SOLUBLE INTERLEUKIN 6 (IL-6) RECEPTOR INFLUENCES THE EXPRESSION OF THE PROTOONCOGENE junB AND THE PRODUCTION OF FIBRINOGEN IN THE HepG2 HUMAN HEPATOMA CELL LINE AND PRIMARY RAT HEPATOCYTES

Igaz, Péter; Tóth, Sára; Rose-John, Stefan; Madurka, Ildikó; Fejér, György; Szalai, Csaba; Falus, András

doi:10.1006/cyto.1997.0330

Cited by 13 publications

(7 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The studies of Igaz et al 38 also shows antagonistic activity of sIL‐6R. Addition of IL‐6 resulted in an induction of junB mRNA expression using HepG2 cells and primary rat hepatocytes.…”

Section: Agonistic and ‘Non‐agonistic’ Properties Of Sil‐6rmentioning

confidence: 85%

“…The relatively new assumption that sIL‐6R itself, without IL‐6, might exert signaling on cells is supported by three studies. It could be shown that the presence of sIL‐6R induced the expression of junB 6.66‐fold relative to the control in HepG2 cells (which are known not to produce endogenous IL‐6 38 ). Another study done by Holub et al , 34 also showed surprising effects of sIL‐6R on HepG2 cells.…”

Section: Agonistic and ‘Non‐agonistic’ Properties Of Sil‐6rmentioning

confidence: 99%

See 1 more Smart Citation

sIL‐6R: more than an agonist?

Knüpfer

Preiss

2007

Immunol Cell Biol

View full text Add to dashboard Cite

On target cells, interleukin‐6 (IL‐6) interacts with its receptor complex consisting of the membrane‐bound IL‐6 receptor (IL‐6R) and the signal transducing protein gp130. IL‐6R can exist as a soluble protein (sIL‐6R), which binds the ligand IL‐6. This soluble complex can bind to gp130 on cells that lack the membrane‐bound IL‐6R and initiate signaling. This process is named transsignaling. The significance of transsignaling via sIL‐6R is underlined by different publications and exceeds very probably the significance of the membrane‐bound IL‐6R. It is the general assumption that sIL‐6R acts as an agonist in combination with IL‐6 resulting in an enhancement of the IL‐6 effects. In this article, we suppose ‘non‐agonistic’ properties. There are several publications that give reasons to speculate that sIL‐6R (a) has IL‐6‐antagonistic effects, (b) has orphan properties and (c) interacts with yet unknown binding partners different from IL‐6. Knowledge about additional properties of sIL‐6R will enlarge the biologic understanding of this molecule and might give an explanation for the sometimes contrasting effects of the cytokine IL‐6.

show abstract

Section: Agonistic and ‘Non‐agonistic’ Properties Of Sil‐6rmentioning

confidence: 85%

Section: Agonistic and ‘Non‐agonistic’ Properties Of Sil‐6rmentioning

confidence: 99%

sIL‐6R: more than an agonist?

Knüpfer

Preiss

2007

Immunol Cell Biol

View full text Add to dashboard Cite

show abstract

“…The PCR-competitor for HDC was generated by performing a PCR reaction facilitating mismatch priming between the primers for HDC and human genomic DNA described earlier for junB oncogene [27,28]. Biefly, human genomic DNA was produced from Jurkat cell line (human Th1 leukemia).…”

Section: Quantitative Rt-pcr For Hdcmentioning

confidence: 99%

Both interferon (IFN) α and IFN γ inhibit histidine decarboxylase expression in the HT168 human melanoma cell line

Héninger¹,

Falus²,

Darvas³

et al. 2000

Inflammation Research

View full text Add to dashboard Cite

show abstract

“…Elevated IL-6 levels in patients are related to future cardiovascular complications [13]. Both hepatocytes and endothelial cells are able to produce IL-6 [24,25]. Previously, we have shown that endothelial cells produce large quantities of IL-6 after infection with viruses [4].…”

Section: Discussionmentioning

confidence: 99%

Acute‐phase response of human hepatocytes after infection with Chlamydia pneumoniae and cytomegalovirus

Verkerk

Visseren

Bouter

et al. 2003

Eur J Clin Investigation

View full text Add to dashboard Cite

We conclude that in addition to direct vascular wall infection by C. pneumoniae and CMV, virus-related development of atherosclerosis might also be initiated by chronic liver infection and subsequent production of inflammatory and procoagulant mediators released in the circulation. This may be another pathophysiological link for the observed relation between infections and the development of atherosclerosis.

show abstract

SOLUBLE INTERLEUKIN 6 (IL-6) RECEPTOR INFLUENCES THE EXPRESSION OF THE PROTOONCOGENE junB AND THE PRODUCTION OF FIBRINOGEN IN THE HepG2 HUMAN HEPATOMA CELL LINE AND PRIMARY RAT HEPATOCYTES

Cited by 13 publications

References 0 publications

sIL‐6R: more than an agonist?

sIL‐6R: more than an agonist?

Both interferon (IFN) α and IFN γ inhibit histidine decarboxylase expression in the HT168 human melanoma cell line

Acute‐phase response of human hepatocytes after infection with Chlamydia pneumoniae and cytomegalovirus

Contact Info

Product

Resources

About