glutamic acid decarboxylase/sarcoma

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Glutamic acid decarboxylase activity is stimulated in quail retina neuronal cells transformed by Rous sarcoma virus and is regulated by pp60v-src.

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Rous sarcoma virus (RSV) stimulates in quail embryo neuro-retina (NR) cultures the specific activity of glutamic acid decarboxylase (GAD), the enzyme responsible for the synthesis of gamma-aminobutyric acid, a major inhibitory neurotransmitter in NR and in central nervous system. In quail embryo NR

Cells with neuronal properties in permanent cultures of quail embryo neuroretinas infected with Rous sarcoma virus.

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Neuroretina cells from 7-day quail embryos infected 'in vitro' with the mutant ts NY-68 of Rous sarcoma virus, were established into permanent cultures. An initial stage of cellular proliferation was followed by a period of minimal multiplication. After recovery from this crisis, cell proliferation

Leucoencephalopathy, transverse myelopathy, and peripheral neuropathy in association with glutamic acid decarboxylase-65 (GAD) antibodies in children with cancer.

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Neurologic toxicity may occur as a direct effect of cancer and its therapy or indirectly because of a dysfunctional immune system. The authors report the development of axonal neuropathy, myelopathy, and leucoencephalopathy associated with glutamic acid decarboxylase-65 (GAD) antibodies in 4

Expression of neuronal markers in chick and quail embryo neuroretina cultures infected with Rous sarcoma virus.

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Cultures of neuroretina (NR) cells from 7-day chick and quail embryos were infected with ts NY-68, a thermosensitive mutant of Rous sarcoma virus (RSV) which transformed NR cells at 36 degrees C. The following differentiation markers for neurones were studied: tetanus toxin-binding sites at the cell

A neuronal clone derived from a Rous sarcoma virus-transformed quail embryo neuroretina established culture.

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Neuroretina (NR) is an evagination of the central nervous system (CNS) which is composed of photoreceptors, glial (Müller) cells and horizontal, bipolar, amacrine and ganglion neuronal cells. We describe here the usefulness of Rous sarcoma virus (RSV) in the establishment of a neuronal clone from

Differentiation of retrovirus-infected avian neuroretina cells.

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The effects of oncogenic retroviruses on the expression of differentiation markers were studied in monolayer cultures of chick and quail embryo neuroretinas. Transformation by Rous sarcoma virus (RSV) did not affect the appearance of synapses, and the expression of glutamic acid decarboxylase was

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