ライフサイエンスコーパス: GCH

1 GCH III is a tetramer of identical subunits; each monome

2 eted overexpression of GTP cyclohydrolase 1 (GCH), the rate limiting enzyme in BH4 synthesis, increas

3 We have studied the GTP-cyclohydrolase 1 (GCH-1) gene in 30 patients with the diagnosis of clinica

4 is formally identical to that catalyzed by a GCH II ortholog (SCO 6655) from Streptomyces coelicolor;

5 nd mapping onto the structure of the E. coli GCH II protein allowed identification of a switch residu

6 ith atypical phenylketonuria due to complete GCH-1 deficiency.

7 ing BH4 synthetic enzyme GTP cyclohydrolase (GCH) became undetectable in the sweat gland neurons duri

8 rgeted overexpression of GTP cyclohydrolase (GCH) I increased levels of the endothelial NO synthase c

9 GTP cyclohydrolase (GCH) III from Methanocaldococcus jannaschii, which catal

10 Endothelial GCH overexpression increased endothelial NO synthase cou

11 ESs was higher than in water, especially for GCH.

12 s in vascular tissue and plasma samples from GCH/ApoE-KO animals.

13 f a patient with adult giant-cell hepatitis (GCH), a rare form of hepatitis with presumed viral etiol

14 ical role(s) of the gene clusters that house GCH II homologues will be discussed.

15 d from the Genomic Comparison Hybridization (GCH) experiment and performed using the Affymetrix platf

16 een associated with goblet cell hyperplasia (GCH) in small studies.

17 enic overexpression of GTP-cyclohydrolase I (GCH), prevented hypoxia-induced pulmonary hypertension.

18 mino acid identity to GTP cyclohydrolase II (GCH II), which catalyzes the committed step in the biosy

19 l hyperplasia in experimental vein grafts in GCH/apolipoprotein E-knockout mice.

20 ion of macrophage marker CD68 mRNA levels in GCH/ApoE-KO mice.

21 ne of our DRD patients without a mutation in GCH-1 had the 3-bp deletion recently detected in DYT1, t

22 domain containing proteins, are observed in GCH III.

23 RANTES (CCL5) were significantly reduced in GCH/ApoE-KO aortic tissue.

24 ed variants (Asp-->Asn) of these residues in GCH III are less active than wild-type.

25 Interestingly, GCH-1 overexpression abrogated these detrimental effects

26 s, revealed by tracking studies in Tie2-LacZ/GCH-Tg/apolipoprotein E-knockout recipient mice or donor

27 hypothesized that the primary determinant of GCH in ever smokers with or without airflow obstruction

28 Our data are consistent with duplication of GCH II in S. coelicolor promoting evolution of a new fun

29 We further extended our investigation of GCH-1 to the 5' and 3' regulatory regions and report the

30 uction poorly correlate with the presence of GCH or COPD.

31 d SCO 2687) produce the canonical product of GCH II, 2,5-diamino-6-ribosylamino-4(3H)-pyrimidinone 5'

32 rvival and recipient-derived repopulation of GCH transgenic ECs, revealed by tracking studies in Tie2

33 howed a stronger supramolecular structure of GCH and a high ratio of B-glucose in both DESs.

34 howed a stronger supramolecular structure of GCH and a high ratio of beta-glucose in both DESs.

35 The structure of GCH III complexed with GTP solved at 2 A resolution clea

36 The structure of GCH III extends the repertoire of possible reactions wit

37 es coelicolor; however, SCO 6655, like other GCH II proteins, is a zinc-containing protein.

38 a clear set of mutational events that permit GCH II to produce either FAPy or APy.

39 olate was more pathogenic than the reference GCH-1 isolate.

40 weat glands reduce BH4 levels by suppressing GCH expression during development.

41 OCA-salt mice, but both were preserved in Tg-GCH mice despite DOCA-salt treatment.

42 othelium-specific GTPCH I overexpression (Tg-GCH).

43 gnificantly improved in DOCA-salt-treated Tg-GCH mice, in parallel with reduced O2(-) levels.

44 fects were prevented in DOCA-salt-treated Tg-GCH mice.

45 ls but was preserved in DOCA-salt-treated Tg-GCH mice.

46 These data also indicate that GCH expression, which is often coordinately regulated wi

47 solved at 2 A resolution clearly shows that GCH III adopts a distinct fold that is closely related t

48 These results suggest that GCH is induced by active smoke exposure and does not nec

49 metal ions in the active site suggests that GCH III utilizes two metal ion catalysis.

50 to be an important causative factor for the GCH-1 mutations in DRD.

51 ced vein graft atherosclerosis in transgenic GCH/ApoE-KO mice compared to ApoE-KO controls.

52 acterized: d-glucose:choline chloride:water (GCH) and d-glucose:citric acid:water (GCiH).

53 dothelial BH4 in hph-1 mice by crossing with GCH transgenic mice rescued pulmonary hypertension induc

54 In contrast, livers of patients with GCH display strong GP73 immunoreactivity in multinucleat