scholarly journals Binding and regulation of cellular functions by monoclonal antibodies against human tumor necrosis factor receptors.

1990 ◽  
Vol 172 (5) ◽  
pp. 1517-1520 ◽  
Author(s):  
M R Shalaby ◽  
A Sundan ◽  
H Loetscher ◽  
M Brockhaus ◽  
W Lesslauer ◽  
...  
Keyword(s):  
Monoclonal Antibodies ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Human Tumor ◽  
Membrane Receptors ◽  
Tnf Alpha ◽  
Human Tumor Necrosis Factor ◽  
Cellular Functions ◽  
Tumor Necrosis Factor Receptors ◽  
Necrosis Factor

The present study was undertaken to further characterize the interaction of monoclonal antibodies (mAbs) against tumor necrosis factor (TNF) receptors with different targets, and to assess their ability to influence TNF effects on U937 and human endothelial cell (HEC) functions. Actions of recombinant TNF-alpha on U937 and HEC were effectively inhibited by Htr-5 and Utr-1, and to a greater extent by a combination of both mAbs. These observations indicate that TNF interaction with antigenically different components of membrane receptors (p55 and p75) represents a crucial step in transduction of signals for TNF toxicity against U937 and TNF activation of HEC functions.

scholarly journals Recombinant human tumor necrosis factor alpha regulates c-myc expression in HL-60 cells at the level of transcription

Blood ◽  
1987 ◽  
Vol 70 (1) ◽  
pp. 200-205
Author(s):  
A Tobler ◽  
D Johnston ◽  
HP Koeffler
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Human Tumor ◽  
Tnf Alpha ◽  
Mrna Levels ◽  
Human Tumor Necrosis Factor ◽  
Mrna Accumulation ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

Recombinant human tumor necrosis factor alpha (TNF alpha) effectively inhibits clonal growth of leukemic cells from patients and several cell lines, including the promyelocytic HL-60 cells. Decreased expression of the c-myc oncogene is linked to growth arrest and terminal cellular differentiation. The present study characterizes the effect of TNF alpha on the regulation of the c-myc gene in HL-60 cells. TNF alpha (100 U/mL) rapidly inhibited messenger RNA (mRNA) accumulation of c-myc with a 50% reduction in less than one hour. Dose-response studies showed that a 50% reduction of c-myc mRNA occurred in the range of 15 U/mL. In vitro nuclear run-on experiments showed that this decrease of c-myc-mRNA accumulation was the result of a reduced rate of transcription of c-myc by TNF alpha. Further studies demonstrated that TNF alpha did not post-transcriptionally alter levels of c-myc mRNA, and the inhibitory action of TNF alpha on c-myc expression in HL-60 cells did not depend on new protein synthesis. In the conditions of all the experiments, TNF alpha did not affect cell viability. By contrast, TNF alpha (500 U/mL) did not decrease mRNA levels of c-myc in an HL-60 variant cell line whose growth was not inhibited by TNF alpha; also TNF alpha (500 U/mL) increased c-myc-mRNA levels in normal fibroblasts whose growth is known to be stimulated by TNF alpha. These findings, in concert with prior studies, show a close association between growth inhibition of HL-60 cells and decreased levels of mRNA coding for c-myc.

Monoclonal antibodies to human tumor necrosis factor α: In vitro and in vivo application

Cytokine ◽  
1990 ◽  
Vol 2 (3) ◽  
pp. 162-169 ◽  
Author(s):  
Achim Möller ◽  
Franz Emling ◽  
Dietmar Blohm ◽  
Erich Schlick ◽  
Klaus Schollmeier
Keyword(s):  
Monoclonal Antibodies ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Human Tumor ◽  
Human Tumor Necrosis Factor ◽  
Factor Α ◽  
Necrosis Factor
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