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  • 1
    Electronic Resource
    Electronic Resource
    Potassium Channels Cloned from NG108-15 Neuroblastoma-Glioma Hybrid Cells (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 707 (1993), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1993.tb38042.x
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  • 2
    Electronic Resource
    Electronic Resource
    Single calcium-activated potassium channel in cultured mammary epithelial cells (1989)
    Springer
    Pflügers Archiv 414 (1989), S. 118-124 
    Details
    ISSN: 1432-2013
    Keywords: Mammary epithelial cells ; Patch clamp ; K+ channel ; Ca2+ activation ; Na+ block ; A23187 ; Inward rectification ; Epidermal growth factor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The properties of Ca2+-activated K+ channels in mouse mammary epithelial cells in primary culture were studied by the patch-clamp technique. In cell-attached patches, spontaneous channel openings were sometimes observed; the slope conductance of the currents was about served; the slope conductance of the currents was about 12 pS at negative membrane potentials with a physiological solution (152 mM Na+, 5.4 mM K+) in the pipette. External application of A23187, a calcium ionophore, activated this channel. In excised inside-out patches, the channel was activated by increasing the internal Ca2+ concentration (10−7 to 10−6 M). No voltage dependence of the channel activity was observed. Internal Na+ blocked the outward K+ current in a voltage dependent manner and this block led to the non-linear I–V relationship at positive membrane potentials. The channel was blocked by internal Ba2+ (0.1 mM) and tetracthylammonium (TEA+, 20–50 mM). Ba2+ reduced the open probability but not the single channel conductance, whereas TEA+ reduced the single channel conductance. The single channel conductance of this channel, measured from the inward current with a high-K+ solution (150 mM K+) in the pipette, was large (about 40 pS), and showed inward rectification. These results suggest that this channel is different from the usual small conductance Ca2+-activated K+ channels observed in many other cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00580952
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  • 3
    Electronic Resource
    Electronic Resource
    The increase in the intracellular Ca2+ concentration induced by mechanical stimulation is propagated via release of pyrophosphorylated nucleotides in mammary epithelial cells (1994)
    Springer
    Pflügers Archiv 427 (1994), S. 533-542 
    Details
    ISSN: 1432-2013
    Keywords: Intracellular calcium ; Fura-2 ; Mammary epithelial cells ; Mechanical stimulation ; Purinoceptor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Mechanical stimulation of one mammary tumor cell in culture induced an increase in its intracellular calcium concentration which spread to surrounding cells. The increase in calcium can also be induced by addition of a solution in which cultured mammary tumor cells were stimulated by repeated pipetting (solution after pipetting cells, SAPC). The activity of the SAPC was completely abolished by treatment with snake venom phosphodiesterase or pyrophosphatase. Uridine triphosphate (UTP), uridine diphosphate (UDP) and ATP (1 μM each) were detected in the SAPC, whereas 5′-UMP and 5′-AMP were produced by phosphodiesterase digestion. A mixture of UTP, UDP and ATP (1 μM each) elicited a calcium response which was comparable to that induced by SAPC, while UTP, UDP or ATP alone at 1 μM elicited a small increase in calcium concentration in mammary tumor cells. Suramin, a competitive antagonist of P2 purinoceptors, diminished the spreading of the calcium wave induced by mechanical stimulation. It also blocked the responses to SAPC, UTP, UDP and ATP. These findings suggest that the mechanical stimulation results in the release of UTP, UDP and ATP into the extracellular space which mediates induction of the spreading calcium response via P2U-type purinoceptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374271
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  • 4
    Electronic Resource
    Electronic Resource
    Spontaneous calcium oscillations and mechanically and chemically induced calcium responses in mammary epithelial cells (1993)
    Springer
    Pflügers Archiv 422 (1993), S. 295-304 
    Details
    ISSN: 1432-2013
    Keywords: Intracellular calcium oscillation ; Fura-2 ; Mammary epithelial cells ; Purinergic receptor ; Mechanical response ; Calcium wave ; Bradykinin ; LaCl3
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Changes of intracellular calcium activity (Ca i 2+ ) in mouse mammary epithelial cells in primary culture (normal) and in an established cell line (MMT060562, cancerous) were investigated by microfluorometry and image analysis of fura-2 fluorescence. In both types of cells, some populations exhibited occasional Ca i 2+ oscillations with a period of 50–160 s. Slight mechanical stimulation of a cell with a fine glass pipette induced a Ca i 2+ increase, which spread from the stimulated cell to the surrounding cells with a speed of 7–12 μm/s. ATP (〉1 μmol/l) and ADP, but not AMP induced a Ca i 2+ increase in both cell types. Bradykinin was highly effective (〉 10 nmol/l) only in the cancerous mammary epithelial cells. In Ca2+-free solution, all these Ca i 2+ responses remained unchanged at the first application, and decreased abruptly at the second trial. La3+ (〉0.5 mmol/l) suppressed the response to ATP but not the response to bradykinin. Addition of extracellular Mn2+ rapidly quenched the fura-2 fluorescence in the cell even in a non-stimulated state. Influx of Mn2+ did not increase during Ca i 2+ responses. These results indicate that the sources of Ca i 2+ responses in mammary epithelial cells are intracellular stores, which exchange Ca2+ with the extracellular medium.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374284
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  • 5
    Electronic Resource
    Electronic Resource
    Oscillating activity of a calcium-activated K+ channel in normal and cancerous mammary cells in culture (1991)
    Springer
    The journal of membrane biology 119 (1991), S. 133-139 
    Details
    ISSN: 1432-1424
    Keywords: Ca2+-activated K+ channel ; Ca2+ oscillation ; inward rectification ; charybdotoxin ; apamin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary Calcium-activated potassium channels were the channels most frequently observed in primary cultured normal mammary cell and in the established mammary tumor cell, MMT060562. In both cells, single-channel and whole-cell clamp recordings sometimes showed slow oscillations of the Ca2+-gated K+ current. The characteristics of the Ca2+-activated K+ channels in normal and cancerous mammary cells were quite similar. The slope conductances changed from 8 to 70 pS depending on the mode of recording and the ionic composition in the patch electrode. The open probability of this channel increased between 0.1 to 1 μm of the intracellular Ca2+, but it was independent of the membrane potential. Charybdotoxin reduced the activity of the Ca2+-activated K+ channel and the oscillation of the membrane current, but apamin had no apparent effect. The application of tetraethylammonium (TEA) from outside and BaCl2 from inside of the cell diminished the activity of the channel. The properties of this channel were different from those of both the large conductance (BK or MAXI K) and small conductance (SK) type Ca2+-activated K+ channels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01871412
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  • 6
    Electronic Resource
    Electronic Resource
    Induction of differentiation by radiation and hyperthermia in neuroblastoma - glioma hybrid cells (1994)
    New York, NY [u.a.] : Wiley-Blackwell
    Cell Biochemistry and Function 12 (1994), S. 137-142 
    Details
    ISSN: 0263-6484
    Keywords: Radiation ; hyperthermia ; neuroblastoma-glioma ; intracellular calcium ; Chemistry ; Biochemistry and Biotechnology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: The effects of either radiation or hyperthermia on the differentiation potential of NG108-15, a neuroblastoma-glioma hybrid cell line, were studied. After radiation and hyperthermia, the outgrowth of neurites from NG108-15 cells was potentiated, and polarizing current and voltage pulses induced a distinct action potential and a diphasic (inward following outward) current, respectively. An increase in the specific activity of acetylcholinesterase was also observed. In addition, both treatments induced an elevation of the concentration of intracellular calcium in some cells. The increase in intracellular calcium concentration caused by applying the calcium ionophore, A23187, induced differentiation. It is suggested that both the radiation- and the hyperthermia-induced increases of electrical excitability and acetylcholinesterase activity may have originated from an increase in intracellular Ca2+ concentration.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/cbf.290120209
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  • 7
    Electronic Resource
    Electronic Resource
    Release of arachidonic acid via Ca2+ increase stimulated by pyrophosphonucleotides and bradykinin in mammary tumour cells (1995)
    New York, NY [u.a.] : Wiley-Blackwell
    Cell Biochemistry and Function 13 (1995), S. 279-286 
    Details
    ISSN: 0263-6484
    Keywords: ATP ; UTP ; bradykinin ; calcium ; arachidonic acid ; mammary cell ; Chemistry ; Biochemistry and Biotechnology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: The relationship between the increase of intracellular Ca2+ and the release of arachidonic acid by bradykinin and pyrophosphonucleotides was studied in cultured mammary tumour cells, MMT060562. Bradykinin, ATP, UTP and UDP induced an increase of intracellular Ca2+ and the release of arachidonic acid from phospholipids into the extracellular fluid. Release of arachidonic acid was also induced by the application of the Ca2+ ionophore, A23187. Liberation of arachidonic acid by bradykinin and ATP was reduced by mepacrine, a blocker of phospholipase A2 and W-7, a calmodulin antagonist.It is suggested that the increase in cytosolic Ca2+-induced release of arachidonic acid occurs through activation of calmodulin-dependent phospholipase A2.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/cbf.290130409
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  • 8
    Electronic Resource
    Electronic Resource
    Modification of frequency augmentation-potentiation by GTPγS in the frog neuromuscular junction (1995)
    New York, NY [u.a.] : Wiley-Blackwell
    Cell Biochemistry and Function 13 (1995), S. 105-109 
    Details
    ISSN: 0263-6484
    Keywords: Nerve terminal ; transmitter release ; G protein ; frequency augmentation-potentiation ; Chemistry ; Biochemistry and Biotechnology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: The effect of modifiers of guanine nucleotide-binding proteins (G proteins) on the frequency augmentation-potentiation of transmitter release were studied in the frog neuromuscular junction. Using GenetransferR as a carrier the mean quantal content of the endplate potential increased by penetration of GTPγS into the presynaptic nerve terminal. Neither GTPγS alone nor carrier alone had any effect. The relationship of log (mean quantal content) versus stimulation frequency changed from a single linear to a dual linear function, suggesting that the immediately releasable pool was modified. GDPβS + carrier also had similar effects, but was less potent. Aluminium fluoride was without effect. Extracellularly recorded presynaptic nerve action potentials remained unchanged with GTPγS + carrier. Also, GTPγS + carrier did not affect the action potential nor the cytosolic Ca2+ concentration in differentiated NG108-15 hybrid cells. It is suggested that some smg-type G protein-dependent processes are involved in determining frequency augmentation-potentiation.
    Additional Material: 2 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/cbf.290130207
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  • 9
    Electronic Resource
    Electronic Resource
    Effects of hyperthermia on intracellular calcium concentration and responses of cancerous mammary cells in culture (1992)
    New York, NY [u.a.] : Wiley-Blackwell
    Cell Biochemistry and Function 10 (1992), S. 225-232 
    Details
    ISSN: 0263-6484
    Keywords: Hyperthermia ; intracellular calcium ; fura-2 ; ATP ; D-myo-inositol 1,4,5-triphosphate ; Chemistry ; Biochemistry and Biotechnology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Effects of hyperthermia on the intracellular calcium concentration (Cai) of an established mouse breast cancer cell line, MMT060562, were studied using fura-2 fluorescence microscopy and the whole-cell clamp technique. A sudden change of temperature from 37 to 45°C induced a transient increase in the fluorescence ratio permeability of the cell membrane and inward current. Deletion of extracellular calcium abolished the fluorescence ratio response to the rise in temperture. Cai of some cells increased after hyperthermia treatment at 44-48°C for 20 min, but the average increase of Cai was negligible. After hyperthermia treatment, spontaneous oscillation of Cai, chemical responses to ATP and bradykinin and the mechanically-induced spreading reponse diminished. However, the mechanically induced increase of Cai within the stimulated cell remained even after hyperthermia treatment. Suppression of the ATP-induced Cai response recovered to about half the original level within 12 h. Blockage of protein synthesis with cycloheximide (100 μM) had no effect on the recovery. The D-myo-inositol 1,4,5-triphosphate (IP3)-dependent increase of Cai remained intact even after hyperthermia treatment. It is concluded that hyperthermia treatment increases both the permeability of the cell membrane and Cai, but decreases the sensitivity of cells to ATP and bradykinin, presumably due to modification of the signal transduction mechanism.
    Additional Material: 9 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/cbf.290100403
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  • 10
    Electronic Resource
    Electronic Resource
    Proliferation-associated increase in sensitivity of mammary epithelial cells to inositol-1,4,5-trisphosphate (1993)
    New York, NY [u.a.] : Wiley-Blackwell
    Cell Biochemistry and Function 11 (1993), S. 55-62 
    Details
    ISSN: 0263-6484
    Keywords: Inositol-1,4,5-trisphosphate ; intracellular calcium ; mammary epithelial cells ; cell proliferation ; Chemistry ; Biochemistry and Biotechnology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Injection of D-myo-inositol-1,4,5-trisphosphate (IP3) was found to induce a transient increase of intracellular Ca2+ concentration in cancerous mammary cells (MMT060562) and in normal mammary cells treated with epidermal growth factor. Responses to injection of either D-myo-inositol-1,4-bisphosphate (IP2) or D-myo-inositol-1,3,4,5-tetrakisphosphate (IP4) were small or absent. Furthermore, normal mammary cells cultivated with low-protein serum replacement alone or in the presence of differentiation-inducing hormones (insulin + cortisol + prolactin) were less sensitive to IP3.Thapsigargin induced a transient increase of Ca2+ due to the release of Ca2+ from an intracellular pool. There was no difference in the peak heights of the thapsigargin-induced Ca2+ increase when mammary cells were cultivated in the presence or absence of epidermal growth factor or insulin + cortisol + prolactin. These findings suggest that the releasable intracellular Ca2+ pool remained unchanged whereas sensitivity to IP3 increases during the proliferation stage.Mechanical stimulus of a mammary cell induces an increase of intracellular Ca2+ in the stimulated cell. A certain stimulating factor is released from the mechanically stimulated cell into the extracellular space, and it induces an increase of Ca2+ in surrounding cells.18 In contrast, the IP3-induced Ca2+ increase in both cancerous and epidermal growth factor-treated normal mammary cells did not spread to adjacent cells. Therefore, increase of Ca2+ is not sufficient to account for the release of stimulating substances from mammary cells in the mechanically-induced spreading response.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/cbf.290110107
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