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:First, we report a series of ChIP-seq results in LbetaT2 cells. Briefly, we performed ChIP-seq experiments with antibodies specific for Foxk2, Sin3a, Tet1 and Uhrf1 in LbetaT2 cells. We found that a total of 343 different promoters including Nab2 that are co-targeted by Foxk2, Sin3a, Tet1 and Uhrf1. Next, hMeDIP-seq and ChIP-seq experiments with antibodies specific for 5hmC and H3K18ub in the pituitary tissues of wild-type and Foxk2 knockout mice were performed. The results showed that compared to the wild-type mice, knockout of Foxk2 reduced the enrichment of 5hmC and H3K18ub on the Foxk2 target gene.This study revealed a critical switch control of FOXK2 for GnRH pulse frequency-dependent LH production and gave us a new understanding of the role of Foxk2 in chromatin status and gene transcription.
Project description:To seek molecular mechanisms underlying the sick sinu syndrome phenotypes observed in Dnajb6 heterozygous knockout mice, we performed whole transcriptome RNA-sequencing experiments using right atrial tissues isolated from Dnajb6 heterozygous knockout mic and WT control mice at 1 year of age.
Project description:The goal of these Hi-ChIP experiments was to determine changes in cohesin-mediated chromatin contacts caused by AHDC1/Gibbin knockout.
Project description:We performed knockout and wild type expression experiments in yeast grown in soribtol to identify genes invovled in controling osmotic stress response.
