A rapid redistribution of the transferrin receptor to the cell surface of HL-60 cells and K562 cells upon treatment with dimethyl sulfoxide due to slowing of endocytosis

Deborah J. Vestal, Bruce H. Davis, Caroline Enns

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Treatment of two human leukemia cell lines with 1.25% dimethyl sulfoxide at 37 °C results in a rapid increase in the number of transferrin receptors on the cell surface detected by fluoroscein-labeled anti-transferrin receptor antibodies. Both HL-60 cells, a human myeloid cell line, and K562 cells, a human erythroid-myeloid cell line, showed a 25-65% increase in cell surface transferrin binding in parallel experiments. Scatchard plot analysis of the data indicates that the number of receptors increases while the affinity of transferrin for the receptor remains the same. This rapid increase in the number of receptors at the cell surface appears to be due to a slowing of endocytosis rather than an increase in externalization of the receptor.

Original languageEnglish (US)
Pages (from-to)278-284
Number of pages7
JournalArchives of Biochemistry and Biophysics
Volume276
Issue number1
DOIs
StatePublished - 1990
Externally publishedYes

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Transferrin Receptors
K562 Cells
HL-60 Cells
Endocytosis
Dimethyl Sulfoxide
Cells
Myeloid Cells
Cell Line
Erythroid Cells
Cell Surface Receptors
Transferrin
Leukemia
Antibodies
Experiments

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

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title = "A rapid redistribution of the transferrin receptor to the cell surface of HL-60 cells and K562 cells upon treatment with dimethyl sulfoxide due to slowing of endocytosis",
abstract = "Treatment of two human leukemia cell lines with 1.25{\%} dimethyl sulfoxide at 37 °C results in a rapid increase in the number of transferrin receptors on the cell surface detected by fluoroscein-labeled anti-transferrin receptor antibodies. Both HL-60 cells, a human myeloid cell line, and K562 cells, a human erythroid-myeloid cell line, showed a 25-65{\%} increase in cell surface transferrin binding in parallel experiments. Scatchard plot analysis of the data indicates that the number of receptors increases while the affinity of transferrin for the receptor remains the same. This rapid increase in the number of receptors at the cell surface appears to be due to a slowing of endocytosis rather than an increase in externalization of the receptor.",
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T1 - A rapid redistribution of the transferrin receptor to the cell surface of HL-60 cells and K562 cells upon treatment with dimethyl sulfoxide due to slowing of endocytosis

AU - Vestal, Deborah J.

AU - Davis, Bruce H.

AU - Enns, Caroline

PY - 1990

Y1 - 1990

N2 - Treatment of two human leukemia cell lines with 1.25% dimethyl sulfoxide at 37 °C results in a rapid increase in the number of transferrin receptors on the cell surface detected by fluoroscein-labeled anti-transferrin receptor antibodies. Both HL-60 cells, a human myeloid cell line, and K562 cells, a human erythroid-myeloid cell line, showed a 25-65% increase in cell surface transferrin binding in parallel experiments. Scatchard plot analysis of the data indicates that the number of receptors increases while the affinity of transferrin for the receptor remains the same. This rapid increase in the number of receptors at the cell surface appears to be due to a slowing of endocytosis rather than an increase in externalization of the receptor.

AB - Treatment of two human leukemia cell lines with 1.25% dimethyl sulfoxide at 37 °C results in a rapid increase in the number of transferrin receptors on the cell surface detected by fluoroscein-labeled anti-transferrin receptor antibodies. Both HL-60 cells, a human myeloid cell line, and K562 cells, a human erythroid-myeloid cell line, showed a 25-65% increase in cell surface transferrin binding in parallel experiments. Scatchard plot analysis of the data indicates that the number of receptors increases while the affinity of transferrin for the receptor remains the same. This rapid increase in the number of receptors at the cell surface appears to be due to a slowing of endocytosis rather than an increase in externalization of the receptor.

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