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Genome-wide profiling of Kdm2a binding and H3K36me2 of hypoxia-cultured B cells derived from miR-155-sufficient and -deficient mice [ChIP-seq]

ABSTRACT: Genome-wide profiling of Kdm2a binding and H3K36me2 of hypoxia-cultured B cells derived from miR-155-sufficient and -deficient mice [ChIP-seq]

PROVIDER: PRJNA961712 | ENA |

REPOSITORIES: ENA

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Genome-wide profiling of Kdm2a binding and H3K36me2 of hypoxia-cultured B cells derived from miR-155-sufficient and -deficient mice [ChIP-seq]

Project description:To investigate the impact caused by miR-155 ablation, B cells from miR-155-sufficient and -deficient mice were cultured in hypoxic conditions and analyzed for profiling the binding of a miR-155 target, Kdm2a, to genomic loci and the distribution pattern of H3K36me2, which Kdm2a demethylates.

2024-10-30 | GSE230527 | GEO

The Role of KDM2A and H3K36me2 Demethylation in Modulating MAPK Signaling during Neurodevelopment [ChIP-seq]

Project description:To investigate how KDM2A regulates downstream genes and affects NPC function and the role of KDM2A in histone methylation, we performed KDM2A and H3K36me2 ChIP-Seq. By analyzing both datasets together, we identified 2,051 overlapping peaks that were shared by both KDM2A and H3K36me2, The enriched genes were found to be associated with generating neurons, central nervous system development and cell proliferation. Furthermore, disease enrichment analysis revealed significant associations with ASD, ID and other neurodevelopmental disorders, indicating KDM2A's roles in neural development.

2024-02-18 | GSE229835 | GEO

KDM2A plays a dual role in regulating the expression of malignancy-related genes in esophageal squamous cell carcinoma

Project description:KDM2A is a histone demethylase, which primarily catalyzes the demethylation of H3K36me2. Abnormal expression of KDM2A is observed in many types of cancers; however, the molecular events connected to KDM2A expression remain unclear. In this work, to gain further insight into the molecular mechanism underlying the function of KDM2A, we analyzed the expression and function of KDM2A in esophageal squamous cell carcinoma (ESCC) cells.

2023-03-31 | GSE207721 | GEO

The Role of KDM2A and H3K36me2 Demethylation in Modulating MAPK Signaling during Neurodevelopment [RNA-seq]

Project description:To explore how KDM2A regulates downstream genes and impacts NPC function, we generated KDM2A knockdown H9 ESC lines using shRNA lentivirus. We designed five siRNAs and selected the two most effective ones for shRNA creation, which were then packaged into shRNA lentivirus (sh1, sh4). Subsequently, we induced these cells into NPCs and cerebral organoids. Through RNA-seq and DEG analysis, we observed that DEGs in NPCs were associated with the MAPK signaling pathway, a finding also present in cerebral organoids. We conducted a disease enrichment analysis on the obtained gene lists, revealing enrichment in neurodevelopmental disorders such as intellectual disability (ID) and autism spectrum disorder (ASD). This finding indirectly suggests that KDM2A plays a role in early neurodevelopmental processes.

2024-02-18 | GSE229834 | GEO

The Role of KDM2A and H3K36me2 Demethylation in Modulating MAPK Signaling during Neurodevelopment.

Project description:The Role of KDM2A and H3K36me2 Demethylation in Modulating MAPK Signaling during Neurodevelopment.

| PRJNA956289 | ENA

The Role of KDM2A and H3K36me2 Demethylation in Modulating MAPK Signaling during Neurodevelopment [ChIP-seq]

Project description:The Role of KDM2A and H3K36me2 Demethylation in Modulating MAPK Signaling during Neurodevelopment [ChIP-seq]

| PRJNA956291 | ENA

The Role of KDM2A and H3K36me2 Demethylation in Modulating MAPK Signaling during Neurodevelopment [RNA-seq]

Project description:The Role of KDM2A and H3K36me2 Demethylation in Modulating MAPK Signaling during Neurodevelopment [RNA-seq]

| PRJNA956292 | ENA

Transcriptome analysis of histone demethylase Kdm2a knockout in mouse embryonic stem cells

Project description:H3K36 methylation plays an important role in gene regulation. The role of H3K36 demethylase Kdm2b has been well studied. However, the role of Kdm2a in embryonic stem cells are still unkonwn. To study the function of Kdm2a in embryonic stem cells. We used CRISPR-gRNA system to knockout Kdm2a. We analyzed the gene expression change and identified target genes and repeats of Kdm2a. We uncovered a novel role of Kdm2a in regulating gene expression in embryonic stem cells.

2019-08-20 | GSE117148 | GEO

Structural basis of paralog-specific KDM2A/B nucleosome recognition

Project description:The nucleosome acidic patch is a major interaction hub for chromatin, providing a platform for enzymes to dock and orient for nucleosome-targeted activities. In order to define the molecular basis of acidic patch recognition proteome-wide, we performed an amino acid resolution acidic patch interactome screen. We discovered that the histone H3 lysine 36 (H3K36) demethylase KDM2A, but not its closely related paralog, KDM2B, requires the acidic patch for nucleosome binding. These KDM2 family JumonjiC (JmjC) domain lysine demethylases are critical to heterochromatin formation and are commonly misregulated in cancer. Despite fundamental roles in transcriptional regulation in health and disease, the molecular mechanisms governing nucleosome substrate specificity of KDM2A/B, or any other JmjC lysine demethylases, remain unclear. We used a covalent JmjC inhibitor to solve cryo-EM structures of KDM2A and KDM2B trapped in action on the nucleosome. Our structures show that KDM2-nucleosome binding is paralog-specific and facilitated by dynamic nucleosomal DNA unwrapping and histone charge shielding that mobilize the H3K36 sequence for demethylation.

2023-02-14 | PXD032791 | Pride

Histone H3K36me2 demethylase KDM2A promotes bladder cancer progression through epigenetically silencing RARRES3.

Project description:Epigenetic dysregulation contributes to bladder cancer tumorigenesis. H3K36me2 demethylase KDM2A functions as an important epigenetic regulator of cell fate in many types of tumors. However, its role in bladder cancer remains unknown. Here, we revealed a positive correlation between KDM2A gene copy number gain and upregulation of KDM2A mRNA expression in bladder cancer. Moreover, a super-enhancer (SE) driving KDM2A transcription was found in high-grade bladder cancer, resulting in a significantly higher expression of KDM2A mRNA compared to that in low-grade bladder tumors. KDM2A knockdown (KD) decreased the proliferation, invasion, and spheroid formation of high-grade bladder cancer cells and inhibited tumor growth in mouse xenograft models. Furthermore, we identified RARRES3 as a key KDM2A target gene. KDM2A suppresses RARRES3 expression via demethylation of H3K36me2 in the RARRES3 promoter. Intriguingly, RARRES3 KD attenuated the inhibitory effects of KDM2A depletion on the malignant phenotypes of high-grade bladder cancer cells. The combination of the KDM2A inhibitor IOX1 and the RARRES3 agonist all-trans retinoic acid (ATRA) synergistically inhibited the proliferation of high-grade bladder cancer cells, suggesting that the KDM2A/RARRES3 axis may be a promising therapeutic target for the treatment of high-grade bladder cancer.

| S-EPMC9192503 | biostudies-literature

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