GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE297nnn/GSE297724/primary200OKGenomicsMus musculusGenome binding/occupancy profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE297724GEOGSEfalseFOXK1 regulates effector T cell differentiation and function by repressing autophagy programs via the Akt-mTOR signaling pathway [Foxk1_ChIP-seq]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.2026/09/01GSE297724GSM8997450GSM899744930172297724Mus musculus