Pattern of Islr knockout mouse colon gene expression
Ontology highlight
ABSTRACT: To further understand different gene expression of islr knockout mouse colon and normal colon, we have employed colon samples microarray expression profiling as a discovery platform to identify different genes with Islr knockout mouse colon and normal colon. Comparison with normal colon, significantly upgene is 779 and downgene is 996 in knockout group.
Project description:To further understand different gene expression of miR-31 knockout mouse colon and normal colon, we have employed colonic epithelium microarray expression profiling as a discovery platform to identify different genes with miR-31 knockout mouse colon and normal colon.comparision with normal colonic epithelium,upgene is 285 and downgene is 178 in knockout group.
Project description:To further understand different gene expression of miR-22 knockout mouse BAT and normal BAT, we have employed BAT samples microarray expression profiling as a discovery platform to identify different genes with miR-22 knockout mouse BAT and normal BAT.comparision with normal BAT,significantly upgene is 522 and downgene is 720 in knockout group.
Project description:To further understand different gene expression of Extramammary Paget disease skin and normal skin, we have employed whole skin microarray expression profiling as a discovery platform to identify different genes with Extramammary Paget disease skin and normal skin.comparision with normal skin, upgene is 4572 in disease group, downgene is 6473. mTOR pathway, RAS pathway, PI3K-AKT pathway, IL6-JAK-Stat3 pathway and so on are activated, WNT Pathway is inhibited.
Project description:To further understand expression patterns of musashi1 overexpression (DTG) in mouse skin,we have employed microarray expression profiling as a discovery platform to identify different genes expression with DTG mouse and Control mouse. Comparision with Control mouse,upgene is 3772 in DTG mouse, downgene is 5529. mTOR pathway, RAS pathway, PI3K-AKT pathway,IL6-JAK-Stat3 pathway and so on are activated, WNT Pathway is inhibited.
Project description:In order to investigate the role of FOXA2 in the occurrence and development, we infected gallbladder cancer cells with recombinant lentivirus to construct FOXA2 overexpression SGC-996. We then performed gene expression profiling analysis using data obtained from RNA-seq of 6 different gallbladder cancer cells from SGC-996-NC or SGC-996-OE groups.
Project description:Purpose: To explore the molecular mechanisms of ISLR protein, RNA sequencing was performed to analyze the geome-wide change of ISLR secreted supernatant treated HEK293FT cells compared to those of control supernatant treated cells. Methods: Total mRNA was extracted from HEK293FT cells in triplicate respectively. Then RNA quality was assessed using an Agilent Bioanalyzer 2100 and the sample reads were sequenced using Illumina Hiseq 4000 platform. As a reasult, we got the transcript data using Hisat2 followed by Stringtie. qRT–PCR validation was performed using TaqMan and SYBR Green assays. Results: We mapped about 60 million sequence reads per sample to the human genome and identified about 58,000 transcripts in HEK293FT cells. Many transcripts showed different expression between ISLR secreted supernatant and control treated HEK293FT cells, with a fold change ≥2 and p value <0.05. Gene set enrichment analysis (GSEA) showed a significantly positive enrichment of Hippo target genes. Conclusion: Our study present the datiled transcripts analysis of HEK293FT cells, with biologic replicates. Based on RNA-seq transcriptome characterization , we conclude a molecular mechanism of ISLR regulating multiple pathways related to tissue repair.
Project description:Satellite cells are adult muscle stem cells responsible for muscle regeneration after acute or chronic injuries. The balance between stem cell self-renewal and differentiation impacts the kinetics and efficiency of skeletal muscle regeneration. This study elucidated the function of Islr in satellite cell asymmetric division. Satellite cell specific deletion of Islr compromises muscle regeneration in adult mice by impairing the satellite cell pool. Islr is pivotal for satellite cell proliferation and its deletion promotes asymmetric cell fate segregation of satellite cells. A mechanistic search revealed that Islr interacts and stabilizes the Sparc protein, which activates p-ERK1/2 signaling required for asymmetric division. In combination, the findings have identified Islr as a key regulator of satellite cell asymmetric division through the Sparc/p-ERK1/2 signaling pathway, which provides a new insight into satellite cell biology and open avenues for the treatment of myopathy.