Molecular Basis of Membrane-Associated Diseases - download pdf or read online

By E. Van Obberghen, R. Ballotti, Y. Le Marchand-Brustel, J. C. Scimeca (auth.), Prof. Dr. Angelo Azzi, Prof. Zdenek Drahota, Prof. Sergio Papa (eds.)

ISBN-10: 364274415X

ISBN-13: 9783642744150

ISBN-10: 3642744176

ISBN-13: 9783642744174

Biological membranes are usually effected by means of ailments. Molecular occasions resulting in or coming up from pathological adjustments during varied illnesses are as but now not truly understood. This efficient learn by way of major specialists covers adjustments of the mobile atmosphere, membranes and the metabolic features in the course of tissue development and differentiation in addition to elements of irregular organelle functionality in lysosomal garage illnesses, peroxisomal and mitochondrial problems, enzyme defects and regulatory defects of receptors because of oncogenes.

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Extra resources for Molecular Basis of Membrane-Associated Diseases

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1986). The association of the Ph' chromosome with ALL is not as frequent as with CML, since only 15% of the cases of ALL are ph +. Within these cases some carry the typical bcr-abl rearrangement and'express P2IO, but a subset does not show any bcr rearrangement. In these patients the chromosome 22 breakpoint appears to be located further upstream, to the left of the breakpoint cluster region (Erikson et al. 1986). It has been recently shown that leukemic cells from these patients express a new altered c-abl protein (P190), oflower molecular weight than P2IO, which still displays enhanced in vitro tyrosine kinase activity, but with different specificity (Clark et al.

J Neurosci 6:2543-2550 Goedert M, Fine A, Hunt SP, Ullrich A (1986) Nerve growth factor mRNA in peripheral and central rat tissues and in the human central nervous system: lesion effects in the rat brain and levels in Alzheimer's disease. Mol Brain Res 1:85-92 Green SH, Rydel RE, Connolly JL, Greene LA (1986) PCI2 mutants that possess low- but not high-affinity nerve growth factor receptors neither respond to nor internalize nerve growth factor. J Cell Bioi 102:830-843 Greenberg ME, Greene LA, Ziff EB (1985) Nerve growth factor and epidermal growth factor induce rapid transient changes in proto-oncogene transcription in PCI2 cells.

1985, 1987; Pierce et al. 1985; Mathey-Prevot et al. 1986; Rovera et al. 1987). The associa tion ofP21 0, a constitutively active tyrosine kinase, with CML cells, strongly suggests that such an enzymatic activity may be involved in their uncontrolled proliferation, perhaps releasing them from their dependence on specific limiting growth factors. Recent gene transfer experiments involving expression of the bcr-abl protein in NIH/3T3 fibroblasts, show that P2IO differs from Pl60 v-abl, since it is not capable of causing fibroblast transformation (Daley et al.

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Molecular Basis of Membrane-Associated Diseases by E. Van Obberghen, R. Ballotti, Y. Le Marchand-Brustel, J. C. Scimeca (auth.), Prof. Dr. Angelo Azzi, Prof. Zdenek Drahota, Prof. Sergio Papa (eds.)

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