Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA401832 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:CIC and ATXN1L knockout gene expression data [NHA]
| PRJNA401831 | ENA
Project description:CIC and ATXN1L knockout gene expression data
| PRJNA401478 | ENA
Project description:Many neurological diseases attack specific brain regions despite widespread expression of the disease-related protein. Spinocerebellar ataxia type 1 (SCA1) primarily affects the cerebellum, though Ataxin-1 (ATXN1) is widely expressed. We previously showed that intensified interaction between mutant ATXN1 and Capicua (CIC) drives SCA1 pathogenesis in the cerebellum, whereas ATXN1 loss augments amyloid beta production in the hippocampus and cortex. CIC, however, forms a complex with ATXN1 and its paralog, Ataxin-1-like (ATXN1L)—yet knockout of either yields completely different phenotypes. To determine whether this could be due to CIC having two isoforms, we generated mice bearing either the long (CIC-L) or short (CIC-S) isoform. Loss of CIC-L led to cognitive deficits, whereas loss of CIC-S caused perinatal lethality, phenocopying, ATXN1 and ATXN1L knockout mice, respectively. Furthermore, CIC-L preferentially interacts with ATXN1, and CIC-S with ATXN1L. Our data underscore the importance of isoform–paralog interplay in studying regional vulnerability in neurodegenerative diseases.
2026-07-29 | GSE310453 | GEO
Project description:CIC has recently been implicated as a negative prognostic factor in multiple cancers. CIC and ATXN1L have been reported as interactors in several cellular contexts including development and disease state. To investigate the relationship between CIC and ATXN1L on a transcriptomic level, CIC-KO and ATXN1L-KO cell lines were generated. Gene expression profiling of CIC-KO and ATXN1L-KO cell lines was performed by microarray and differentially expressed genes were compared. We found a high degree of overlap in differentially expressed genes in CIC-KO and ATXN1L-KO suggesting loss of either interacting partner to lead to similar transcriptomic changes.
2017-09-30 | GSE103514 | GEO
Project description:CIC has recently been implicated as a negative prognostic factor in multiple cancers. CIC and ATXN1L have been reported as interactors in several cellular contexts including development and disease state. To investigate the relationship between CIC and ATXN1L on a transcriptomic level, CIC-KO and ATXN1L-KO cell lines were generated. Gene expression profiling of CIC-KO and ATXN1L-KO cell lines was performed by microarray and differentially expressed genes were compared. We found a high degree of overlap in differentially expressed genes in CIC-KO and ATXN1L-KO suggesting loss of either interacting partner to lead to similar transcriptomic changes.
2017-09-30 | GSE103513 | GEO
Project description:Aberrations in Capicua (CIC) have recently been implicated as a negative prognostic factor in a multitude of cancer types through activation of the MAPK signalling cascade and derepression of oncogenic ETS transcription factors. The Ataxin-family protein ATXN1L has previously been reported to interact with CIC in developmental and disease contexts to facilitate the repression of CIC target genes. To further investigate this relationship, we performed functional in vitro studies utilizing ATXN1LKO and CICKO human cell lines and characterized a reciprocal functional relationship between CIC and ATXN1L.
2020-03-31 | GSE140471 | GEO
Project description:Early detection of viral infection and rapid activation of host antiviral defenses are critical for limiting viral replication and spread. At a cellular level, this is achieved through host pattern recognition receptors that sense viral nucleic acid as foreign and initiate antiviral defenses through transcriptional upregulation of antiviral cytokines interferons (IFNs) and interferon stimulated genes (ISGs). However, aberrant production of IFN in the absence of viral infection leads to auto-inflammation and can be detrimental to the host. Here, we show that the DNA binding transcriptional repressor complex composed of Capicua (CIC) and Ataxin-1 like (ATXN1L) bind to 8-nucleotide motif near IFN and ISG promoters and block aberrant expression under homeostasis. However, during respiratory viral infections, this active repression is relieved by rapid degradation of the CIC-ATXN1L complex via the activation Mitogen‑activated protein kinase (MAPK) pathway, thereby priming the host cells ready to mount robust antiviral responses through canonical interferon regulatory factors (IRF), and signal transducer and activator of transcription (STAT) transcription factors. Importantly, murine Cic-Atxn1L also repress expression from IFN and ISGs promoters, demonstrating the conservation of this regulatory mechanism in murine species. Together, our studies define a new paradigm for regulation of IFN and ISGs through the evolutionarily conserved CIC-ATXN1L DNA binding transcription repressor complex under homeostasis and viral infection conditions.
2025-03-24 | GSE271897 | GEO
Project description:Expression data from CIC wild type and knockout cell lines
| PRJNA318740 | ENA
Project description:Early detection of viral infection and rapid activation of host antiviral defenses are critical for limiting viral replication and spread. At a cellular level, this is achieved through host pattern recognition receptors that sense viral nucleic acid as foreign and initiate antiviral defenses through transcriptional upregulation of antiviral cytokines interferons (IFNs) and interferon stimulated genes (ISGs). However, aberrant production of IFN in the absence of viral infection leads to auto-inflammation and can be detrimental to the host. Here, we show that the DNA binding transcriptional repressor complex composed of Capicua (CIC) and Ataxin-1 like (ATXN1L) bind to 8-nucleotide motif near IFN and ISG promoters and block aberrant expression under homeostasis. However, during respiratory viral infections, this active repression is relieved by rapid degradation of the CIC-ATXN1L complex via the activation Mitogen‑activated protein kinase (MAPK) pathway, thereby priming the host cells ready to mount robust antiviral responses through canonical interferon regulatory factors (IRF), and signal transducer and activator of transcription (STAT) transcription factors. Importantly, murine Cic-Atxn1L also repress expression from IFN and ISGs promoters, demonstrating the conservation of this regulatory mechanism in murine species. Together, our studies define a new paradigm for regulation of IFN and ISGs through the evolutionarily conserved CIC-ATXN1L DNA binding transcription repressor complex under homeostasis and viral infection conditions.
2025-03-24 | GSE271899 | GEO
Project description:Early detection of viral infection and rapid activation of host antiviral defenses are critical for limiting viral replication and spread. At a cellular level, this is achieved through host pattern recognition receptors that sense viral nucleic acid as foreign and initiate antiviral defenses through transcriptional upregulation of antiviral cytokines interferons (IFNs) and interferon stimulated genes (ISGs). However, aberrant production of IFN in the absence of viral infection leads to auto-inflammation and can be detrimental to the host. Here, we show that the DNA binding transcriptional repressor complex composed of Capicua (CIC) and Ataxin-1 like (ATXN1L) bind to 8-nucleotide motif near IFN and ISG promoters and block aberrant expression under homeostasis. However, during respiratory viral infections, this active repression is relieved by rapid degradation of the CIC-ATXN1L complex via the activation Mitogen‑activated protein kinase (MAPK) pathway, thereby priming the host cells ready to mount robust antiviral responses through canonical interferon regulatory factors (IRF), and signal transducer and activator of transcription (STAT) transcription factors. Importantly, murine Cic-Atxn1L also repress expression from IFN and ISGs promoters, demonstrating the conservation of this regulatory mechanism in murine species. Together, our studies define a new paradigm for regulation of IFN and ISGs through the evolutionarily conserved CIC-ATXN1L DNA binding transcription repressor complex under homeostasis and viral infection conditions.
2025-03-24 | GSE271898 | GEO