Tumour Necrosis Factor-a and Heat-Shock Protein 70-2 Gene Polymorphisms in a Family with Rheumatoid Arthritis

2004 ◽  
Vol 51 (3) ◽  
pp. 263-269 ◽  
Author(s):  
A. Balog ◽  
J. Gál ◽  
Zsófia Gyulai ◽  
Szilvia Zsilák ◽  
Yvette Mándi
Keyword(s):  
Rheumatoid Arthritis ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Tumour Necrosis Factor ◽  
Heat Shock Protein 70 ◽  
Gene Polymorphisms ◽  
Tumour Necrosis ◽  
Necrosis Factor

Interleukin 1 and tumour necrosis factor increase phosphorylation of the small heat shock protein

FEBS Letters ◽  
1989 ◽  
Vol 258 (2) ◽  
pp. 269-273 ◽  
Author(s):  
Paramjit Kaur ◽  
William J. Welch ◽  
Jeremy Saklatvala
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Interleukin 1 ◽  
Small Heat Shock Protein ◽  
Necrosis Factor

scholarly journals Tumour necrosis factor alpha gene polymorphisms in rheumatoid arthritis: association with susceptibility to, or severity of, disease?

Rheumatology ◽  
1997 ◽  
Vol 36 (5) ◽  
pp. 516-521 ◽  
Author(s):  
B. M. Brinkman ◽  
T. W. Huizinga ◽  
S. S. Kurban ◽  
E. A. van der Velde ◽  
G. M. Schreuder ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumour Necrosis Factor ◽  
Gene Polymorphisms ◽  
Tumour Necrosis ◽  
Tumour Necrosis Factor Alpha ◽  
Necrosis Factor Alpha ◽  
Severity Of Disease ◽  
Factor Alpha ◽  
Alpha Gene ◽  
Necrosis Factor

scholarly journals Phosphorylation of the small heat-shock protein is regulated by interleukin 1, tumour necrosis factor, growth factors, bradykinin and ATP

1991 ◽  
Vol 277 (3) ◽  
pp. 635-642 ◽  
Author(s):  
J Saklatvala ◽  
P Kaur ◽  
F Guesdon
Keyword(s):  
Growth Factor ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Interleukin 1 ◽  
Small Heat Shock Protein ◽  
Prolonged Treatment ◽  
Hsp 27 ◽  
Necrosis Factor

Interleukin 1 (IL1) increased phosphorylation of the small heat-shock protein (hsp 27) in MRC5 fibroblasts. The increase was maintained for at least 30 min, but levels had returned to pre-stimulation values by 2 h. When hsp 27 was metabolically labelled with [3H]leucine, about 15% was phosphorylated in resting confluent cells; this rose to 90% upon stimulation by IL1. Peptide maps of the three differently charged phosphorylated forms were consistent with their arising by phosphorylation of increasing numbers of serine residues. IL1 had the same effect on hsp 27 in pig articular chondrocytes, endothelial cells from human umbilical vein and an epidermoid carcinoma cell line (KB). Certain other agents were found selectively to increase phosphorylation of hsp 27 in MRC5 cells besides IL1 [and tumour necrosis factor (TNF)]. Platelet-derived growth factor had a similar effect to that of IL1; bradykinin, acid fibroblast growth factor and ATP caused an intermediate effect; phorbol myristate acetate (PMA) and 1-oleoyl-2-acetylglycerol had smaller effects. Dibutyryl cyclic AMP and forskolin had no effects on hsp 27 phosphorylation. When cells had been depleted of protein kinase C (PKC) by prolonged treatment with PMA, stimulation by IL1, TNF or bradykinin still increased hsp 27 phosphorylation. The stimulation by all three agents was also unaffected by the PKC inhibitor staurosporine. IL1, TNF and bradykinin each caused hsp 27 phosphorylation by a pathway independent of PKC. The results are consistent with IL1 activating a serine kinase which remains to be identified.

Heat shock protein 70 gene polymorphisms in rheumatoid arthritis

1997 ◽  
Vol 50 (1) ◽  
pp. 71-73 ◽  
Author(s):  
J. Vinasco ◽  
Y. Beraun ◽  
A. Nieto ◽  
A. Fralle ◽  
E. Pareja ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Heat Shock Protein 70 ◽  
Gene Polymorphisms

Endogenous tumour necrosis factor regulates heat-inducible heat shock protein 72 synthesis

1998 ◽  
Vol 14 (3) ◽  
pp. 309-317 ◽  
Author(s):  
N. Watanabe ◽  
N. Tsuji ◽  
S. Akiyama ◽  
H. Sasaki ◽  
T. Okamoto ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Heat Shock Protein 72 ◽  
Necrosis Factor

scholarly journals A single tumour necrosis factor haplotype influences the response to adalimumab in rheumatoid arthritis

2007 ◽  
Vol 67 (4) ◽  
pp. 478-484 ◽  
Author(s):  
C Miceli-Richard ◽  
E Comets ◽  
C Verstuyft ◽  
R Tamouza ◽  
P Loiseau ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumour Necrosis Factor ◽  
Gene Polymorphisms ◽  
Tumour Necrosis ◽  
Shared Epitope ◽  
Pharmacogenetic Study ◽  
Genetic Predictors ◽  
Extended Haplotypes ◽  
Phase Iiib ◽  
Necrosis Factor

Objective:To determine whether tumour necrosis factor (TNF) gene polymorphisms and/or the shared epitope are genetic predictors of the response to adalimumab (ADA) in rheumatoid arthritis (RA).Methods:This ancillary study to the Research in Active Rheumatoid Arthritis (ReAct) Phase IIIb study included a large cohort of Caucasian patients with RA from France (n = 388) treated with ADA plus methotrexate (MTX) (n = 182), ADA plus any other DMARD (n = 98) or ADA alone (n = 108). The primary outcome was ACR50 at 12 weeks. Patients underwent genotyping for HLA-DRB1 and three TNF gene polymorphisms (–238A/G,–308A/G and–857C/T). Extended haplotypes involving HLA-DRB1 and TNF loci were reconstructed using the PHASE program.Results:A total of 151 patients (40%) had an ACR50 response at week 12. Neither the number of HLA-DRB1 shared epitope copies nor presence of the three TNF polymorphisms tested separately was significantly associated with ACR50 response at week 12. However, haplotype reconstruction of the TNF locus revealed that the GGC haplotype (–238G/–308G/–857C) in a homozygous form (i.e. present in more than half of the patients) was significantly associated with a lower ACR50 response to ADA at 12 weeks (34% vs. 50% in patients without the haplotype) (p = 0.003; pa = 0.015). This effect was more important in the subgroup of patients concomitantly treated with MTX.Conclusion:This large pharmacogenetic study provides preliminary data indicating that a single TNF locus haplotype (–238G/–308G/–857C), present on both chromosomes is associated with a lower response to ADA, mainly in patients treated with ADA and MTX.

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