Human Nucleotide Expansion Disorders (Nucleic Acids and by Michael Fry, Karen Usdin
By Michael Fry, Karen Usdin
Human neurological and neuromuscular problems because of nucleotide growth are the point of interest of becoming curiosity of working towards physicians and of biomedical researchers. This quantity represents a complete and updated description of some of the better-studied issues. The authors speak about molecular, scientific and pathological elements of the ailments in addition to our present figuring out in their underlying mechanisms.
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Complex cis- and trans-acting factors effecting these differences are only beginning to be revealed. R. Sinden et al. Given the clear role for replication in repeat instability, as evidenced by differences in stability as a function of orientation with respect to the direction of replication (Kang et al. 1995a; Maurer et al. 1996; Freudenreich et al. 1997; Miret et al. 1997; Hashem et al. 2002; Cleary et al. 2002; Panigrahi et al. 2002), and a role for transcription (Bowater et al. 1997; Mochmann and Wells 2004), the distance and orientation of repeats with respect to replication origins might be a critical cis-acting factor in repeat instability.
DNA excision repair proteins. The bacterial damage-recognition protein UvrA binds to heteroduplex substrates containing (CAG)n repeat loops, where n = 1, 2, or 17, with a Kd of about 10–20 nM, about 2 orders of magnitude higher than that for binding to duplex d(CTG)n · d(CAG)n (Oussatcheva et al. 2001). Moreover, when plasmid containing a d(CTG)23 or a d(CAG)23 heteroduplex loop was introduced into E. coli cells, the loops were effectively excised in cells containing functional UvrA. Loops were less effectively excised in cells deﬁcient in UvrA (Oussatcheva et al.
Coli and yeast has been interpreted to be initiated by DNA secondary structure formation in the lagging template strand (Samadashwily et al. 1997; Pelletier et al. 2003; Krasilnikova and Mirkin 2004). The pathway shown in Fig. 7 discusses pausing as a leading strand event because DNA secondary structure in the lagging strand may not be expected to permanently block fork progression since lagging-strand replication can start on either side of the structure. The restart of stalled forks is also important for mammalian cells, and pathways analogous to those discussed for E.