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Homo sapiens

ABSTRACT: Integrator complex subunit 12 is a key regulator of human protein synthesis pathways

PROVIDER: PRJNA318778 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3400060_1.fastq.gz	Fastqsanger.gz
	SRR3400060_2.fastq.gz	Fastqsanger.gz
	SRR3400070_1.fastq.gz	Fastqsanger.gz
	SRR3400070_2.fastq.gz	Fastqsanger.gz
	SRR3400051.fastq.gz	Fastqsanger.gz

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Integrator complex subunit 12 is a key regulator of human protein synthesis pathways

Project description:Genome wide association studies of human lung function have identified a signal on 4q24 but the mechanistic basis for this signal is unclear. This region contains the Integrator Complex subunit 12 gene (INTS12) and nearby polymorphisms associated with lung function correlate with INTS12 expression. We aimed to define INTS12 function in human bronchial epithelial cells. RNAseq pathway analyses of INTS12 depleted cells revealed robust downregulation of several protein synthesis related pathways, including the aminoacyl tRNA synthetases and PERK regulated gene expression. Indeed, INTS12 knockdown using mRNA silencing repressed cellular translation and proliferation. ChIPseq gene-centric analyses revealed INTS12 binding to be near transcriptional start sites. The binding was found to be enriched for differentially expressed loci identifying the genes it regulates, a finding previously unknown for this particular member of Integrator complex. These findings contribute to the biology behind genetic association

2017-06-12 | GSE80386 | GEO

Integrator complex regulates NELF-mediated RNA Polymerase II pause/release and processivity at coding genes [RNA-seq]

Project description:RNAPII pausing/termination shortly after initiation is a hallmark of gene regulation. However, the molecular mechanisms involved are still to be uncovered. Here, we show that NELF interacts with Integrator complex subunits (INTScom) forming a stable complex with RNPII and Spt5. The interaction between NELF and INTScom subunits is RNA and DNA independent. Using both HIV-1 promoter and genome wide analyses, we demonstrate that Integrator subunits specifically control NELF-mediated RNAPII pause/release at coding genes. The strength of RNAPII pausing is determined by the nature of the NELF-associated complex. Interestingly, in addition to controlling RNAPII pause release INTS11 catalytic subunit of the INTScom is required for the synthesis of full length mRNA. Finally, INTScom-target genes are enriched in HIV-1 TAR/ NELF-binding element and in a 3’box sequence required for snRNA biogenesis. Revealing these unexpected functions of INTScom in regulating RNAPII pausing/release and completion of mRNA synthesis of NELF-target genes will contribute to our understanding of the gene expression cycle. Genome-wide expression in HeLa cells in the absence of Integrator 11, or NELF or mock (control) depleted by strand-specific RNASeq (Illumina)

2015-05-19 | E-GEOD-60585 | biostudies-arrayexpress

Integrator complex regulates NELF-mediated RNA Polymerase II pause/release and processivity at coding genes [ChIP-seq]

Project description:RNAPII pausing/termination shortly after initiation is a hallmark of gene regulation. However, the molecular mechanisms involved are still to be uncovered. Here, we show that NELF interacts with Integrator complex subunits (INTScom) forming a stable complex with RNPII and Spt5. The interaction between NELF and INTScom subunits is RNA and DNA independent. Using both HIV-1 promoter and genome wide analyses, we demonstrate that Integrator subunits specifically control NELF-mediated RNAPII pause/release at coding genes. The strength of RNAPII pausing is determined by the nature of the NELF-associated complex. Interestingly, in addition to controlling RNAPII pause release INTS11 catalytic subunit of the INTScom is required for the synthesis of full length mRNA. Finally, INTScom-target genes are enriched in HIV-1 TAR/ NELF-binding element and in a 3’box sequence required for snRNA biogenesis. Revealing these unexpected functions of INTScom in regulating RNAPII pausing/release and completion of mRNA synthesis of NELF-target genes will contribute to our understanding of the gene expression cycle. Binding profiles of Integrator subunits in HeLa cells by ChIP-Seq (Illumina) Please note that the MACS14*.tar.gz contains MACS output bed and xls files and the 'readme.txt' contains a detailed description of each file.

2015-05-19 | E-GEOD-60584 | biostudies-arrayexpress

Integrator complex subunit 12 knockout overcomes a transcriptional block to HIV latency reversal

Project description:Integrator complex subunit 12 knockout overcomes a transcriptional block to HIV latency reversal

| PRJNA1161690 | ENA

INTS13 Mutations Causing a Developmental Ciliopathy Disrupt Integrator Complex Assembly

Project description:Oral-facial-digital syndromes (OFD) are a heterogeneous group of congenital disorders characterized by malformations of the face and oral cavity, and digit anomalies. To date, mutations in 12 ciliary-related genes have been identified to cause several OFD types suggesting OFDs constitute a subgroup of developmental ciliopathies. Through homozygosity mapping and exome sequencing performed on two families with variable OFD type 2, we identified distinct germline mutations in INTS13, a subunit of the Integrator Complex. This 14-component complex associates with RNAPII and can cleave nascent RNA to modulate gene expression. We determined that INTS13 utilizes a discrete domain within its C-terminus to bind the Integrator cleavage module, which is disrupted by the identified germline INTS13 mutations. Depletion of INTS13 disrupts ciliogenesis in human cultured cells and causes dysregulation of a broad collection of ciliary genes. Accordingly, its knockdown in Xenopus embryos lead to motile cilia anomalies. Altogether, we show that mutations in INTS13 cause an autosomal recessive ciliopathy, which reveal key interactions within Integrator components.

2021-07-11 | GSE154197 | GEO

Integrator complex subunit 12 knockout overcomes a transcriptional block to HIV latency reversal [CRISPR]

Project description:Integrator complex subunit 12 knockout overcomes a transcriptional block to HIV latency reversal [CRISPR]

| PRJNA1158849 | ENA

Transcriptomic effects of INTS1 knockout in zebrafish larvae

Project description:Precise regulation of RNA polymerase II (RNAPII) is fundamental to transcriptional fidelity in eukaryotes. The Integrator complex, a conserved multi-subunit assembly, safeguards transcriptional integrity through its interaction with RNAPII, mediating transcription initiation, nascent RNA cleavage, and 3′ end processing. INTS1, the largest subunit of the Integrator complex, is critical for its function, and its mutations are linked to human neurodevelopmental disorders, yet, the underlying transcriptional effects remain poorly defined. Here, we characterize the global transcriptional effects of INTS1 deficiency in zebrafish. INTS1 loss leads to widespread gene expression changes, including of genes linked to hyperactivity and pathways associated with Attention-Deficit/Hyperactivity Disorder. We observe mutant-specific first intron retentions and transcript extensions. These findings underscore a central role for INTS1 in coordinating transcriptional regulation, and highlight the essential function of the Integrator complex in maintaining transcriptome integrity. Together, they offer insights into how INTS1 disruption may contribute to behavioral and physiological abnormalities.

2025-09-01 | GSE297343 | GEO

Homo sapiens

Project description:hnRNP C is a key regulator of protein synthesis in mitosis

| PRJNA326128 | ENA

Integrator complex subunit 12 knockout overcomes a transcriptional block to HIV latency reversal [AutoCUT&Tag]

Project description:Integrator complex subunit 12 knockout overcomes a transcriptional block to HIV latency reversal [AutoCUT&Tag]

| PRJNA1161694 | ENA

Integrator complex subunit 12 knockout overcomes a transcriptional block to HIV latency reversal [RNA-seq]

Project description:Integrator complex subunit 12 knockout overcomes a transcriptional block to HIV latency reversal [RNA-seq]

| PRJNA1158793 | ENA