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ALG1 — IL6

Text-mined interactions from Literome

Penkowa et al., Glia 1999 (Brain Injuries) : The opposing effect of IL-6 on MT-I+II and MT-III levels in the damaged brain suggests MT isoform-specific functions
Daffada et al., FEBS Lett 1999 : We found that IL-1alpha, IL-1beta and IL-6 increased both metallothionein-1 (MT-1) and metallothionein-2 (MT-2) mRNA in HepG2 cells ... IL-6 induced only low levels of both MT-1 and MT-2 mRNA
Penkowa et al., Glia 2000 (Brain Injuries...) : The changes in neuronal tissue damage and in brain regeneration observed in IL-6KO mice are likely caused by the IL-6 dependent decrease in MT-I+II expression, indicating IL-6 and MT-I+II as neuroprotective factors during brain injury
Okumura et al., Biochim Biophys Acta 2011 : Interleukin-6 , which induces MT-I transcription independently of MTF-1, did not reduce histone H3 levels in the promoter
Sato et al., Int J Immunopharmacol 1994 : MT-I was also induced in lung and heart by TNF, but little by IL-6
Sato et al., Int J Immunopharmacol 1996 : This suggests a synergistic effect of IL-6 and Dex on MT-I synthesis in the heart
Hernández et al., Neurochem Int 1998 (Brain Injuries...) : The results suggest that IL-1 and IL-6 are important regulators of brain MT-I+II and that these cytokines could mediate MT-I+II induction after an immunological insult
Carrasco et al., Brain Res Mol Brain Res 1998 : In contrast to LPS, brain MT-I induction by restraint stress was not affected significantly by IL-6 or TNFR1 deficiencies, suggesting that these cytokines are not important during the stress response in the brain
Carrasco et al., Exp Neurol 1998 : The effect of interleukin-6 (IL-6) on metallothionein-I (MT-I) and MT-III expression in the brain has been studied in transgenic mice expressing IL-6 under the regulatory control of the glial fibrillary acidic protein gene promoter ( GFAP-IL6 mice ), which develop chronic progressive neurodegenerative disease
Lee et al., Biochem J 1999 : This study suggests that the effects of LPS on hepatic MT-I gene expression are mediated by IL-6 and involve the activation of STAT binding to the proximal promoter