Cell membrane potential changes follow Epstein-Barr virus binding

Upon binding to receptor-bearing target cells, viruses cause cell membrane potential changes. Epstein-Barr Virus causes a biphasic membrane potential change in receptor-bearing B lymphocytes but not receptor-negative T lymphocytes, as measured by flow cytometry or cyanine dye uptake. Membrane potential changes from EBV binding to receptor-bearing cells resemble electrical responses of other cells following ligand binding to transmembrane receptors.     

Cell determination and differentiation: a concept of gene clusters]

This paper formulates a conception of cluster organization of the genetic material, responsible for cell determination and differentiation in multicellular organisms. According to this conception, gene controlling each particular stage of these processes are functionally integrated via genes-activators into gene groups (clusters) of different levels of hierarchy. Besides, some hypotheses of molecular mechanisms providing the action of these gene groups have been put forward. Attempts were made to elucidate some phenomena of cell differentiation, specifically a drop or a complete loss of dividing ability in highly specialized cells, in addition to a property of the cell to remember the history of its own development inside the organism, and to inherit the ancestor's direction of differentiation. Attention was paid to a mechanism (originating from this conception) of the emergency of malignant tumors, which means that cells giving rise to tumors are known to evade primarily their involvement in the process of further specialization. Besides, mechanisms of a molecular supply of positional information are examined. Phylogenetic aspects concerning the standing of the fragment of genetic apparatus controlling cell specialization, and the development of its inner hierarchy that involves subordination of some clusters to other ones.     

Cell growth arrest by sialic acid clusters in ganglioside GM3 mimetic polymers

Ganglioside GM3, one of the sialic acid containing glycosphingolipids, is known to form clusters in lipid microdomains, which serve as platforms for effective signal transduction. In an attempt to clarify the GM3 cluster effect, we enzymatically synthesized GM3 mimetic polymer (GM3-p), with an acrylamide backbone from LacCer mimetic polymer (LacCer-p). Interestingly, GM3-p, but not LacCer-p, reversibly inhibited proliferation of NIH3T3 cells, which are normally resistant to exogenously added GM3. Moreover, we found that the introduction of carbonic acid into the acrylamide chain aided well-oriented cluster formation and enhanced the inhibitory effect of GM3-p. Since sialyllactosyl polymer and GM4 mimetic polymer, but not GM2 mimetic polymer, also inhibited cell proliferation, sialic acid-galactose units must be essential for the biological activity of GM3-p. These results suggest that the formation of sialic acid-galactose clusters is necessary for the suppressive effect of GM3-p. GM3-p treatment did not affect the serum-dependent activation of ERK1/2 or c-fos expression, but caused a reduction in the gene and/or protein expression of cyclin D1, cyclin E, cyclin-dependent kinase (cdk)4, and cdk2, which are involved in the cell cycle. Therefore, GM3-p inhibits cell proliferation by reducing cyclin D1-cdk4 and cyclin E-cdk2 complexes without affecting growth factor signaling from serum to c-fos.     

Using flow cytometry to follow the apoptotic cascade

Abstract

Flow cytometry has been extensively used to follow the apoptotic cascade and to enumerate apoptotic cells, both in cell cultures and, to a lesser extent, in tissue biopsies. An overview of the apoptotic cascade and how flow cytometric measurements can be used to observe the different elements of this process is presented.