Human Lymphoid Cell Lines in Biochemical Genetics

1981 ◽  
Vol 23 (1) ◽  
pp. 35-38 ◽  
Author(s):  
Ichiro Matsuda ◽  
Izumi Akaboshi ◽  
Jiro Yamamoto ◽  
Noriyuki Nagata
Keyword(s):  
Cell Lines ◽  
Lymphoid Cell ◽  
Biochemical Genetics ◽  
Human Lymphoid Cell ◽  
Lymphoid Cell Lines

Adhesion of human lymphoid cell lines to immobilized carbohydrates and to bone-marrow stromal cell layers by surface sugar receptors

1993 ◽  
Vol 54 (6) ◽  
pp. 1017-1021 ◽  
Author(s):  
Sigrun Gabius ◽  
Ralf Wawotzny ◽  
Sabine Wilholm ◽  
Ulrikc Martin ◽  
Bernhard Wörmann ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Cell Lines ◽  
Lymphoid Cell ◽  
Stromal Cell ◽  
Bone Marrow Stromal Cell ◽  
Marrow Stromal Cell ◽  
Human Lymphoid Cell ◽  
Cell Layers ◽  
Sugar Receptors ◽  
Lymphoid Cell Lines

scholarly journals Arene–Ru(II)–chloroquine complexes interact with DNA, induce apoptosis on human lymphoid cell lines and display low toxicity to normal mammalian cells

2010 ◽  
Vol 104 (9) ◽  
pp. 967-977 ◽  
Author(s):  
Alberto Martínez ◽  
Chandima S.K. Rajapakse ◽  
Roberto A. Sánchez-Delgado ◽  
Armando Varela-Ramirez ◽  
Carolina Lema ◽  
...  
Keyword(s):  
Cell Lines ◽  
Lymphoid Cell ◽  
Mammalian Cells ◽  
Human Lymphoid Cell ◽  
Low Toxicity ◽  
Lymphoid Cell Lines

scholarly journals Cytotoxicity of farnesyltransferase inhibitors in lymphoid cells mediated by MAPK pathway inhibition and Bim up-regulation

Blood ◽  
2011 ◽  
Vol 118 (18) ◽  
pp. 4872-4881 ◽  
Author(s):  
Husheng Ding ◽  
Jennifer Hackbarth ◽  
Paula A. Schneider ◽  
Kevin L. Peterson ◽  
X. Wei Meng ◽  
...  
Keyword(s):  
Cell Lines ◽  
Lymphoid Cell ◽  
Mapk Pathway ◽  
Lymphoid Cells ◽  
Farnesyltransferase Inhibitors ◽  
Death Domain ◽  
Nucleotide Exchange ◽  
Human Lymphoid Cell ◽  
Induced Apoptosis ◽  
Lymphoid Cell Lines

Abstract The mechanism of cytotoxicity of farnesyltransferase inhibitors is incompletely understood and seems to vary depending on the cell type. To identify potential determinants of sensitivity or resistance for study in the accompanying clinical trial (Witzig et al, page 4882), we examined the mechanism of cytotoxicity of tipifarnib in human lymphoid cell lines. Based on initial experiments showing that Jurkat variants lacking Fas-associated death domain or procaspase-8 undergo tipifarnib-induced apoptosis, whereas cells lacking caspase-9 or overexpressing Bcl-2 do not, we examined changes in Bcl-2 family members. Tipifarnib caused dose-dependent up-regulation of Bim in lymphoid cell lines (Jurkat, Molt3, H9, DoHH2, and RL) that undergo tipifarnib-induced apoptosis but not in lines (SKW6.4 and Hs445) that resist tipifarnib-induced apoptosis. Further analysis demonstrated that increased Bim levels reflect inhibition of signaling from c-Raf to MEK1/2 and ERK1/2. Additional experiments showed that down-regulation of the Ras guanine nucleotide exchange factor RasGRP1 diminished tipifarnib sensitivity, suggesting that H-Ras or N-Ras is a critical farnesylation target upstream of c-Raf in lymphoid cells. These results not only trace a pathway through c-Raf to Bim that contributes to tipifarnib cytotoxicity in human lymphoid cells but also identify potential determinants of sensitivity to this agent.

scholarly journals THE RELATIONSHIP BETWEEN ß2-MICROGLOBULIN AND IMMUNOGLOBULIN IN CULTURED HUMAN LYMPHOID CELL LINES

1973 ◽  
Vol 137 (3) ◽  
pp. 838-843 ◽  
Author(s):  
T. H. Hütteroth ◽  
H. Cleve ◽  
S. D. Litwin ◽  
M. D. Poulik
Keyword(s):  
Cell Surface ◽  
Cell Lines ◽  
Specific Antibody ◽  
Lymphoid Cell ◽  
Lymphoid Cells ◽  
Human Lymphoid Cell ◽  
Membrane Antigens ◽  
The Relationship ◽  
Lymphoid Cell Lines

ß2-microglobulin was detected on the cell surface and in the medium of human lymphoid cells established in long-term culture. The secretion of ß2-microglobulin was relatively uniform when different cell lines were compared, whereas IgG production varied widely. κ- and µ-membrane antigens were modulated by specific antibody; ß2-microglobulin was not modulated. Anti-κ and anti-µ antisera had no effect on the expression of membrane ß2-microglobulin, nor had anti-ß2-microglobulin antiserum any effect on the expression of κ- and µ-membrane antigens.

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