Amino Acid Sequence Gly-Arg-Lys-Lys-Arg-Arg-Gln-Arg-Arg-Arg-Pro-Pro-Arg-Pro-Lys-Arg-Pro-Thr-Thr-Leu-Asn-Leu-Phe-Pro-Gln-Val-Pro-Arg-Ser-Gln-Asp-NH2 Biochem/physiol Actions The L-JNKi 1 and the protease resistant, all-D retro-inverso form, D-JNKi peptides represent the only potent inhibitors specific for JNK (JNK1, JNK2 and JNK3). Different from chemical inhibitors that directly affect kinase activity e.g. by competing with the ATP-binding site of the protein kinase, they rather inhibit the interaction between JNK and its substrate, resulting in a JNK K.O. phenotype. In contrast to pure diffusion they are actively transported into cells, where they remain until their proteolytic degradation. The c-Jun N-terminal kinases (JNK1, 2, 3), members of the mitogen-activated protein kinase (MAPK) superfamily, are activated by a wide variety of extracellular stimuli such as inflammatory cytokines, heat shock and ischemia.Targets of JNKs are mostly transcription factors, including c-Jun, activating transcription factor(ATF) 2, and ETS-containing factors such as Elk1. Other targets having function regulated by JNK-mediated phosphorylation include insulin receptor substrate 1 and Bcl-2. |
Amino Acid Sequence Gly-Arg-Lys-Lys-Arg-Arg-Gln-Arg-Arg-Arg-Pro-Pro-Arg-Pro-Lys-Arg-Pro-Thr-Thr-Leu-Asn-Leu-Phe-Pro-Gln-Val-Pro-Arg-Ser-Gln-Asp-NH2 Biochem/physiol Actions The L-JNKi 1 and the protease resistant, all-D retro-inverso form, D-JNKi peptides represent the only potent inhibitors specific for JNK (JNK1, JNK2 and JNK3). Different from chemical inhibitors that directly affect kinase activity e.g. by competing with the ATP-binding site of the protein kinase, they rather inhibit the interaction between JNK and its substrate, resulting in a JNK K.O. phenotype. In contrast to pure diffusion they are actively transported into cells, where they remain until their proteolytic degradation. The c-Jun N-terminal kinases (JNK1, 2, 3), members of the mitogen-activated protein kinase (MAPK) superfamily, are activated by a wide variety of extracellular stimuli such as inflammatory cytokines, heat shock and ischemia.Targets of JNKs are mostly transcription factors, including c-Jun, activating transcription factor(ATF) 2, and ETS-containing factors such as Elk1. Other targets having function regulated by JNK-mediated phosphorylation include insulin receptor substrate 1 and Bcl-2. |