identify the differentially expressed genes and pathways influenced by MCM7 depletion. The results revealed notable alterations in gene expression, particularly in fibrosis- and inflammation-related pathways. Our study identified MCM7 as a key regulator of IL11 expression through the SHCBP1-RACGAP1-STAT3 signaling pathway, which contributes to the activation of hepatic stellate cells and the advancement of liver fibrosis. These findings underscore the critical role of MCM7 in liver fibrosis by promoting IL11 expression, thereby driving the activation of hepatic stellate cells and the progression of fibrosis. Overall, this research sheds light on a mechanistic pathway where MCM7 plays a pivotal role in liver fibrosis progression through the regulation of IL11 expression under inflammatory conditions.

2025-08-09 | GSE276001 | GEO

Elucidating the Roles of MCM7 and SHCBP1 in Liver Fibrosis through LC-MS Analysis

Project description:Liver fibrosis, characterized by the excessive deposition of extracellular matrix, presents a significant challenge due to its intricately complex and poorly understood mechanisms. In this study, we aimed to elucidate the roles of Minichromosome Maintenance Complex Component 7 (MCM7) and SHC SH2-Domain Binding Protein 1 (SHCBP1) in liver fibrosis, focusing on their regulatory networks and interactions. Stable hepatocyte cell lines with overexpression of MCM7 and SHCBP1 were constructed. Through targeted LC-MS analysis of MCM7, significant changes were observed in the protein interaction profiles, . MCM7 was found to interact with SHCBP1, which was further analyzed using LC-MS to detail its role in binding to RACGAP1. This interaction activates the SHCBP1-RACGAP1-STAT3 signaling axis, leading to increased IL11 expression. Elevated IL11 levels contribute to the activation of hepatic stellate cells (HSCs) and the progression of liver fibrosis. Our findings demonstrate that through mass spectrometry, MCM7 is identified as a crucial regulatory factor in liver fibrosis, promoting IL11 expression via the SHCBP1-RACGAP1-STAT3 signaling pathway. Both MCM7 and SHCBP1 involvement in driving HSC activation and fibrosis progression. Overall, our study highlights a mechanistic pathway where MCM7 and SHCBP1 collaborate to regulate IL11 expression, thereby influencing the progression of liver fibrosis. These insights emphasize the critical regulatory roles of MCM7 and SHCBP1, offering potential therapeutic targets for combating fibrotic liver diseases.

2025-08-09 | PXD055175 | Pride

mRNA Sequencing Analysis of MCM7 Knockdown in Primary Hepatocytes Under IL-6 Stimulation

Project description:mRNA Sequencing Analysis of MCM7 Knockdown in Primary Hepatocytes Under IL-6 Stimulation

| PRJNA1154255 | ENA

Analysis of Metabolically Stressed Primary Hepatocytes with IL-1β Recombinant Protein for 24 Hours

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2025-03-12 | GSE282137 | GEO

RNA-seq of ex vivo cultured lung CD140a+ mesenchymal cells (fibroblasts) upon stimulation by IL-1β

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Genome wide identification of MCM7 binding sites as replication origins

Project description:Here, we precisely determined MCM7 binding sites inHeLa cells by ChIP-Seq, classified them into firing and dormant replication origins using SNS data deposited, and analyzed their association with various chromatin signatures.

2017-11-23 | GSE107248 | GEO

Analysis of Metabolically Stressed Primary Hepatocytes with IL-1β Recombinant Protein for 24 Hours

Project description:Analysis of Metabolically Stressed Primary Hepatocytes with IL-1β Recombinant Protein for 24 Hours

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Transcriptome analysis in primary fibroblasts from HOIL-1-deficient patients upon TNF-α or IL-1β stimulation

Project description:HOIL-1 deficient disease is a new early onset fatal autosomal recessive human disorder charaterized by chronic auto-inflammation, recurrent invasive bacterial infections and progressive muscular amylopectinosis. We studied the effect of TNF-α and IL-1β on transcriptional changes of primary fibroblasts from HOIL-1-, MYD88- and NEMO-deficient patients. Primary fibroblasts were obtained from HOIL-1, MYD88- and NEMO-deficient patients and healthy donors and stimulated with TNF-α or IL-1β for 2 and 6 hours. RNA were extracted and globin reduced. Labeled cRNA were hybridized to Illumina Human HT-12 Beadchips.

2012-10-28 | E-GEOD-40560 | biostudies-arrayexpress

Genome-wide analysis expression of ileum samples from PGC-1β fl/? and iKOPGC-1β

Project description:Analysis of metabolic pathway gene expression. The hypothesis tested in the present study is to assess mRNA level changes in metabolic genes in enterocytes from intestine specific PGC-1β konckout mice. Total RNA obtained from ileum samples from IKOPGC-1β mice was compared to the total RNA extracted from their wild-type littermates.

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