Similar Datasets
Project description:KDM5B promote tumorigenesis in MCF-7 cells
| PRJNA1210488 | ENA
Project description:CUL4B and KDM5B ChIP-sequencing in MCF-7 cells
| PRJNA1210487 | ENA
Project description:Estrogen receptor-positive (ER+) breast cancer is the predominant subtype of breast cancer. Here, we investigate the functional interplay between lysine demethylase 5B (KDM5B) and the Cullin-RING ligase 4B (CRL4B) complex in modulating cholesterol metabolism to promote ER+ breast cancer progression. We found that disrupting the KDM5B–CRL4B axis impairs cholesterol homeostasis and inhibits tumor growth.
2026-02-18 | GSE286885 | GEO
Project description:Analysis of the effects of KDM5B in melanoma cells at gene expression level. Knockdown of KDM5B provides important information about potential target genes of KDM5B.
2022-03-14 | GSE137393 | GEO
Project description:The biological significance of microglia are highlighted by their critical role as the resident immune cells of the central nervous system. In this capacity, microglia maintain homeostasis through various pathways that include cell migration, phagocytosis as well as secretion of immune-related and signaling factors into the extracellular environment. Microglial reactivity is associated with a variety of functional outcomes that are highly context-dependent and therefore microglia can exhibit a wide range of phenotypes. Epigenetic regulation through DNA methylation and histone modifications has recently been implicated in this complex control of microglial reactivity. Specifically, in relation to histone methylation status, the histone demethylase KDM5B has been implicated in many pathophysiological states including alcohol use disorder (AUD), cancer, and inflammatory disorders; however, the cell type-specific role of KDM5B in microglial reactivity has yet to be fully investigated. In this study, transcriptomic and proteomic analyses were used to characterize the effects of KDM5B knockdown on microglial pathways using CRISPR editing of adult-derived murine microglial cells to generate a Kdm5b knockout pool. From this multi-omic analysis, over 34,000 genes and 9,000 proteins were identified across all replicates of wild-type (WT) and KDM5B-depleted microglia. Additionally, various stimuli including LPS, IL4, and alcohol were used to study the effects of KDM5B knockdown on immune reactivity in microglia using deep proteomic analysis. Through this deep characterization, an overall decrease in inflammatory and immune reactivity pathways was observed in KDM5B-depleted microglia, which was then functionally validated through measurement of secreted factors including TNFα, IL6, IL4, IL10, IL16, and SPP1. The results from this study has provided critical insight into KDM5B-mediated effects on microglial function as well as a molecular framework for future studies aimed to understand epigenetic regulation of microglia and implications in neurodegenerative disease pathogenesis and progression.
2026-02-19 | GSE291289 | GEO
Project description:ES cell pluripotency is thought to be regulated in part by H3K4 methylation. However, it is unclear how H3K4 demethylation contributes to ES cell function and participates in iPS cell reprogramming. Here, we show that KDM5B, which demethylates H3K4, is important for ES cell differentiation, and presents a barrier to the reprogramming process. Depletion of Kdm5b leads to an extension in the self-renewal of ES cells in the absence of LIF. Transcriptome analysis revealed the persistent expression of pluripotency-genes and underexpression of developmental genes during differentiation in the absence of Kdm5b, suggesting that KDM5B plays a key role in cellular fate changes. We also observed accelerated reprogramming of differentiated cells in the absence of Kdm5b, demonstrating that KDM5B is a barrier to the reprogramming process. Expression analysis revealed that mesenchymal master regulators associated with epithelial-to-mesenchymal transition (EMT) are downregulated during reprogramming in the absence of Kdm5b. Moreover, global analysis of H3K4me3/2 revealed that enhancers of fibroblast genes are rapidly deactivated in the absence of Kdm5b, and genes associated with EMT lose H3K4me3/2 during the early reprogramming process. These findings provide functional insight into the role for KDM5B in regulating ES cell differentiation and as a barrier to the reprogramming process. ChIP-Seq for H3K4me3 and H3K4me2 in murine shLuc and shKdm5b 4TF-MEFs (tetO-Pou5f1,-Sox2,-Klf4,-c-Myc) at 48h.
2013-10-14 | E-GEOD-47123 | biostudies-arrayexpress
Project description:ES cell pluripotency is thought to be regulated in part by H3K4 methylation. However, it is unclear how H3K4 demethylation contributes to ES cell function and participates in iPS cell reprogramming. Here, we show that KDM5B, which demethylates H3K4, is important for ES cell differentiation, and presents a barrier to the reprogramming process. Depletion of Kdm5b leads to an extension in the self-renewal of ES cells in the absence of LIF. Transcriptome analysis revealed the persistent expression of pluripotency-genes and underexpression of developmental genes during differentiation in the absence of Kdm5b, suggesting that KDM5B plays a key role in cellular fate changes. We also observed accelerated reprogramming of differentiated cells in the absence of Kdm5b, demonstrating that KDM5B is a barrier to the reprogramming process. Expression analysis revealed that mesenchymal master regulators associated with epithelial-to-mesenchymal transition (EMT) are downregulated during reprogramming in the absence of Kdm5b. Moreover, global analysis of H3K4me3/2 revealed that enhancers of fibroblast genes are rapidly deactivated in the absence of Kdm5b, and genes associated with EMT lose H3K4me3/2 during the early reprogramming process. These findings provide functional insight into the role for KDM5B in regulating ES cell differentiation and as a barrier to the reprogramming process. RNA-Seq of undifferentiated and embryoid body (EB) differentiated murine shLuc and shKdm5b ES cells
2013-10-14 | E-GEOD-47124 | biostudies-arrayexpress
Project description:Microglia maintain brain homeostasis through coordinated pathways, including cell migration, phagocytosis, and secretion of immune-related signaling factors. Microglial reactivity is associated with a variety of functional outcomes that are highly context-dependent with epigenetic regulation through DNA methylation and histone modificationsimplicated in this complex control of microglial plasticity. Specifically, in relation to histone methylation, lysine-specific demethylase 5B (KDM5B) has been associated with several pathophysiological states, including neurodevelopmental and inflammatory disorders, cancer, and alcohol use disorder; however, the cell-type-specific role of KDM5B in microglial reactivity has not been investigated. In this study, transcriptomic and proteomic analyses were used to characterize the effects of KDM5B depletion on microglial pathways in clustered regularly interspaced short palindromic repeats (CRISPR)-edited adult-derived murine microglial cells. Additionally, various immunomodulatory stimuli, including lipopolysaccharide, interleukin-4, and alcohol, were used to study the effects of KDM5B depletion on immune reactivity in microglia using deep proteomics and bioinformatic analysis. Through this comprehensive characterization, KDM5B-depleted microglia exhibited broad remodeling of immune reactivity, including reduced intracellular and secreted inflammatory responses to lipopolysaccharide as well as distinct modulation of alcohol- and interleukin-4-induced pathways, that was functionally demonstrated by altered cytokine secretion profiles. Results from this study provide critical insight into KDM5B-mediated immunological effects on microglial function.
2026-03-02 | PXD058485 | Pride
Project description:RNA-seq analysis was performed to identify key signaling responding to PRMT6 knockdown in MDA-MB-231
2023-05-24 | GSE210948 | GEO
Project description:ES cell pluripotency is thought to be regulated in part by H3K4 methylation. However, it is unclear how H3K4 demethylation contributes to ES cell function and participates in iPS cell reprogramming. Here, we show that KDM5B, which demethylates H3K4, is important for ES cell differentiation, and presents a barrier to the reprogramming process. Depletion of Kdm5b leads to an extension in the self-renewal of ES cells in the absence of LIF. Transcriptome analysis revealed the persistent expression of pluripotency-genes and underexpression of developmental genes during differentiation in the absence of Kdm5b, suggesting that KDM5B plays a key role in cellular fate changes. We also observed accelerated reprogramming of differentiated cells in the absence of Kdm5b, demonstrating that KDM5B is a barrier to the reprogramming process. Expression analysis revealed that mesenchymal master regulators associated with epithelial-to-mesenchymal transition (EMT) are downregulated during reprogramming in the absence of Kdm5b. Moreover, global analysis of H3K4me3/2 revealed that enhancers of fibroblast genes are rapidly deactivated in the absence of Kdm5b, and genes associated with EMT lose H3K4me3/2 during the early reprogramming process. These findings provide functional insight into the role for KDM5B in regulating ES cell differentiation and as a barrier to the reprogramming process.
2013-10-14 | GSE47124 | GEO