Anti-Tyk2: Mouse Tyk2 Antibody

Tyk2-deficient mice, unlike other Jak kinase mutants, are developmentally normal. It was shown that Tyk2 was not absolutely essential for type I IFN signaling in mice. Thus, the function of Tyk2 in mice appears to be compensated for in vivo, partly by other kinase(s), most likely other Jak(s). However, Tyk2 plays obligatory roles in multiple cytokine signals involved in innate and acquired immunity of humans, which differs substantially from Tyk2 function in mice.⁴ Furthermore, it was shown that Tyk2 function is critical for the downregulation of metabolic genes upon immune challenge, in particular genes involved in lipid metabolism. Thus, there may be an important regulatory role for Tyk2 in modulating the relationship between immunity and metabolism.⁵ Additionally, Tyk2 acts in non-haematopoetic systems. It was shown that Abeta-induced activation of STAT3 and caspase-3-dependent neuronal death can be inhibited in tyk2–/– neurons, which suggest the potential involvement of Tyk2/STAT3 signaling in AD pathophysiology.⁶ Moreover, Tyk2/Jak signaling may also participate in protein synthesis signaling. It was shown that PKR acts as a substrate of activated Jaks, and is phosphorylated at Tyr 101 and Tyr 293. PKR tyrosine phosphorylation provides an important link between IFN signaling and translational control through the regulation of eIF2alpha phosphorylation.⁷