ライフサイエンスコーパス: AADC

1 AADC deficient patients fail to produce normal levels of

2 AADC immunopositive (AADC +) cells were also counted in

3 AADC levels did not decrease during development, and adu

4 AADC secreted much higher levels of IL-10, but lower lev

5 e conclude that even minute levels of active AADC are sufficient to allow for substantial amounts of

6 ation approaches, we demonstrate that TH and AADC associate with VMAT(2)-containing synaptic vesicles

7 In rat striata, TH and AADC co-immunoprecipitate with VMAT(2), whereas in PC 12

8 T(2) involved in the interaction with TH and AADC.

9 s using 6-[(18)F]fluorodopa (FDOPA) (another AADC substrate) to measure how striatal PET signal and a

10 atal form of infantile Parkinsonism known as AADC deficiency.

11 LAT1 transport but is not decarboxylated by AADC.

12 be mediated by 5-HT1B receptors expressed by AADC cells.

13 The production of 5-HT by AADC cells, together with an upregulation of 5-HT2 recep

14 trophysiology, we show that 5-HT produced by AADC cells increases the excitability of spinal motoneur

15 A single infusion of BALB/c AADC to quiescent B10 recipients induced alloantigen-spe

16 , relies in part on DOPA decarboxylase (DDC, AADC), an enzyme that is required for normative neural o

17 lasms that possess amino acid decarboxylase (AADC) activity and can theoretically be imaged by (18)F-

18 ed with aromatic L-amino acid decarboxylase (AADC) and VMAT-2 genes.

19 enzyme aromatic-L-amino acid decarboxylase (AADC) and, when incubated with the dopamine precursor, 3

20 (TPH) and aromatic amino acid decarboxylase (AADC) are expressed in taste cells.

21 The aromatic L-amino-acid decarboxylase (AADC) defect appears to be consistently smaller than the

22 Aromatic l-amino acid decarboxylase (AADC) deficiency is an inborn error of monoamine neurotr

23 Aromatic l-amino acid decarboxylase (AADC) deficiency is an inherited disease that causes dep

24 The rat aromatic l-amino acid decarboxylase (AADC) gene contains alternative promoters which direct e

25 in the aromatic l-amino acid decarboxylase (AADC) gene result in a severe depletion of its namesake

26 TH) and L-aromatic amino acid decarboxylase (AADC) in animals housed under long photoperiod (LD) or S

27 vity of aromatic l-amino acid decarboxylase (AADC) in the corpus striatum (CS) and substantia nigra (

28 ctions of aromatic amino acid decarboxylase (AADC) in the proximal tubule, previous studies have not

29 on of the aromatic amino acid decarboxylase (AADC) inhibitor m-hydroxybenzylhydrazine attenuated thes

30 enzyme aromatic l-amino acid decarboxylase (AADC) occur not only near the central canal, as reported

31 enzyme aromatic l-amino acid decarboxylase (AADC) or the TH cofactor tetrahydrobiopterin (BH4) could

32 Aromatic amino acid decarboxylase (AADC) then converts di-OH-phenylalanine into DA.

33 lation by aromatic amino acid decarboxylase (AADC), an enzyme overexpressed in these malignancies.

34 e (TH), aromatic l-amino acid decarboxylase (AADC), and GTP cyclohydrolase I (GCH1) transcription; in

35 ates of aromatic l-amino acid decarboxylase (AADC), the level of which is enhanced in endocrine tumor

36 enzyme aromatic L-amino acid decarboxylase (AADC), which synthesizes trace amines directly from diet

37 g enzyme, aromatic amino acid decarboxylase (AADC).

38 TH), aromatic amino acid dopa decarboxylase (AADC), and GTP cyclohydrolase 1 (CH1) in a single transc

39 rmation pathway (acetoacetate decarboxylase [AADC] and coenzyme A-transferase [CoAT]) of Clostridium

40 C; also known as L-amino acid decarboxylase; AADC) is involved in the synthesis of dopamine, norepine

41 Aromatic L-amino acid decarboxylases (AADCs) are key enzymes operating at the interface betwee

42 0, encoding pyridoxal 5'-phosphate-dependent AADCs with high homology to the recently identified Petu

43 mg/kg) and phencyclidine (4 mg/kg) elevated AADC activity in both the CS and SN (2- to 3-fold).

44 tic neurons were strongly immunoreactive for AADC.

45 There is no optimal treatment for AADC deficiency and few truly good models in which to in

46 tants represent a novel, mild model of human AADC deficiency.

47 ated virus (AAV) vector containing the human AADC gene (AAV2-hAADC) in four children with AADC defici

48 AADC immunopositive (AADC +) cells were also counted in the median eminence.

49 The phenotypic change in AADC cells appears to result from a loss of inhibition b

50 This decline in AADC+ cells may play a role in SD-induced changes in hyp

51 Similarly pronounced increases in AADC activity in CS (1.9-fold) and SN (2.8-fold) were de

52 Even more striking increases in AADC were noted with 40 mg/kg amantadine (3.8-fold for C

53 g alpha2-adrenoceptors, profoundly increases AADC activity, more especially in the SN than CS.

54 nzyme L-aromatic amino acid decarboxylase (L-AADC) in neural and nonneural tissue, on blood pressure

55 dministration of carbidopa, which inhibits L-AADC outside the blood-brain barrier, blunted both the i

56 nsection of the rat spinal cord at S2 level, AADC cells distal to the lesion acquire the ability to p

57 we generated mice with selective deletion of AADC in the kidney proximal tubules (referred to herein

58 Despite the significant downregulation of AADC in these strains, there were no concomitant effects

59 which do not express the nonneuronal form of AADC by transient transfection.

60 ecific expression of the nonneuronal form of AADC mRNA is HNF-1.

61 which do not express the nonneuronal form of AADC resulted in activation of transfected AADC nonneuro

62 re inhibited by benserazide, an inhibitor of AADC.

63 that all three strains exhibit low levels of AADC compared to the plasmid control [ATCC 824(pSOS95del

64 In contrast, FMT remains a purer measure of AADC function.

65 In vivo migration of AADC to secondary lymphoid tissue was not impaired.

66 The number of AADC + cells was also reduced in the median eminence of

67 duced a significant decline in the number of AADC + cells.

68 Inhibition of monoamine receptors or of AADC, or even an increase in inhaled oxygen, produces su

69 ce insight into the regulatory properties of AADC and demonstrate their therapeutic potential in vasc

70 efinitive diagnosis and clinical symptoms of AADC deficiency (hypotonia, dystonia, and oculogyric cri

71 porter 2 defects, suggesting upregulation of AADC function in PD.

72 or muscarinic receptors is without effect on AADC in either brain region.

73 ect the number of TH immunopositive (TH+) or AADC + cells in the caudal periventricular nuclei.

74 A 966 (5 mg/kg, not 1 mg/kg) modestly raised AADC activity in CS (0.45-fold) and not SN.

75 ssion of the nonneuronal promoter of the rat AADC gene in the kidney epithelial cell line LLC-PK1 and

76 dicate that this phenotypic change in spinal AADC cells is initiated by the loss of descending 5-HT p

77 tal neurons transduced with this vector, TH, AADC, and CH1 proteins can all be detected.

78 ence of fragments involved in the VMAT(2)/TH/AADC interaction.

79 These findings indicate that AADC cells are a potential source of 5-HT at spinal leve

80 These findings suggest that AADC does not limit acetone formation and, thus, we targ

81 The AADC-expanded allogeneic CD4+CD25+ T cells showed enhanc

82 ly by CTLA4-Ig, administered 1 day after the AADC.

83 roduce asRNAs of various lengths against the AADC (adc) transcript.

84 ss a stable but minimally active form of the AADC protein.

85 8)F-FDOPA PET results, pretreatment with the AADC inhibitor S-carbidopa did not affect the (18)F-l-FE

86 , the three different asRNAs directed toward AADC, along with previously reported clostridial asRNAs,

87 f AADC resulted in activation of transfected AADC nonneuronal promoter constructs.

88 tyrosine to DOPA and subsequently to DA via AADC.

89 fted with either control cells or cells with AADC alone.

90 AADC gene (AAV2-hAADC) in four children with AADC deficiency (aged 4-6 years).

91 t improve motor development in children with AADC deficiency.

92 of (18)F-FDOPA significantly correlated with AADC expression (n = 15 nonhepatic tumors; maximum stand

93 -FDOPA PET were measured and correlated with AADC messenger RNA level in tumor tissue.

94 By correlating with AADC expression, (18)F-FDOPA PET might serve as a useful

95 probably independent of any interaction with AADC.

96 n dopamine and serotonin levels of mice with AADC deficiency.

97 is highly prevalent in Chinese patients with AADC deficiency.