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IL6 — TYR

Text-mined interactions from Literome

Choi et al., Pigment Cell Res 2005 (Melanoma) : The results reveal that ELA may be an effective inhibitor of hyperpigmentation caused by UV irradiation or by pigmented skin disorders through a mechanism involving IL-6 mediated downregulation of Mitf rather than a direct inhibition of tyrosinase activity
Chen et al., Br J Pharmacol 2006 : Pretreatment of ECs with Mag dose dependently inhibited IL-6 induced Tyr705 and Ser727 phosphorylation in STAT3 without affecting the phosphorylation of JAK1, JAK2, and ERK1/2
Liu et al., Oncogene 2010 (Prostatic Neoplasms) : Small interfering RNA mediated knockdown of Ack1 or Src showed that Ack1 mediates heregulin- and Gas6 induced AR Tyr-267 phosphorylation, whereas Src mediates Tyr-534 phosphorylation induced by EGF, IL-6 and bombesin
Serrano-Marco et al., Diabetologia 2012 (Insulin Resistance) : In addition, treatment with this drug abolished IL-6 induced STAT3 phosphorylation of Tyr7°5 and Ser7²7 and prevented the increase in SOCS3 caused by this cytokine
Nishimura et al., Biochim Biophys Acta 1990 : Iodination of Tyr-32 gave no significant effect on IL-6 activity, suggesting that Tyr-32 is not responsible for IL-6 activity
Fahmi et al., Cell Signal 2013 (Hypertrophy...) : Furthermore, IL-6/sIL-6R induced phosphorylation of STAT1 Tyr and STAT3 Tyr were enhanced by SB203580
Andrés et al., Exp Dermatol 2013 (MAP Kinase Signaling System...) : Tyr705 phosphorylation was induced by IL-6 and IL-20 in a Jak2 dependent manner, and moreover, phosphorylation of Tyr705 produced a strong increase in STAT3 transcriptional activity
Swope et al., J Immunol 1989 (Melanoma) : IL-6 significantly inhibited the basal level of tyrosinase and partially abrogated the alpha-MSH induced tyrosinase activity ... IL-1 alpha, GM-CSF, and IL-6 or IL-1 alpha and GM-CSF added together did not significantly affect the MSH induced tyrosinase activity
Swope et al., J Invest Dermatol 1994 : Previously we demonstrated that neonatal human melanocyte proliferation and tyrosinase activity are inhibited by interleukin-1 alpha, tumor necrosis factor-alpha, and interleukin-6