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Interleukin 6 is expressed in high levels in psoriatic skin and stimulates proliferation of cultured human keratinocytes.
Interleukin 6 could directly contribute to the epidermal hyperplasia seen in psoriatic epithelium as well as affect the function of dermal inflammatory cells.
Paradigm shifts in the cell biology of STAT signaling.
  • P. Sehgal
  • Biology
    Seminars in cell & developmental biology
  • 1 August 2008
Activation of the human "beta 2-interferon/hepatocyte-stimulating factor/interleukin 6" promoter by cytokines, viruses, and second messenger agonists.
The region between -225 and -113 in IFN-beta 2, which contains DNA motifs similar to the regulatory elements in the human c-fos gene, appears to contain the major cis-acting regulatory elements responsible for the activation of the IFN -beta 2 promoter by several different cytokines, viruses, and second messenger agonists.
Repression of the interleukin 6 gene promoter by p53 and the retinoblastoma susceptibility gene product.
Transient transfection experiments suggest that p53 and RB may be involved as transcriptional repressors in modulating IL-6 gene expression during cellular differentiation and oncogenesis.
Amniotic fluid interleukin 6 in preterm labor. Association with infection.
Evaluation of AF IL-6 levels may have diagnostic and prognostic value in the management of women in preterm labor and implicate IL- 6 in the host response to intrauterine infection.
Cellular Physiology of STAT3: Where’s the Cytoplasmic Monomer?*
It is discovered that there is little monomeric STAT3 in the cytosol of liver cells, and an alternative model for STAT signaling is suggested in which STAT3 proteins function in the cytoplasm as heteromeric complexes with accessory scaffolding proteins, including the chaperone GRP58.
Cytokine Signaling
The data show pre-association of STATs with plasma membrane rafts in flotation fractions, and suggest that Tyr phosphorylation may not in itself be sufficient to cause the departure of PY-STATs from plasma membrane floating rafts.
On the mechanism for efficient repression of the interleukin-6 promoter by glucocorticoids: enhancer, TATA box, and RNA start site (Inr motif) occlusion.
Surprisingly, chimeric genes containing MRE II, which lacks a recognizable GACGTCA cyclic AMP- and phorbol ester-responsive motif, were strongly induced by both phorbl ester and forskolin, suggesting that MREII (ACATTGCACAATCT) may be the prototype of a novel cycle-responsive element.