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HDAC6 regulates NF-κB signalling by HDAC-dependent and independent mechanisms to control chondrocyte IL-1-induced MMP and inflammatory gene expression [TSA exp]

ABSTRACT: HDAC6 regulates NF-κB signalling by HDAC-dependent and independent mechanisms to control chondrocyte IL-1-induced MMP and inflammatory gene expression [TSA exp]

PROVIDER: PRJNA775078 | ENA |

REPOSITORIES: ENA

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HDAC6 regulates NF-κB signalling by HDAC-dependent and independent mechanisms to control chondrocyte IL-1-induced MMP and inflammatory gene expression [TSA exp]

Project description:Analysis of the effect of HDAC inhibitor TSA on IL-1-induced gene expression in SW1353 chondrocytes.

2021-10-29 | GSE186689 | GEO

HDAC6 regulates NF-κB signalling by HDAC-dependent and independent mechanisms to control chondrocyte IL-1-induced MMP and inflammatory gene expression [HDAC siRNA exp]

Project description:HDAC6 regulates NF-κB signalling by HDAC-dependent and independent mechanisms to control chondrocyte IL-1-induced MMP and inflammatory gene expression [HDAC siRNA exp]

| PRJNA775079 | ENA

KLF9-GRK5-HDAC6 axis aggravates osteoarthritis pathogenesis by promoting chondrocyte extracellular matrix degradation and apoptosis

Project description:Osteoarthritis (OA) is a degenerative joint disease that affects the cartilage and surrounding tissues. The transcription factor Kruppel-like family factor 9 (KLF9) has been identified as a regulator of tumorigenesis. However, its role in OA is still not fully understood. Herein, this study aimed to access the potential role and molecular mechanism by which KLF9 regulates OA development. KLF9 was upregulated in cartilage tissues of OA patients and medial meniscotibial ligament (MMTL)-induced OA rats, as well as in IL-1β-treated chondrocytes. Furthermore, knockdown of KLF9 inhibited OA-related cartilage injury, as evidenced by inhibiting chondrocyte extracellular matrix (ECM) degradation, increasing chondrocyte viability, and decreasing apoptosis. Conversely, overexpression of KLF9 had the opposite effect. The downstream mechanism of KLF9 was confirmed. KLF9 mediated the transcription of G protein-coupled receptor kinase 5 (GRK5) by directly targeting the GRK5 promoter. GRK5 knockdown eliminated the effects of KLF9 overexpression on chondrocyte dysfunction. It was also found that GRK5 combined with histone deacetylase 6 (HDAC6) and promoted HDAC6 phosphorylation. The use of the HDAC6 inhibitor TubastatinA also abolished the effects of GRK5 overexpression on chondrocyte ECM degradation and apoptosis. These results demonstrate that the KLF9-GRK5-HDAC6 axis plays a crucial role in promoting the progression of OA.

2025-01-15 | GSE285234 | GEO

HDAC6 regulates NF-κB signalling by HDAC-dependent and independent mechanisms to control chondrocyte IL-1-induced MMP and inflammatory gene expression [HDAC siRNA exp]

Project description:Analysis of the effect of HDAC6 knockdown on IL-1-induced gene expression in SW1353 chondrocytes.

2021-10-29 | GSE186688 | GEO

HDAC6 regulates NF-κB signalling by HDAC-dependent and independent mechanisms to control chondrocyte IL-1-induced MMP and inflammatory gene expression

Project description:HDAC6 regulates NF-κB signalling by HDAC-dependent and independent mechanisms to control chondrocyte IL-1-induced MMP and inflammatory gene expression

| PRJNA775073 | ENA

Hdac6 regulates Tip60-p400 function in stem cells (sequencing)

Project description:The Tip60 (also known as Kat5) lysine acetyltransferase functions broadly as a transcriptional co-activator that acetylates histones. In contrast, Tip60 functions in embryonic stem cells (ESCs) both to silence genes that promote differentiation and to activate genes required for proliferation. The mechanism by which Tip60 functions as a repressor is unknown. Here we show that the class II histone deacetylase Hdac6 co-purifies with Tip60-p400 complex from ESCs and is necessary for complete silencing of most differentiation genes targeted by Tip60. In contrast to differentiated cells, where Hdac6 is mainly cytoplasmic and does not interact with Tip60, Hdac6 is largely nuclear in ESCs and neural stem cells (NSCs) and interacts with Tip60-p400 in both cell types. Hdac6 is enriched at promoters bound by Tip60-p400 in ESCs, but while Tip60 binds on both sides of transcription start sites (TSSs), Hdac6 binding overlaps with only the downstream Tip60 peak. Surprisingly, Hdac6 does not deacetylate histones at these sites, but rather is required for Tip60 binding. These data suggest that nuclear exclusion of Hdac6 during differentiation plays a major role in modulation of Tip60-p400 function. We determined the genome-wide localization of Tip60 and Hdac6 in mouse ES cells, and examined genomic binding profiles of Tip60 and Hdac6 upon indicated knockdown by ChIP-seq. We examined genomic binding profiles of p400 upon indicated knockdown by ChIP-seq.

2013-11-20 | E-GEOD-42209 | biostudies-arrayexpress

KLF9-GRK5-HDAC6 axis aggravates osteoarthritis pathogenesis by promoting chondrocyte extracellular matrix degradation and apoptosis

Project description:KLF9-GRK5-HDAC6 axis aggravates osteoarthritis pathogenesis by promoting chondrocyte extracellular matrix degradation and apoptosis

| PRJNA1202090 | ENA

HDAC6 Inhibition Disrupts HDAC6-P300 Interaction Reshaping the Cancer Chromatin Landscape (ChIP-Seq)

Project description:Histone deacetylases (HDACs) are crucial regulators of gene expression, DNA synthesis, and cellular processes, making them essential targets in cancer research. HDAC6, specifically, influences protein stability and chromatin dynamics. Despite HDAC6's potential therapeutic value, its exact role in gene regulation and chromatin remodeling needs further clarification. This study examines how HDAC6 inactivation influences lysine acetyltransferase P300 stabilization and subsequent effects on chromatin structure and function in cancer cells. We employed the HDAC6 inhibitor ITF3756, siRNA, or CRISPR/Cas9 gene editing to inactivate HDAC6 in different epigenomic backgrounds. Constantly, this inactivation led to significant changes in chromatin accessibility, particularly increased acetylation of histone H3 lysines 9, 14, and 27 (ATAC-seq and H3K27Ac ChIP-seq analysis). Transcriptomics, proteomics, and gene ontology analysis revealed gene changes in cell proliferation, adhesion, migration, and apoptosis. Significantly, HDAC6 inactivation altered P300 ubiquitination, stabilizing P300 and leading to downregulating genes critical for cancer cell survival. Our study highlights the substantial impact of HDAC6 inactivation on the chromatin landscape of cancer cells and suggests a role for P300 in contributing to the anticancer effects. The stabilization of P300 with HDAC6 inhibition proposes a potential shift in therapeutic focus from HDAC6 itself to its interaction with P300. This finding opens new avenues for developing targeted cancer therapies, improving our understanding of epigenetic mechanisms in cancer cells.

2024-08-19 | GSE273645 | GEO

HDAC6 Inhibition Disrupts HDAC6-P300 Interaction Reshaping the Cancer Chromatin Landscape (ATAC-Seq)

2024-08-19 | GSE273644 | GEO

HDAC6 and HSP90 control the functions of Foxp3+ T regulatory cells

Project description:Foxp3+ T-regulatory cells (Tregs) are key to immune homeostasis such that their diminished numbers or function can cause autoimmunity and allograft rejection. Foxp3+ Tregs express histone/protein deacetylases (HDACs) that regulate chromatin remodeling, gene expression and protein function. Pan-HDAC inhibitors developed for oncology enhance Treg production and suppression but have limited non-oncologic applications given their broad effects. We show, using HDAC6-deficient mice and WT mice treated with HDAC6-specific inhibitors, that HDAC6 inhibition promotes Treg suppressive activity in models of inflammation and autoimmunity, including multiple forms of experimental colitis and fully MHC-incompatible cardiac allograft rejection. Many of the beneficial effects of HDAC6 targeting are also achieved by inhibition of the HDAC6-regulated protein, HSP90. Hence, selective targeting of a single HDAC isoform, HDAC6, or its downstream target, HSP90, can promote Treg-dependent suppression of autoimmunity and transplant rejection. RNA from three independent samples from magnetically separated CD4+CD25+ Treg of HDAC6 knock out, compared to wild type (C57BL6) control

2011-05-01 | E-GEOD-27896 | biostudies-arrayexpress

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