HMGB1 prefers to interact with structural RNAs and regulates rRNA methylation modification and translation in HeLa cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA494169 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26338463_1.fastq.gz | Fastqsanger.gz | |||
| SRR26338463_2.fastq.gz | Fastqsanger.gz | |||
| SRR26338464_1.fastq.gz | Fastqsanger.gz | |||
| SRR26338464_2.fastq.gz | Fastqsanger.gz | |||
| SRR26338465_1.fastq.gz | Fastqsanger.gz |
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Project description:High-mobility group B1 (HMGB1) is both a DNA binding nuclear factor modulating transcription and a crucial cytokine that mediates the response to both infectious and noninfectious inflammation.Recently data show that HMGB1is a RNA-binding protein also affecting splicing.Howerer we still lack understanding of the functional roles of HMGB1 in protein translation.To address theses we applied Improved RNA immunoprecipitation by UV cross-linking and deep sequencing (iRIP-seq) experiment revealed that HMGB1 selectively bound to mRNAs and structured RNAs. We also integrated RNA-seq data from knockdown and overexpress HMGB1 to show that HMGB1 affected some genes expression. Taken these data together, our findings highlight that HMGB1 binds to multiple RNA species including mRNA and snoRNA
2024-04-10 | GSE120693 | GEO
Project description:BackgroundHigh-mobility group B1 (HMGB1) is both a DNA binding nuclear factor modulating transcription and a crucial cytokine that mediates the response to both infectious and noninfectious inflammation such as autoimmunity, cancer, trauma, and ischemia reperfusion injury. HMGB1 has been proposed to control ribosome biogenesis, similar as the other members of a class of HMGB proteins.ResultsHere, we report that HMGB1 selectively promotes transcription of genes involved in the regulation of transcription, osteoclast differentiation and apoptotic process. Improved RNA immunoprecipitation by UV cross-linking and deep sequencing (iRIP-seq) experiment revealed that HMGB1 selectively bound to mRNAs functioning not only in signal transduction and gene expression, but also in axon guidance, focal adhesion, and extracellular matrix organization. Importantly, HMGB1-bound reads were strongly enriched in specific structured RNAs, including the domain II of 28S rRNA, H/ACA box snoRNAs including snoRNA63 and scaRNAs. RTL-P experiment showed that overexpression of HMGB1 led to a decreased methylation modification of 28S rRNA at position Am2388, Cm2409, and Gm2411. We further showed that HMGB1 overexpression increased ribosome RNA expression levels and enhanced protein synthesis.ConclusionTaken together, our results support a model in which HMGB1 binds to multiple RNA species in human cancer cells, which could at least partially contribute to HMGB1-modulated rRNA modification, protein synthesis function of ribosomes, and differential gene expression including rRNA genes. These findings provide additional mechanistic clues to HMGB1 functions in cancers and cell differentiation.
| S-EPMC10996203 | biostudies-literature
Project description:High Mobility Group Box 1 (HMGB1) is a highly abundant and evolutionarily conserved non-histone chromatin component with the ability to bind and bend DNA. The protein is involved in fundamental nuclear processes including nucleosome sliding, transcription, replication, V(D)J recombination and DNA transposition. To assess the functional impact of HMGB1 on transcription we performed gene expression profile analyses of HeLa cells stably transfected with an anti-HMGB1 shRNA expressing plasmid or a control plasmid. 2 stable clones: control HeLa, Hmgb1-knocked down HeLa, 3 technical replicates. Hmgb1 knockdown HeLa cells were prepared by stable transfection with the plasmid Hmgb1shRNA-pSuperior.puro or, as a mock control, with the empty vector pSuperior.puro (Invitrogen). Transfection was made starting from 500 thousands (500K) or 5 milions (5mil) cells. Transfected cells were selected with puromycin and single resistant clones were picked, amplified and analyzed for HMGB1 expression by western blot. A clone containing less then 10% of the wt amount of HMGB1 was selected for further experiments. Total RNAs were extracted using Quiagen RNeasy kit and analyzed on the Illumina BeadsArray platform in 2 technical replica (2 arrays).
2011-06-28 | E-GEOD-18721 | biostudies-arrayexpress
Project description:High Mobility Group Box 1 (HMGB1) is a highly abundant and evolutionarily conserved non-histone chromatin component with the ability to bind and bend DNA. The protein is involved in fundamental nuclear processes including nucleosome sliding, transcription, replication, V(D)J recombination and DNA transposition. To assess the functional impact of HMGB1 on transcription we performed gene expression profile analyses of HeLa cells stably transfected with an anti-HMGB1 shRNA expressing plasmid or a control plasmid.
2011-06-28 | GSE18721 | GEO
Project description:This study reports the interactome of HMGB1 in prostate and ovarian cancer cells, which includes a variety of proteins involved in diverse cellular processes. Subcellular fractionation is used to map the distribution of interacting proteins. In the nucleus, HMGB1 interacts directly with NuRD complex subunit RBBP7, as confirmed by yeast two-hybrid. Amongst HMGB1 interacting proteins are also subunits of the THOC complex and the septin complex. THOC5 IP-MS experiments confirmed that THOC proteins interact with septins and also with RAB11.
2022-02-17 | PXD026258 | Pride
Project description:Astrocytes are intimately linked with brain blood vessels, a relationship critical for neuronal function. However, astroglial factors driving these physical and functional associations during postnatal brain development have yet to be identified. By characterizing structural and transcriptional changes in mouse cortical astrocytes during the first two postnatal weeks, we find that high-mobility group box 1 (Hmgb1), normally upregulated with injury and involved in adult cerebrovascular repair, is highly expressed in astrocytes at birth and then decreases rapidly. Astrocyte-selective ablation of Hmgb1 at birth affects astrocyte morphology and endfoot placement, alters distribution of endfoot proteins connexin43 and aquaporin-4, induces transcriptional changes in astrocytes related to cytoskeleton remodeling, and profoundly disrupts endothelial ultrastructure. While lack of astroglial Hmgb1 does not affect the blood-brain barrier or angiogenesis postnatally, it impairs neurovascular coupling and behavior in adult mice. These findings identify astroglial Hmgb1 as a key player in postnatal gliovascular maturation.
2023-07-10 | GSE236429 | GEO
Project description:Astrocytes are intimately linked with brain vessels, a relationship that is critical for neuronal health and function. However, key astroglial molecular factors that drive these physical and functional associations during postnatal brain development have not yet been identified. We characterized structural and transcriptional changes in mouse cortical astrocytes and microvessels during the first two postnatal weeks and found that high-mobility group box 1 (Hmgb1), normally upregulated with injury and involved in adult cerebrovascular repair, was highly expressed in astrocytes at birth to then decreased rapidly. Astrocyte-selective ablation of Hmgb1 in newborn mice affected astrocyte morphology and endfoot placement, induced disruption of endfoot proteins connexin43 and aquaporin-4, induced transcriptional changes in astrocytes, and profoundly altered endothelial cell ultrastructure. While lack of astroglial Hmgb1 did not affect the blood-brain barrier or angiogenesis postnatally, it impaired neurovascular coupling and behavior in adult mice. These findings identify astroglial Hmgb1 as a key player in postnatal gliovascular maturation.
2023-06-13 | GSE224784 | GEO
Project description:Testing the consequences of the absence of the chromatin-associated HMGB1 protein on the transcriptome in Arabidopsis. Keywords: Comparison of mutant and wildtype samples. Four replicate RNA extractions were performed of each genotype using independent pools of plants. hmgb1#1 (Cy5) vs. Col-0#1 (Cy3) Col-0#2 (Cy5) vs. hmgb1#2 (Cy3) dye-swap hmgb1#3 (Cy5) vs. Col-0#3 (Cy3) Col-0#5 (Cy5) vs. hmgb1#4 (Cy3) dye-swap Samples were hybridized in two dye-swaps. The data were normalized over all 4 hybridizations to obtain one, single log-ratio(Sample/Reference). The raw data files of all four of the hybridizations are attached to the Sample.
2008-11-23 | E-GEOD-10638 | biostudies-arrayexpress
Project description:High Mobility Group Box 1 (HMGB1) is a highly abundant and evolutionarily conserved non-histone chromatin component with the ability to bind and bend DNA. The protein is involved in fundamental nuclear processes including nucleosome sliding, transcription, replication, V(D)J recombination and DNA transposition. To assess the functional impact of HMGB1 on transcription we performed gene expression profile analyses of mouse embryonic fibroblasts, wild-type or knockout for the Hmgb1 gene 2 genetic backgrounds: wild-type (Wt), Hmgb1-/- (KO), 3 biological replicates (rep1, rep2, rep3; S phase synchronized cells in duplicate only), no technical replicates. Each pair of wt and Hmgb1-/- MEFs was isolated from embryos born from a single Hmgb1+/- mother crossed with a Hmgb1 +/- male. Total RNAs from three pairs of MEFs, derived from three different mothers and cultured up to passage 3, were extracted using mirVana miRNA Isolation Kit (Ambion) and analyzed on the Illumina BeadsArray platform.
2013-10-01 | E-GEOD-18463 | biostudies-arrayexpress
Project description:Mutant ataxin-1 (Atxn1), which causes spinocerebellar ataxia type 1 (SCA1), binds to and impairs the function of high mobility group box 1 (HMGB1), a critical nuclear protein that regulates DNA architectural changes essential for DNA damage repair and transcription. In this study, we established that transgenic or virus vector-mediated supplementation of HMGB1 ameliorates motor dysfunction and elongates lifespan in mutant Atxn1 knock-in (Atxn1-KI) mice. We identified mitochondrial DNA damage repair by HMGB1 as a novel molecular basis for this effect, in addition to the mechanisms already associated with HMGB1 function, such as nuclear DNA damage repair and nuclear transcription. The dysfunction and the improvement of mitochondrial DNA damage repair functions are tightly associated with the exacerbation and rescue, respectively, of symptoms, supporting the involvement of mitochondrial DNA quality control by HMGB1 in SCA1 pathology. Moreover, we show that the rescue of Purkinje cell dendrites and dendritic spines by HMGB1 could be downstream effects. Although extracellular HMGB1 triggers inflammation mediated by toll-like receptor and receptor for advanced glycation end products, upregulation of intracellular HMGB1 does not induce such side effects. Thus, viral delivery of HMGB1 is a candidate approach by which to modify the disease progression of SCA1 even after its onset.
2015-01-05 | E-MTAB-2987 | biostudies-arrayexpress