Project description:To study the gene expression and phenotype roles of KDAC8, CRISPR/Cas9 was used to create knockout cell lines from wild-type HT1080 cells. Four individual isolated knockout clones were pooled to create the line. Comparable wild-type data is available in GSE302260.
Project description:To study the gene expression and phenotype roles of KDAC6, CRISPR/Cas9 was used to create knockout cell lines from wild-type HT1080 cells. Four individual isolated knockout clones were pooled to create the line. Comparable wild-type data is available in GSE302260.
Project description:HDAC8 expression is causative for resistance to BRAF inhibiton and increased migration in BRAF mutant melanoma cell lines. Changes in gene expression were determined upon forced HDAC8 expression in an isogenic cell line.
Project description:In this study, we analyzed inflammatory response to Poly:IC under HDAC8 or HDAC9 silencing keratinocyte and performed pathway analysis by RNA-seq.
Project description:Interventions: experimental group :PD-1 Knockout Engineered T Cells
Primary outcome(s): Number of participants with Adverse Events and/or Dose Limiting Toxicities as a Measure of Safety and tolerability of dose of PD-1 Knockout T cells using Common Terminology Criteria for Adverse Events (CTCAE v4.0) in patients
Study Design: historical control
Project description:Analysis of the effects of genomic elements, gene transcritpion, and DNA replication on gene targeting. The hypothesis tested was that genomic elements and processes either positively or megatively influence AAV-mediated gene targeting. Results show that homologous recombination increases when the target site is transcribed in the opposite orientation of an incoming replication or transcription fork. Total RNA obtained from cultured HT1080 cell lines
Project description:HDAC8, a member of class I HDACs, plays a pivotal role in cell cycle regulation by deacetylating the cohesin subunit SMC3. While cyclins and CDKs are well-established cell cycle regulators, our knowledge of other regulators remains limited. Here we reveal acetylated K202 in HDAC8 as a key cell cycle regulator responsive to stress. K202 acetylation in HDAC8, primarily catalyzed by Tip60, negatively modulates HDAC8 activity, leading to increased SMC3 acetylation and cell cycle arrest. Furthermore, cells mimicking K202 acetylation display significant alterations in gene expression, potentially linked to changes in 3D genome structure, including enhanced chromatid loop interactions. K202 acetylation negatively impacts cell cycle progression by disrupting the expression of cell cycle-related genes and sister chromatid cohesion, resulting in G2/M phase arrest. These findings illuminate the reversible acetylation of HDAC8 as a novel cell cycle regulator, expanding our understanding of stress-responsive cell cycle dynamics.