By D. R. Colman, L. Bernier, J. L. Salzer, S. Gillespie, P. Brophy, D. D. Sabatini (auth.), G. Serlupi Crescenzi (eds.)
The current e-book is predicated at the papers offered in the course of an inter disciplinary assembly which was once held in Rome October 27-30, 1986, on the Istituto Superiore di Sanita lower than the sponsorship of NATO, and with a monetary contribution of the Cassa di Risparmio di Roma. The assembly used to be of serious curiosity simply because, for the 1st time, a bunch of hugely certified scientists focusing on various fields have been amassed jointly to debate the matter of demyelinating illnesses. In thi. context molecular biologists, immunologists, virologists, and lipid chemists may check with clinicians for 4 days each element of demyelinating ailments. They shared result of the newer examine with the wish that extra wisdom of the myelinating method will finally reach discovering new remedies for those ailments. The assembly used to be profitable, might be partially simply because discussions in the course of lunches and dinners supplied a chance for the alternate of recent principles. This used to be obvious within the discussions held after the presen tation of every paper and used to be summarized within the very vigorous around desk which was once hung on the final day. The editor needs to precise his because of the medical committee contributors: N. Baumann, C. Fieschi, G. Macchi, J.M. Matthieu, okay. Suzuki. It used to be their suggestion that made the alternative of contributors and matters such a success. The organizer additionally recognize the organizing aid of NATO in getting ready those complaints. Acknowledgments must be provided to Dr. S. Salvati, Dr. A.M.
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Additional info for A Multidisciplinary Approach to Myelin Diseases
4. Nucleotide sequence of exon 2 of the mouse proteolipid protein gene. The mouse genomic sequence is compared to the rat cDNA sequence, as in Figure 3. The region of ex on 2 that is bracketed for both the mouse genomic and the rat cDNA sequences is the beginning of the mouse PLP eDNA, pBAS1013. In this region, there are no differences between the mouse genomic DNA in the rat cDNA sequences. contains the sequence from nucleotide 269 to 1006. An Sst I site exists in this sequence at position 960, and an ~ I site exists-it position 375.
M. X. Omlin, J. Rambaldi, G. E. , 103:2673-2682 (1986). -M. Roch, M. Brown-Luedi, B. J. -M. Matthieu, Mice heterozygous for the mId mutation have intermediate levels of myelin basic protein mRNA and its translation products, Molec. , 1:137-144 (1986). D. Doolittle and K. M. Heredity 68:331 (1977). F. Lachapelle, C. de Baecque, C. -M. Bourre, A. Delassalle, D. Doolittle, J. J. Hauw, and N. Baumann, Comparison of morphological and biochemical defects of two probably allelic mutations of the mouse, myelin deficient (mId) and shiverer (shi), in: "Neurological Mutations Affecting Myelination, INSERM Symposium N<>14" N.
What remains unknown is the mechanism which turns down the synthesis of myelin components when the period of myelin thickening is completed. The results presented in this report seem to give a clue to this question. This mechanism could involve the discontinuation of an activating factor or the appearance of an inhibitor. In any case, this mechanism is likely to act on gene transcription since the amounts of MBP mRNA (29) and MAG mRNA (36) decrease during development of normal mice. In mId brains, the high levels of messenger for MAG and Wolfgram protein, indicate that the down regulation signal did not reach the transcription apparatus.