OVA-T4 Peptide

OVA-T4 Peptide (SIITFEKL; OVA (257-264) Variant) (0.1 nM; 48 h) induced robust proliferation of OT-I CD8 T cells, and this proliferation was enhanced in the absence of ZFP36 and ZFP36L1^[4].
OVA-T4 Peptide (0.1 nM; 24-48 h) induces CD25 expression and STAT5 phosphorylation in OT-I CD8 T cells, and this process is impaired in the absence of ZFP36 and ZFP36L1^[4].
OVA-T4 Peptide (0.1 nM; 72 h)-induced OT-I CD8 T cell expansion depends on IL-2 availability, which is impaired in the absence of ZFP36 and ZFP36L1^[4].
In OVA-T4 Peptide (100 nM; 24-48 h)-stimulated OT-I CD8⁺ T cells, ITK/RLK activity is dispensable for the switch-like induction of CD69 but is critical for regulating IRF4 expression and proliferative potential^[6].
In naive OT-I CD8⁺ T cells stimulated with OVA-T4 Peptide (100 nM; 1-2 h), NF-κB (p65) activation showed a graded response that could be modulated by TCR signal strength and was selectively attenuated by ITK/RLK inhibition^[6].
In naive OT-I CD8⁺ T cells stimulated with OVA-T4 Peptide (100 nM; 1 h), DAG signaling plays a dominant role in regulating NF-κB translocation, and supplementation with Phorbol 12-myristate 13-acetate (PMA) (HY-18739) can rescue the NF-κB signaling defect caused by ITK/RLK inhibition^[6].


In OVA-T4 Peptide (100 nM; 30-120 min)-stimulated OT-I CD8⁺ T cells, ITK/RLK inhibition reduced the expression of cytokine- and effector-related transcripts (including IRF4) after 2 hours of stimulation^[6].
OVA-T4 Peptide (0.1 nM; 1.5-16 h) induces transcriptional changes in OT-I CD8 T cells, in which ZFP36 and ZFP36L1 regulate a network of cytokine signaling pathway regulators including Socs1, Cish, Socs3, and Pim1^[4].
OVA-T4 Peptide (6 h) only altered the magnitude of cytokine production in mouse OT-I effector CD8⁺ T cells without changing its kinetics^[5].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.