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1 er in another step, likely hydrolysis of the carbinolamine.
2 arbinolamine nitrogen to give the protonated carbinolamine.
3 ble of existing in equilibrium with a cyclic carbinolamine.
4 -1, respectively, in dehydrating the neutral carbinolamine.
5 roups and give rise to 5- or 6-membered ring carbinolamines.
7 such that the oxygen atoms analogous to the carbinolamine and beta-hydroxyl oxygens are positioned n
8 ambiguously identify the postulated covalent carbinolamine and Schiff base intermediates in the aldol
10 ial formation of alpha-iminoglutarate, alpha-carbinolamine, and alpha-ketoglutarate-reduced coenzyme
12 e derived aldehydes to form 5- or 6-membered carbinolamines are critical determinants of biologic pot
14 ve stability of the interconvertible N10-C11 carbinolamine, carbinolamine methyl ether, and imine for
16 -alpha-iminoglutarate and enzyme-NADPH-alpha-carbinolamine complexes at concentrations whose sum acco
17 ent forms of the known alpha-imino and alpha-carbinolamine complexes in which the active site cleft i
18 alpha-iminoglutarate and highly red-shifted carbinolamine complexes observed in both reactions, the
24 s encoding phenylalanine hydroxylase (PhhA), carbinolamine dehydratase (PhhB), and aromatic aminotran
25 ion has been found, supporting the idea that carbinolamine dehydratase activity is not required for H
26 oH2 forms a tetramer, displays pterin-4alpha-carbinolamine dehydratase activity, and binds HNF1alpha
28 osa PhhA plus the recycling enzyme pterin 4a-carbinolamine dehydratase, PhhB, rescues tyrosine auxotr
29 ting assays further indicated that pterin-4a-carbinolamine dehydratase, which regenerates the AAH cof
31 tivity of the bifunctional protein pterin-4a-carbinolamine dehydratase/dimerization cofactor for hepa
32 ed a novel deletion in PCBD1 (pterin-4 alpha-carbinolamine dehydratase/dimerization cofactor of hepat
33 tocyte nuclear factor 1 (DCoH)/pterin-4alpha-carbinolamine dehydratases (PCD)-like protein is the cau
39 ase, which allowed the rates of both initial carbinolamine formation (as part of the imination step)
40 ion by acting as a proton shuttle during the carbinolamine formation step, which enables diamines to
42 ith N-methyl-L-tryptophan, sarcosine, or the carbinolamine formed with L-tryptophan and formaldehyde.
44 y the same group accepting a proton from the carbinolamine hydroxyl to generate alpha-Kg and lysine.
45 in protonation of the hydroxyl group of the carbinolamine in the dehydration step, catalyzing Schiff
46 evidence is presented for the formation of a carbinolamine interchain cross-link in 5'-CpG-3' sequenc
47 esidue or position in the protonation of the carbinolamine intermediate and dehydration of the Schiff
48 strongly for the N-dealkylation of 2a via a carbinolamine intermediate formed by a conventional C-hy
49 to facilitate formation and breakdown of the carbinolamine intermediate to give the Schiff base and t
51 catalyzed step, most likely protonation of a carbinolamine intermediate, is also significantly rate c
52 ction proceeds with C-N bond cleavage in the carbinolamine intermediate, shows excellent functional g
55 ) at C-H bonds in 1-4 leads to nonrearranged carbinolamine intermediates and thereby to "ordinary" N-
56 part, explain the thermal stability of this carbinolamine interstrand cross-link and the stereochemi
57 ally stable surrogates for the corresponding carbinolamine interstrand cross-links arising from the c
60 is the dG linked to the alpha-carbon of the carbinolamine linkage, and Y(19) is the dG linked to the
61 is the dG linked to the gamma-carbon of the carbinolamine linkage; the cross-link is in the 5'-CpG-3
63 p is likely protonation/deprotonation of the carbinolamine nitrogen formed as an intermediate in imin
64 s a general acid and donates a proton to the carbinolamine nitrogen to give the protonated carbinolam
65 isotope effects reveal that collapse of the carbinolamine (or gem-diamine) to give the final product
70 ve of 1b, which cannot give rise to a cyclic carbinolamine, was 2 orders of magnitude less potent tha
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