Extended Data Fig. 4: Loss of SIRT2 enhances LCK activation and downstream TCR signaling through LCKK228 acetylation.
From: SIRT2-mediated deacetylation of LCK governs the magnitude of T cell receptor signaling
a, Immunoblot analysis of phosphorylated and total LCK, LAT and PLCγ1 following TCR stimulation with 2.5 µg/ml CD3 Abs for 2–5 min in CRISPR-Cas9–generated LCK-deficient Jurkat clones (Lck−/−Sirt2+/+, C1 and C2) and double LCK–SIRT2-deficient Jurkat clones (Lck−/−Sirt2−/−, C4, C7 and C8) reconstituted with empty, LCKWT, LCKK228R or LCKK228Q vectors. b, Immunoblot analysis of phosphorylated and total LCK following stimulation with 2.5 µg/ml CD3 Abs for 2–5 min in LCK-deficient primary mouse CD3+ T cells in WT or Sirt2−/− backgrounds reconstituted with empty, LCKWT, LCKK228R or LCKK228Q vectors. GAPDH used as loading control. Data representative of three independent experiments.
