Project description:The TNF superfamily is large, including TNF ligands (n = 19) and TNF receptors (n = 29),as determined following the completion of large-scale sequencing of the human and mouse genomes. These members not only function in immune cells but are also involved in respiratory and intestinal diseases, and some members may act as a double-edged sword. Tumor necrosis factor-like cytokine 1A (TL1A, also known as TNFSF15) is the only known death receptor 3 (DR3, also known as TNFRSF25) ligand (Meylan et al., 2011). The TL1A/DR3 axis plays a role in the regulation of intestinal immunity and fibrosis (Valatas et al., 2019), asthma airway remodeling (Zhang et al., 2022; Herro et al., 2010), and other autoimmune and inflammatory diseases (Herro et al., 2021), exacerbating disease progression. However, some researchers have proposed that the TL1A/DR3 axis has a protective role in some disease models. A novel role for TL1A/DR3 in protection against intestinal injury was reported by Jia et al (Jia et al., 2016). Yang et al. revealed a protective effect of TL1A against intracerebral hemorrhage-induced secondary brain injury and infection (Yang et al., 2021). In addition, TL1A maintains the blood–retinal barrier by modulating SHP-1-Src-VE-cadherin signaling in diabetic retinopathy, as verified by Li et al (Li et al., 2021). However, the role of TL1A/DR3 in ARDS has not been explored.
Project description:LORAX-seq (Yang et al, DOI:https://doi.org/10.1016/j.molcel.2024.01.019) was used to identify the backtracked RNA in DIS3-depleted HCT116 DIS3-AID cells. Briefly, LORAX-seq was performed according to Yang et al. (2024) with following modifications. The Pol II complexes were immunoprecipitated with α‐Rpb1 CTD (ab5408, Abcam), followed by capture using a mixture of Dynabeads Protein-A and G. The magnetic beads were treated with recombinant Human TCEA1 protein (ab204205, Abcam) as per Yang et al. (2024), followed by isolation of eluted RNA using TRIZOL (Invitrogen). RNA was prepared for sequencing using the NEBNext Low-bias Small RNA library prep kit (NEB). The eluted RNA was mixed with QIAseq miRNA Library QC Spike-in (331535, Qiagen) as per manufacturer’s instructions. Sequencing libraries were visualized using an Agilent 2100 Tapestation and sequencing was done using the NextSeq 1000/2000 P2 cartridge (Illumina). We identified longer backtracked RNAs in DIS3-depleted cells than in control cells.
Project description:Comment on published article "Massive genomic rearrangement acquired in a single catastrophic event during cancer development." by Stephens, P.J., Greenman, C.D., Beiyuan, F., Yang, F., Bignell, G.R., Mudie, L.J., Pleasance, E.D., Lau, K.W., Beare, D., Stebbings, L.A., et al. (2011). Cell 144, 27-40. [PMID: 21215367]
2011-06-06 | GSE27560 | GEO
Project description:male and female Transcriptome of Poratrioza sinica Yang et Li.
Project description:ChIP-seq data characterizing the occupancy of TFAM over the mitochondrial and nuclear genomes in HeLa cells. Characterization of mitochondrial and nuclear genome-wide TFAM binding in HeLa cells
Project description:Active regions in the genome are more prone to DNA damage (Schwer et al., 2016), but the mutations occur less often in these regions (Martincorena et al., 2012; Monroe et al., 2022; Xia et al., 2020; Zhang and Yang, 2015), indicating involvement of unknown protective machinery. Chronic DNA damage signaling induces senescence associated secretory phenotype (SASP), which mediates pathophysiological functions of senescent cells during aging (Herranz and Gil, 2018), however, the molecular players governing SASP remain poorly understood. Here we performed a genome wide CRISPR screening by implementing a SASP specific reporter system and a guide RNA library targeting regulatory regions and identify several novel SASP repressors. ZNF512B is one such factor that prioritizes DNA repair around regulatory regions associated with highly expressed genes. ZNF512B selectively recruits NuRD nucleosome remodeling complexes to damage loci and ensure faithful timely manner repair. ZNF512B depletion induces SASP, and its overexpression inhibits SASP in various in vitro and in vivo models by modulating DNA repair. ZNF512B overexpression slows down cutaneous wound healing and reduces damage associated with acute liver injury by repression of SASP. ZNF512B is a known prognostic factor for amyotrophic lateral sclerosis (ALS) (Jiang et al., 2021; Tetsuka et al., 2013; Yang et al., 2015; Yu et al., 2018) and its ablation in human neuromuscular organoids leads to depletion of astroglia compartment, a possible mechanism leading to subsequent defects in neuromuscular pathology in ALS. Taken together these findings have important implications for our understanding of repair bias around functionally constrained regions to safeguard long term genome integrity during aging and age associated pathology.
Project description:A robust set of CNS transcript changes was defined by comparing microarray data that describe the injury response of the rat retina [Vazquez-Chona et al., IOVS 2004; GSE1001], brain [Matzilevich et al., J Neurosci Res 2002; GSE1911], and spinal cord [Di Giovanni et al., Ann Neurol 2003; GDS63]. We determined the CNS injury genes that were expressed in cultured astrocytes from rat cortex [GSM34300] and from human optic nerve head [Yang et al., Physiol Genomics 2004; GDS532]. Keywords: other