𝔖 Bobbio Scriptorium
✦   LIBER   ✦

Properties of Mg2+-dependent cation channels in human leukemia K562 cells

✍ Scribed by Svetlana B. Semenova; Alla F. Fomina; Irina O. Vassilieva; Yuri A. Negulyaev


Publisher
John Wiley and Sons
Year
2005
Tongue
English
Weight
154 KB
Volume
205
Category
Article
ISSN
0021-9541

No coin nor oath required. For personal study only.

✦ Synopsis


Abstract

The endogenous Mg^2+^‐inhibited cation (MIC) current was recently described in different cells of hematopoietic lineage and was implicated in the regulation of Mg^2+^ homeostasis. Here we present a single channel study of endogenously expressed Mg^2+^‐dependent cation channels in the human myeloid leukemia K562 cells. Inwardly directed unitary currents were activated in cell‐attached experiments in the absence of Ca^2+^ and Mg^2+^ in the pipette solution. The current–voltage (I–V) relationships displayed strong inward rectification and yielded a single channel slope conductance of ∼30 pS at negative potentials. The I–V relationships were not altered by patch excision into divalent‐free solution. Channel open probability (P~o~) and mean closed time constant (τ~C~) were strongly voltage‐dependent, indicating that gating mechanisms may underlie current inward rectification. Millimolar concentrations of Ca^2+^ or Mg^2+^ applied to the cytoplasmic side of the membrane produced slow irreversible inhibition of channel activity. The Mg^2+^‐dependent cation channels described in this study differ from the MIC channels described in human T‐cells, Jurkat, and rat basophilic leukemia (RBL) cells in their I–V relationships, kinetic parameters and dependence on intracellular divalent cations. Our results suggested that endogenously expressed Mg^2+^‐dependent cation channels in K562 cells and the MIC channels in other hematopoietic cells might be formed by different channel proteins. © 2005 Wiley‐Liss, Inc.


📜 SIMILAR VOLUMES


Effect of resveratrol on high glucose-in
✍ Wen-Hsiung Chan 📂 Article 📅 2005 🏛 John Wiley and Sons 🌐 English ⚖ 428 KB

## Abstract Hyperglycemia, a symptom of diabetes mellitus, induces hyperosmotic responses, including apoptosis, in vascular endothelial cells and leukocytes. Hyperosmotic shock elicits a stress response in mammalian cells, often leading to apoptotic cell death. In a previous report, we showed that

Tiazofurin-induced autosecretion of IL-6
✍ Talley, C.J.; Turner, E.A.; Hatcher, F.M.; Aguinaga, P.M.; Chakrabarti, P. 📂 Article 📅 1997 🏛 John Wiley and Sons 🌐 English ⚖ 83 KB 👁 1 views

Previous reports have established the synthesis of interleukin-6 (IL-6) and IL-6 receptors (IL-6R) in several human leukemia cells and found that IL-6 and the IL-6R could be expressed in cell lines with erythroid/megakaryocytic features. IL-6 is a pleiotropic cytokine involved in megakaryocytic diff

Arecoline-induced death of human leukemi
✍ Ying-Jung Chen; Long-Sen Chang 📂 Article 📅 2012 🏛 John Wiley and Sons 🌐 English ⚖ 936 KB

## Abstract The goal of the present study is to explore the contribution of tumor necrosis factor‐α (TNFα)‐related pathway to the cytotoxicity of arecoline on human leukemia K562 cells. Arecoline treatment induced death of K562 cells and increased surface expression of TNFα, TNFR1, and TNFR2. Unlik

Mutual contact of murine erythroleukemia
✍ Annarosa Arcangeli; Maria Riccarda Del Bene; Riccardo Poli; Letizia Ricupero; Ma 📂 Article 📅 1989 🏛 John Wiley and Sons 🌐 English ⚖ 885 KB

This study deals with the modulation of the plasma membrane potential (A+,) of murine erythroleukemia (MEL) cells by cell-substratum or cell-cell contact. At& was determined by measuring the distribution of tetraphenylphosphonium (TPP+) across the plasma membrane; it appeared strongly, and inlersely

Changes in glycoprotein fucosylation in
✍ Louise G. Bernier; Arthur K. Sullivan 📂 Article 📅 1988 🏛 John Wiley and Sons 🌐 English ⚖ 655 KB

Previous studies from this and other laboratories have shown that variants of tumor cell lines can be selected for resistance to the lytic action of natural killer (NK) cells. One of these (K562-Clonc I), when made resistant to the toxic effccts of Concanavalin A (Con A-Rl), regained its sensitivity