GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE298nnn/GSE298556/primaryOK200TranscriptomicsMus musculusExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE298556GEOGSEfalseFoxk1 regulates effector T cell differentiation and function by repressing autophagy programs via the Akt-mTOR signaling pathway [Foxk1_RNA-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.2026/09/01GSE298556GSM9017194GSM9017195GSM9017196GSM9017197GSM9017198GSM9017210GSM9017199GSM9017211GSM9017200GSM9017201GSM9017202GSM9017203GSM9017204GSM9017205GSM9017206GSM9017207GSM9017208GSM901720919057298556Mus musculus