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Given the seminal discovery of the critical and non-redundant immunosuppressive role of A2AR (24) and the therapeutic potential of A2AR blockade for T cellbased immunotherapy (25), our study demonstrates a viable strategy by targeting A2AR in combination with inhibition of lipid peroxidation to improve persistence and functionality of ACT against cancer
UBQLN2 dysfunction compromises substrate delivery to the proteasome, resulting in the accumulation of toxic protein aggregates and progressive neurodegeneration
PMID 14752199.
Molecular medicine (Cambridge, Mass.), 19(1), 334345
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