<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE319nnn/GSE319703/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Homo sapiens</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE319703</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>YTHDF1 functions as a non-canonical nuclear checkpoint that couples R-loop homeostasis to innate immune restraint and adaptive immune resistance in cancer（RNA-seq II）</name><description>Innate immune signaling within cancer cells plays an important role in shaping antitumor immunity, yet the nuclear mechanisms that restrain inappropriate immune activation remain incompletely defined. YTHDF1 is an mRNA-binding protein previously characterized as a cytoplasmic m⁶A reader. Emerging evidence indicates that YTHDF1 also functions in the nucleus, where it associates with chromatin and contributes to the regulation of R-loop homeostasis. Loss of YTHDF1 results in R-loop accumulation, genomic instability, cytosolic DNA release, and activation of the cGAS–STING–type I interferon pathway. Mechanistically, YTHDF1 interacts with the chromatin remodeler ARID1A at immune-associated genomic regions, suggesting a cooperative role in maintaining genome stability and regulating immune-related transcriptional programs. To investigate the transcriptomic and chromatin-level consequences of YTHDF1 and ARID1A perturbation, we generated RNA sequencing (RNA-seq) and R-loop CUT&amp;Tag datasets in A549 human lung cancer cells. RNA-seq was performed in two experimental settings: (1) wild-type (WT) and YTHDF1 knockout (YTHDF1-KO) cells; and (2) WT, YTHDF1-KO, ARID1A knockdown (siARID1A), and combined YTHDF1-KO with ARID1A knockdown cells. In parallel, R-loop CUT&amp;Tag profiling was conducted under the same respective conditions to assess genome-wide R-loop distribution. These datasets provide integrated transcriptomic and chromatin profiling resources for studying the roles of YTHDF1 and ARID1A in regulating R-loop dynamics and tumor-intrinsic innate immune signaling</description><dates><publication>2026/07/15</publication></dates><accession>GSE319703</accession><cross_references><GSM>GSM9524103</GSM><GSM>GSM9524102</GSM><GSM>GSM9524105</GSM><GSM>GSM9524104</GSM><GSM>GSM9524110</GSM><GSM>GSM9524101</GSM><GSM>GSM9524112</GSM><GSM>GSM9524111</GSM><GSM>GSM9524107</GSM><GSM>GSM9524106</GSM><GSM>GSM9524109</GSM><GSM>GSM9524108</GSM><GPL>24676</GPL><GSE>319703</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>