Prostaglandin E2 receptors of a human monocytic cell line, U937 cells

1993 ◽  
Vol 21 (1) ◽  
pp. 52S-52S
Author(s):  
CHOY CHENG LOH ◽  
DINO ROTONDO ◽  
ASIM K. DUTTA-ROY
Keyword(s):  
Prostaglandin E2 ◽  
Cell Line ◽  
U937 Cells ◽  
Monocytic Cell ◽  
Monocytic Cell Line ◽  
Human Monocytic Cell Line ◽  
Human Monocytic Cell

Expression of N-Acetyl Transferase in a Human Monocytic Cell-Line, U937

1991 ◽  
Vol 10 (1) ◽  
pp. 33-38 ◽  
Author(s):  
S.L. Kelly ◽  
E. Sim
Keyword(s):  
Cell Line ◽  
The Other ◽  
U937 Cells ◽  
Monocytic Cell ◽  
Monocytic Cell Line ◽  
Human Monocytic Cell Line ◽  
Human Monocytic Cell

1 N-acetyl transferase (NAT) catalyses the acetylation of arylamine and hydrazine drugs and other xenobiotics. The activity of one isozyme (polymorphic NAT) varies amongst indiviudals but the other (monomorphic NAT) does not. 2 The human monocytic cell-line U937 transcribes the gene for monomorphic N-acetyl transferase. 3 Although the gene for polymorphic N-acetyl transferase is present in these cells, its expression is not detected. 4 It is concluded that U937 cells are a useful model for studying the metabolism of arylamines and hydrazines by human monomorphic N-acetyl transferase.

scholarly journals Screening of compounds toxicity against human Monocytic cell line-THP-1 by flow cytometry

10.1251/bpo92 ◽  
2004 ◽  
Vol 6 (1) ◽  
pp. 220-225 ◽  
Author(s):  
Neora Pick ◽  
Scott Cameron ◽  
Dorit Arad ◽  
Yossef Av-Gay
Keyword(s):  
Flow Cytometry ◽  
Cell Line ◽  
Monocytic Cell ◽  
Monocytic Cell Line ◽  
Human Monocytic Cell Line ◽  
Human Monocytic Cell

scholarly journals Alkaline Comet Assay using the monocytic cell line THP-1

2019 ◽  
Author(s):  
Ana Neves-Costa ◽  
Dora Pedroso ◽  
Luis F Moita
Keyword(s):  
Comet Assay ◽  
Cell Line ◽  
Adherent Cell ◽  
Monocytic Cell ◽  
Monocytic Cell Line ◽  
Strand Breaks ◽  
Human Monocytic Cell Line ◽  
Human Monocytic Cell ◽  
Dna Strand

Abstract This protocol details the experimental procedure for performing the comet assay, a very sensitive DNA break assay based on single cell gel electrophoresis.The analysis of DNA strand breaks, both single- and double-strand breaks (SSBs and DSBs, respectively), was performed in immune responsive cells. The cell line used was the human monocytic cell line THP-1, an adherent cell type with many known applications in in vitro studies of innate immunity. The comet assay is a robust procedure that allows the accurate and reproducible quantification of DNA damage. Here we describe not only the comet assay step-by-step protocol, but also some important aspects related to troubleshooting.

Gallic Acid Inhibits Cell Viability and Induces Apoptosis in Human Monocytic Cell Line U937

2011 ◽  
Vol 14 (3) ◽  
pp. 240-246 ◽  
Author(s):  
Nam-Seok Kim ◽  
Seung-Il Jeong ◽  
Byung-Soon Hwang ◽  
Young-Eun Lee ◽  
Shin-Ho Kang ◽  
...  
Keyword(s):  
Cell Viability ◽  
Gallic Acid ◽  
Cell Line ◽  
Monocytic Cell ◽  
Monocytic Cell Line ◽  
Human Monocytic Cell Line ◽  
Human Monocytic Cell

scholarly journals Changes in phospholipid metabolism induced by quinine, 4-aminopyridine and tetraethylammonium in the monocytic cell line THP1

1992 ◽  
Vol 282 (2) ◽  
pp. 443-446 ◽  
Author(s):  
C Pelassy ◽  
N Cattan ◽  
C Aussel
Keyword(s):  
Cell Line ◽  
Phospholipid Metabolism ◽  
Choline Transport ◽  
Monocytic Cell ◽  
Monocytic Cell Line ◽  
K Channels ◽  
Human Monocytic Cell Line ◽  
Human Monocytic Cell

Quinine, 4-aminopyridine and tetraethylammonium, three compounds generally used as effectors of K+ channels, strongly modify phospholipid metabolism. In the human monocytic cell line THP1, the three drugs enhanced the incorporation of [3H]serine into phosphatidylserine and that of [3H]inositol into phosphatidylinositol in the absence of significant changes in the uptake of the 3H labels. On the contrary, the biosynthesis of both phosphatidylcholine and phosphatidylethanolamine was strongly inhibited. This inhibition appeared to be mainly due to the inhibition of both [3H]choline and [3H]ethanolamine uptake by the cells, by impairment of choline transport in a competitive mode.

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