Download A Hard Day's Knight (Nightside, Book 11) by Simon R. Green PDF

By Simon R. Green

John Taylor, P.I., has come into ownership of the mythical Excalibur. to determine why, he'll need to seek advice the final Defenders of Camelot, a bunch of knights who reside in a spot extra scary than the Nightside: London. John has been there in years-and there are reliable purposes for that...

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Additional resources for A Hard Day's Knight (Nightside, Book 11)

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Proc Natl Acad Sci USA 1999;96:11815–11819. Feng JF, Readon M, Yadav SP, Im MJ: Calreticulin down-regulates both GTP binding and transglutaminase activities of transglutaminase II. Biochemistry 1999;38:10743–10749. Baek KJ, Das T, Gray CD, Desai S, Hwang KC, Gacchui R, Ludwig M, Im MJ: A 50 KDa protein modulates guanine nucleotide binding of transglutaminase II. Biochemistry 1996;35:2651–2657. Feng JF, Gray CD, Im MJ: ␣1B-adrenoceptor interacts with multiple sites of transglutaminase II: Characteristics of the interaction in binding and activation.

The interaction of Trp241 with the ␥-glutamyl carbonyl oxygen is obvious, though the positioning and activating effect of Trp332 towards the acceptor substrate is questionable. Nevertheless, it is possible that these and also other Trp residues are essential for the ‘waterproofing’ of the active site. Homologous TGases have ten highly-conserved tryptophans, nine of which are located in the core From Function to Structure of TGases 27 domain sequence. As assessed by fluorescence resonance transfer measurements, the indole moieties of five of these nine tryptophans in TGase 2 (Trp180, Trp241, Trp278, Trp332 and Trp337) are positioned in molecular proximity (within 20 Å) to the catalytic site so that these might have a role in locking out of the water from the proximity of the ␥-glutamyl-TGase thioester intermediate [23, 25]).

The Genes and Expression of Human TGases The genes for the 9 members of the human TGase family (TGM1–7, F13A1 and EPB42, which codes a catalytically inactive protein) reveal high degree of similarity in the numbers, lengths and boundaries of exons. The TGM1 and F13A1 genes consist of 15 exons and 14 introns, whereas the other genes (TGM2–7 and EPB42) consist of 13 exons and 12 introns. Phylogenetical analysis revealed that an early gene duplication event of an ancestral TGM gene gave rise to these two groups and that the different exon number is a consequence of the acquisition of a noncoding first exon and the intersection of exon 9 by an intron sequence, which formed exons 10 and 11 of F13A1 and TGM1 (see ensuing chapters of this book for review and references).

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