Characterization of the defect in a variant of HL-60 promyelocytic leukemia cells with reduced transferrin receptor expression

1992 ◽  
Vol 18 (1) ◽  
pp. 45-63 ◽  
Author(s):  
Kimiko Ishiguro ◽  
Peter T. C. Ho ◽  
Alan C. Sartorelli
Keyword(s):  
Transferrin Receptor ◽  
Promyelocytic Leukemia ◽  
Receptor Expression ◽  
Leukemia Cells ◽  
Transferrin Receptor Expression

Diltiazem inhibits transferrin receptor expression and causes G1 arrest in normal and neoplastic T cells

1986 ◽  
Vol 6 (12) ◽  
pp. 4244-4250
Author(s):  
L M Neckers ◽  
S Bauer ◽  
R C McGlennen ◽  
J B Trepel ◽  
K Rao ◽  
...  
Keyword(s):  
T Cells ◽  
Transferrin Receptor ◽  
Interleukin 2 ◽  
Receptor Expression ◽  
Calcium Flux ◽  
G1 Arrest ◽  
Receptor Mrna ◽  
Interleukin 2 Receptor ◽  
Transferrin Receptor Expression ◽  
Malignant T Cells

Transferrin receptor expression is essential for the proliferation of both normal and malignant T cells. While transferrin receptor expression in normal T cells is tightly coupled to interleukin-2 receptor expression, transferrin receptor expression in malignant cells is usually constitutive and is released from this constraint. Temporally, the appearance of these membrane receptors is preceded by changes in the expression of the proto-oncogenes c-myc and c-myb. In addition, although an increase in the level of intracellular free calcium occurs early in the sequence of T-cell activation, the activation events dependent on this calcium flux have not been resolved. In the present study we report that diltiazem, an ion channel-blocking agent that inhibits calcium influx, arrested the growth in vitro of both normal and malignant human T cells in the G1 phase of the cell cycle. However, diltiazem did not inhibit the expression of c-myc or interleukin-2 receptor mRNA and protein in normal mitogen-activated T cells or the constitutive expression of c-myc and c-myb mRNA in malignant T cells (T acute lymphoblastic leukemia cells). In contrast, diltiazem prevented the induction of transferrin receptor (mRNA and protein) in normal T cells and caused a progressive loss of transferrin receptor (mRNA and protein) in malignant T cells. These data demonstrate that diltiazem can dissociate several growth-related processes normally occurring in G1 and thereby disrupt the biochemical cascade leading to cell proliferation.

Decreased transferrin receptor expression by neuromelanin cells in restless legs syndrome

Neurology ◽  
2004 ◽  
Vol 62 (9) ◽  
pp. 1563-1567 ◽  
Author(s):  
J. R. Connor ◽  
X. S. Wang ◽  
S. M. Patton ◽  
S. L. Menzies ◽  
J. C. Troncoso ◽  
...  
Keyword(s):  
Restless Legs Syndrome ◽  
Transferrin Receptor ◽  
Receptor Expression ◽  
Restless Legs ◽  
Transferrin Receptor Expression

scholarly journals Mechanisms of differential transferrin receptor expression in normal hematopoiesis

2000 ◽  
Vol 267 (23) ◽  
pp. 6762-6774 ◽  
Author(s):  
Nadia M. Sposi ◽  
Luciano Cianetti ◽  
Elena Tritarelli ◽  
Elvira Pelosi ◽  
Stefania Militi ◽  
...  
Keyword(s):  
Transferrin Receptor ◽  
Receptor Expression ◽  
Transferrin Receptor Expression

scholarly journals Selective inhibition of the growth of human erythroid bursts by monoclonal antibodies against transferrin or the transferrin receptor

Blood ◽  
1986 ◽  
Vol 67 (6) ◽  
pp. 1631-1638 ◽  
Author(s):  
KM Shannon ◽  
JW Larrick ◽  
SA Fulcher ◽  
KB Burck ◽  
J Pacely ◽  
...  
Keyword(s):  
Monoclonal Antibodies ◽  
Transferrin Receptor ◽  
Thymidine Incorporation ◽  
Selective Inhibition ◽  
Receptor Expression ◽  
Cell Surface Receptor ◽  
Transferrin Receptors ◽  
Human Erythropoietin ◽  
Surface Receptor ◽  
Transferrin Receptor Expression

Abstract The relative requirements of colonies derived from erythroid (BFU-E) and myeloid (CFU-c) progenitors for transferrin were examined using monoclonal antibodies directed against the transferrin molecule (TF-6) or its cell surface receptor (TFR-A12, TFR1–2B). Growth of erythroid bursts was profoundly reduced at concentrations of all three antibodies that had no effect on CFU-c-derived colonies. When TFR1–2B was layered over cultures established one to seven days previously, further burst development was inhibited, and degeneration of early erythroid colonies was observed. Addition of erythropoietin augmented transferrin receptor expression on cells harvested after 1 to 2 weeks in culture and analyzed by flow cytometry. Recombinant human erythropoietin gave results comparable to those obtained in experiments using human urinary erythropoietin. Analysis of erythroblasts plucked directly from culture plates confirmed the presence of transferrin receptors on BFU-E-derived colonies. Thymidine incorporation was maximal early in the second week of culture and coincided with high transferrin receptor expression. These data demonstrate that transferrin must be available into the second week of culture to support the growth and differentiation of BFU- E-derived erythroid bursts, that the generation of erythroid colonies from BFU-E is more dependent on transferrin than myeloid colony formation from CFU-c, and that erythropoietin modulates the expression of transferrin receptors on growing bursts.

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