retinoblastoma/draslík

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Glycine release from Y79 retinoblastoma cells.

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Glycine release, induced by a high concentration of potassium chloride (K+), was investigated in cultured human Y79 retinoblastoma cells. The cells were labeled by incubation with [2-3H]glycine prior to K+ depolarization. Depolarization with 55 mM K+ caused an immediate, Ca2+-dependent release of

Induction of voltage-dependent sodium channels by in vitro differentiation of human retinoblastoma cells.

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1. Neuronlike differentiation of Y-79 retinoblastoma was chemically induced in vitro, by plating the cells onto a poly-D-lysine and laminin substrate. The changes in voltage-dependent conductances after 48-72 h were examined with the whole-cell tight-seal and the perforated-patch recording

Electrical properties of Y-79 cells, a multipotent line of human retinoblastoma.

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1. Whole-cell and perforated-patch tight-seal recording techniques were used to characterize the voltage-dependent membrane conductances of the Y-79 cells, a human retinoblastoma line composed of pluripotential retinal precursor cells. 2. Membrane resistance and capacitance were measured under

Potassium-induced apoptosis in rat cerebellar granule cells involves cell-cycle blockade at the G1/S transition.

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The role of regulators controlling the G1/S transition of the cell cycle was analyzed during neuronal apoptosis in post-mitotic cerebellar granule cells in an attempt to identify common mechanisms of control with transformed cells. Cyclin D1 and its associated kinase activity CDK4 (cyclin-dependent

Electrolyte imbalances in the aqueous humour in retinoblastoma.

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The sodium and potassium concentrations and the lactic dehydrogenase (LDH) activity were estimated in the aqueous and serum of five children with retinoblastoma. Two patients who had a high aqueous LDH activity also showed grossly elevated potassium levels in their aqueous. Though the exact reason

The p38(MAPK) signaling pathway regulates neuronal apoptosis through the phosphorylation of the retinoblastoma protein.

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We investigated the role of SB202190, a selective p38 mitogen-activated protein kinase (MAPK) inhibitor in cerebellar granule neurons (CGC) in response to serum potassium deprivation (S/K deprivation), an apoptotic stimulus. CGC apoptosis after S/K deprivation was shown to be mediated through cell

Eag1 Gene and Protein Expression in Human Retinoblastoma Tumors and its Regulation by pRb in HeLa Cells.

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Retinoblastoma is the most common pediatric intraocular malignant tumor. Unfortunately, low cure rates and low life expectancy are observed in low-income countries. Thus, alternative therapies are needed for patients who do not respond to current treatments or those with advanced cases of the

Glycogen synthase kinase-3 is involved in the regulation of the cell cycle in cerebellar granule cells.

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Recent studies have demonstrated that neuronal reentry in the cell cycle and specifically the expression of the transcription factor E2F-1, constitutes a pathway that may be involved in neuronal apoptosis after serum and potassium withdrawal. Other enzymes such as glycogen synthase kinase-3beta

Identification of inhibitor-of-differentiation 2 (Id2) as a modulator of neuronal apoptosis.

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Inhibitor-of-differentiation 2 (Id2) belongs to a family of transcriptional modulators that are characterized by a helix loop helix region but lack the basic amino acid domain. During development, Id2 antagonizes differentiation mediated by the retinoblastoma protein, probably by scavenging

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