{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE298nnn/GSE298556/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE298556"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Foxk1 regulates effector T cell differentiation and function by repressing autophagy programs via the Akt-mTOR signaling pathway [Foxk1_RNA-seq]","description":"Upon T Cell Receptor (TCR) engagement, the Akt-mTOR signaling cascade initiates downstream events that orchestrate metabolic reprogramming in T cells through the coordinated activation of distinct transcription factors (TFs). Here, we demonstrate that Foxk1 is an integrating component of the Akt-mTOR signaling program, mediating T cell activation and differentiation. Foxk1 deficiency leads to impaired effector functions in both CD4⁺ and CD8⁺ T cells, associated with defects in metabolic reprogramming. We demonstrate that this is due to Foxk1’s ability to repress autophagy-related genes within hours following TCR stimulation. Conversely, overexpression or enforced nuclear localization of Foxk1 enhances effector-like phenotype of T cells, leading to better anti-tumor responses. Our results demonstrate the central role played by Foxk1 in initiating T cell activation and in shaping their differentiation trajectory.","dates":{"publication":"2026/09/01"},"accession":"GSE298556","cross_references":{"GSM":["GSM9017194","GSM9017195","GSM9017196","GSM9017197","GSM9017198","GSM9017210","GSM9017199","GSM9017211","GSM9017200","GSM9017201","GSM9017202","GSM9017203","GSM9017204","GSM9017205","GSM9017206","GSM9017207","GSM9017208","GSM9017209"],"GPL":["19057"],"GSE":["298556"],"taxon":["Mus musculus"]}}