Mus musculus
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ABSTRACT:
PROVIDER: PRJNA310599 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The mammalian LINC complex controls mechanosensing at a genome-wide level: miRNA-sequencing
| PRJNA310700 | ENA
Project description:The mammalian LINC complex controls mechanosensing at a genome-wide level
| PRJNA310699 | ENA
Project description:Mechanotransduction leads to a variety of biological responses including changes in cell shape, migration, tissue development, immune responses, and gene expression. Dysregulation of mechanotransduction is implicated in the progression of various diseases such as cancer and cardiovascular diseases. The actin cytoskeleton plays a crucial role in transmitting mechanical stimuli. Actin filaments, essential for cell motility and shape changes, respond to mechanical cues by remodeling, influencing gene expression via the LINC complex and mechanosensitive transcription factors. This study employs the DSP-MNase DNA-seq method to explore the relationship between cellular mechanosensing and chromatin architecture.
2024-08-28 | GSE257539 | GEO
Project description:Mechanical cues influence the shape, growth, and function of tissues and organs and are necessary for the development of engineered tissues. Yet, how cells sense mechanical cues and transduce them into changes in gene expression is not well understood. It is known that mechanical forces transmitted to the nucleus induce chromatin remodeling, promote DNA repair, contribute to the motion of intranuclear organelles and cause direct dissociation of protein complexes inside nuclei. Yet, the extent to which such signals impact gene expression is not understood. Because mechanical forces from the cytoskeleton to the nucleus interior are transmitted by the LINC (linker of nucleoskeleton-to-cytoskeleton) complex, we disrupted the LINC complex and performed genome wide expression studies using RNA sequencing. LINC disruption altered the expression of hundreds of genes at a genome-wide scale. We asked how LINC disruption affected the mechanosensitivity of individual genes by quantifying fold changes in gene expression on soft and stiff substrates. Remarkably, LINC disruption tended to preserve gene mechanosensitivity, but to reverse its direction. LINC disruption did not cause changes in nuclear shape, nor eliminated nuclear shape sensitivity to substrate rigidity. Our results show for the first time that the LINC complex regulates mechano-sensing at a genome-wide level, and argue for a distinct mechanism that does not require changes in nuclear morphology.
2017-01-20 | GSE77472 | GEO
Project description:Mechanical cues influence the shape, growth, and function of tissues and organs and are necessary for the development of engineered tissues. Yet, how cells sense mechanical cues and transduce them into changes in gene expression is not well understood. It is known that mechanical forces transmitted to the nucleus induce chromatin remodeling, promote DNA repair, contribute to the motion of intranuclear organelles and cause direct dissociation of protein complexes inside nuclei. Yet, the extent to which such signals impact gene expression is not understood. Because mechanical forces from the cytoskeleton to the nucleus interior are transmitted by the LINC (linker of nucleoskeleton-to-cytoskeleton) complex, we disrupted the LINC complex and performed genome wide expression studies using RNA sequencing. LINC disruption altered the expression of hundreds of genes at a genome-wide scale. We asked how LINC disruption affected the mechanosensitivity of individual genes by quantifying fold changes in gene expression on soft and stiff substrates. Remarkably, LINC disruption tended to preserve gene mechanosensitivity, but to reverse its direction. LINC disruption did not cause changes in nuclear shape, nor eliminated nuclear shape sensitivity to substrate rigidity. Our results show for the first time that the LINC complex regulates mechano-sensing at a genome-wide level, and argue for a distinct mechanism that does not require changes in nuclear morphology.
2017-01-20 | GSE77520 | GEO
Project description:To test the hypothesis that circRNAs might encode functional peptides in mammalian cells, we studied the long intergenic non-protein coding RNA, p53 induced transcript (LINC-PINT), which was previously reported as a tumor suppressor and connected p53 activation with polycomb repressive complex 2 (PRC2). We selected this long noncoding RNA (lncRNA) for further analysis because LINC-PINT has a long exon 2 which in accordance with the bioinformatical analyzed circular RNA standard.The following immunoblotting showed 87aa peptide level also decreased, indicating that this peptide is encoded by circPINTexon2. We name this circRNA encoded peptide PINT87aa.
2015-11-04 | GSE74610 | GEO
Project description:To test the hypothesis that circRNAs might encode functional peptides in mammalian cells, we studied the long intergenic non-protein coding RNA, p53 induced transcript (LINC-PINT), which was previously reported as a tumor suppressor and connected p53 activation with polycomb repressive complex 2 (PRC2). We selected this long noncoding RNA (lncRNA) for further analysis because LINC-PINT has a long exon 2 which in accordance with the bioinformatical analyzed circular RNA standard.The following immunoblotting showed 87aa peptide level also decreased, indicating that this peptide is encoded by circPINTexon2. We name this circRNA encoded peptide PINT87aa. To investigate the possible regulatory role of PINT87aa, we did the expression micro array in PINT87aa stably transfect U251 or U87 glioblastoma cells and their control cells. The array analysis reveals that PINT87aa may involve in the cell cycle regulation, anti-apoptosis effects and multiple oncogenic signaling pathway activation.
2015-11-04 | E-GEOD-74610 | biostudies-arrayexpress
Project description:Inappropriate or sustained activation of innate immunity is a pathologic feature of several common cardio-metabolic disorders. Little is known, however, about transcriptomic modulation during inflammatory stress in disease-relevant human tissues. We applied deep RNA sequencing (RNA-seq) during low-dose experimental endotoxemia (LPS) in healthy humans to interrogate, in an unbiased manner, inflammatory tissue-level transcriptome responses of relevance to complex cardio-metabolic diseases. We utilized adipose and blood samples from three individuals who underwent a standardized inpatient endotoxemia protocol. Our comprehensive analysis revealed substantial, highly tissue- and subject-specific LPS-modulated changes in the expression of protein-coding genes and linc-RNAs as well as alternative splicing (AS). We also confirmed adipocytes and macrophages as potential cell sources of selective LPS-modulated linc-RNAs and AS events. Finally, we defined disease relevance of a subset of findings in obese adipose tissue and through interrogation of overlap with genome-wide association study loci for cardio-metabolic traits. Our findings provide novel insights into tissue-level genomic regulation, not detectable through analysis of DNA variations alone, of relevance to common cardio-metabolic diseases. Using RNA-seq data to study LPS-modulated changes in lincRNA expression for adipose and blood of a healthy individual.
2014-01-02 | E-GEOD-50792 | biostudies-arrayexpress
Project description:A promoter level mammalian expression atlas (mouse, sRNA-Seq)
| PRJDB4060 | ENA
Project description:Glioblastoma multiforme (GBM) is the most common and aggressive malignant brain tumor among adults, which is characterized by high invasion, migration and proliferation abilities. One important process that contributes to the invasiveness of GBM is the epithelial to mesenchymal transition (EMT). EMT is regulated by a set of defined transcription factors which tightly regulate this process, among them is the basic helix-loop-helix family member, TWIST1. Here we show that TWIST1 is methylated on lysine-33 at chromatin by SETD6, a methyltransferase with expression levels correlating with poor survival in GBM patients. RNA-seq analysis in U251 GBM cells suggested that both SETD6 and TWIST1 regulate cell adhesion and migration processes. We further show that TWIST1 methylation attenuates the expression of the long-non-coding RNA, LINC-PINT, thereby suppressing EMT in GBM. Mechanistically, TWIST1 methylation represses the transcription of LINC-PINT by increasing the occupancy of EZH2 and the catalysis of the repressive H3K27me3 mark at the LINC-PINT locus. Under un-methylated conditions, TWIST1 dissociates from the LINC-PINT locus, allowing the expression of LINC-PINT which leads to increased cell adhesion and decreased cell migration. Together, our findings unravel a new mechanistic dimension for selective expression of LINC-PINT mediated by TWIST1 methylation.
2022-08-12 | PXD029361 | Pride