Project description:Using a genome-wide CRISPR activation screen, we identified ZNF296, a transcription factor prominently expressed in epithelial cancers, as a key regulator of tumor resistance to NK cell-mediated cytotoxicity. To investigate the role of ZNF296 in regulating chromatin accessibility and its effects on gene transcription, we performed ATAC-seq on ZNF296-overexpressing (ZNF296-OE) and control A549 cells. These data provide insights into the epigenetic mechanisms underlying ZNF296-mediated tumor immune evasion.

2025-09-06 | GSE283057 | GEO

A tumor specific super-enhancer drives immune evasion by guiding synchronous expression of PD-L1 and PD-L2

Project description:A tumor specific super-enhancer drives immune evasion by guiding synchronous expression of PD-L1 and PD-L2

2019-07-30 | GSE135016 | GEO

Proteostatic Stress Response Drives T Cell Exhaustion and Immune Evasion

Project description:Proteostatic Stress Response Drives T Cell Exhaustion and Immune Evasion

| PRJNA1295348 | ENA

Mal2 drives immune evasion by reducing antigen presentation on tumor cells

Project description:Mal2 drives immune evasion by reducing antigen presentation on tumor cells

| PRJNA602751 | ENA

Histone methylation antagonism drives tumor immune evasion in squamous cell carcinomas

Project description:Histone methylation antagonism drives tumor immune evasion in squamous cell carcinomas

| PRJNA773062 | ENA

KRAS drives immune evasion in a genetic model of pancreatic cancer

Project description:KRAS drives immune evasion in a genetic model of pancreatic cancer

| PRJNA548394 | ENA

ZNF296 drives immune evasion in epithelial cancer cells [ChIP-seq]

Project description:Using a genome-wide CRISPR activation screen, we identified ZNF296, a transcription factor highly expressed in epithelial cancers, as a key regulator of tumor resistance to NK cell-mediated cytotoxicity. To uncover its direct targets, we performed ChIP-seq in A549 cells overexpressing ZNF296-Flag, revealing its preferential binding to specific genomic regions. IP-MS further demonstrated that ZNF296 interacts with the NuRD complex, which suppresses gene expression via histone deacetylase activity.To test whether ZNF296 mediates transcriptional repression through the NuRD complex, we conducted ChIP-seq for HDAC1, a core component of the complex, in ZNF296-overexpressing (ZNF296-OE) and control A549 cells. These analyses revealed genomic targets co-regulated by ZNF296 and the NuRD complex, providing insights into its mechanism of transcriptional regulation.

2025-09-06 | GSE283059 | GEO

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