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By Jeffery C. Hall

Advances in Genetics raises its concentrate on sleek human genetics and its relation to drugs with the merger of this long-standing serial with Molecular Genetic medication . This merger affirms theAcademic Press dedication to submit vital experiences of the broadest curiosity to geneticists and their colleagues in affiliated disciplines.

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And Haines, 1. L. (199% Consortium fine localisation of X-linked Charcot-Marie-Tooth disease (CMTXI ): Additional support that connexin32 is the defect in CMTXI. Hum. Hered. 45:121-128. , Bourre, J. , and Baumann, N. (1979). Absence of the major dense line in the myelin of the mutant mouse shiwever. Neurosci. Lett. 12:107-I 12. , and Werner, R. (1994). A connexin32 mutation associated with Charcot-Marie-Tooth disease does not affect channel formation in oocytes. FERS Lett. 35 1:90-94. , and Vandenberghe, A.

Prevalence and origin of de now duplications in Charcot-Marie-Tooth disease type 1A: First report of a de now duplication associated with a maternal origin. Am. J. Hum. Genet. 58:472-476. , and Schachner, M. (1987). The peripheral myelin glycoprotein Po expresses the L2IHNK-1 and L3 carbohydrate structures shared by neural adhesion molecules. Neurosci. Lett. 82:77-82. Bone, L. , Lensch, M. , Chance, P. , and Fischbeck, K. H. (1995). New connexin mutations associated with X-linked Charcot-Marie-Tooth disease.

1. Molecular Genetics of the Peripheral Neuropathies 35 in combination with frequent cutting enzymes) is commonly used in laboratories, but results may be limited by the difficulty in interpreting dosage differences or by the informativeness of the marker itself. 0, effectively combines these two methods by using frequent cutting enzymes and by producing novel fragments in CMTlA and HNPP patients. 8 kb are observed in 80% (84/105) of CMTlA patients and 95% (19/20) of HNPP patients, respectively; the remainder of CMTlA/HNPP patients with the duplication/deletion are detected by dosage differences.

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