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1 the active site in these binary complexes of glutaryl-CoA dehydrogenase.
2 f a proton at C-4, this is not the case with glutaryl-CoA dehydrogenase.
3 ylation of glutaryl-CoA that is catalyzed by glutaryl-CoA dehydrogenase.
4  medium chain acyl-CoA dehydrogenase and the glutaryl-CoA dehydrogenase.
5      We demonstrated glutaconyl-CoA bound to glutaryl-CoA dehydrogenase after anaerobic reduction of
6                                              Glutaryl-CoA dehydrogenase also has intrinsic enoyl-CoA
7 tion of a spectral species between wild type glutaryl-CoA dehydrogenase and a E370D mutant are consis
8 sm via beta-oxidation, a non-decarboxylating glutaryl-CoA dehydrogenase and a subsequent glutaconyl-C
9 tic pathway catalyzed by the E370D mutant of glutaryl-CoA dehydrogenase and compared them with those
10          Thus short-chain, medium-chain, and glutaryl-CoA dehydrogenase are rapidly inactivated by 2-
11                  2-Pentynoyl-CoA inactivates glutaryl-CoA dehydrogenase at a rate that considerably e
12                                              Glutaryl-CoA dehydrogenase catalyzes the oxidation and d
13                                              Glutaryl-CoA dehydrogenase catalyzes the oxidation of gl
14 nsistent with the idea that this distance in glutaryl-CoA dehydrogenase contributes to the enhanced r
15 y diagnosis, one-third of Amish infants with glutaryl-CoA dehydrogenase deficiency (GA1) develop stri
16         Here, we show that loss of DHTKD1 in glutaryl-CoA dehydrogenase-deficient HEK-293 cells leads
17           Glu370Asp and Glu370Gln mutants of glutaryl-CoA dehydrogenase exhibit 7% and 0.04% residual
18 eening the conditions for crystallization of glutaryl-CoA dehydrogenase from Burkholderia pseudomalle
19                          Of nine known ACDs, glutaryl-CoA dehydrogenase (GCD) is unique: in addition
20 were already present at that time: ancestral glutaryl-CoA dehydrogenase (GCD), isovaleryl-CoA dehydro
21 ood disorder caused by defective activity of glutaryl CoA dehydrogenase (GCDH) which disturb lysine (
22 ation on the lysine oxidation pathway enzyme glutaryl-CoA dehydrogenase (GCDH) and show increased GCD
23 an disease, glutaric aciduria type I (GA-1), glutaryl-CoA dehydrogenase (GCDH) deficiency disrupts th
24 l-coenzyme A (crotonyl-CoA)-producing enzyme glutaryl-CoA dehydrogenase (GCDH) with downregulation of
25 nd to and stabilize the mitochondrial enzyme glutaryl-CoA dehydrogenase (GCDH), the computational sit
26 transferase (SUGCT) and become substrate for glutaryl-CoA dehydrogenase (GCDH), the enzyme that is de
27 anoma addiction to the mitochondrial protein glutaryl-CoA dehydrogenase (GCDH), which functions in ly
28 id metabolism resulting from a deficiency of glutaryl-CoA dehydrogenase (GCDH).
29  DHTKD1, an enzyme upstream of the defective glutaryl-CoA dehydrogenase, has been investigated as a p
30                                              Glutaryl-CoA dehydrogenase is also differentiated from o
31                  This distance for wild type glutaryl-CoA dehydrogenase is not known.
32                                              Glutaryl-CoA dehydrogenase is the only member of the acy
33 ces (e.g., in short-chain, medium-chain, and glutaryl-CoA dehydrogenases) or on the G helix (long-cha
34  dehydrogenation reaction catalyzed by human glutaryl-CoA dehydrogenase was investigated using a seri
35 llowing decarboxylation of glutaconyl-CoA by glutaryl-CoA dehydrogenase was investigated.
36     The involvement of water in catalysis by glutaryl-CoA dehydrogenase was previously unrecognized a
37 parison of steady-state kinetic constants of glutaryl-CoA dehydrogenase with glutaryl-CoA and the alt