ライフサイエンスコーパス: NPH

1 NPH I hydrolyzes ATP to release transcripts during trans

2 NPH I shows sequence similarity with the DEXH-box family

3 NPH I uses ATP hydrolysis to mediate transcript release,

4 NPH-AD may cover an important subset of patients who car

5 NPH-I is a member of the DExH box family of nucleic acid

6 NPH-II exhibited profound asymmetry in displacing hybrid

7 NPH-II increases the rate of U1A dissociation by more th

8 NPH-II is a prototypical member of the DExH/D subgroup o

9 NPH-II is the prototypal RNA helicase of the DExH box pr

10 NPH-II is thus believed to make primary contacts with ba

11 NPH-II mutations that inactivated the phosphohydrolase i

12 NPH-II was incapable of displacing a 34-bp double-strand

13 NPH-II-Ala proteins were expressed in baculovirus-infect

14 er two OGLDs, and pre-mix 0.97 (0.46, 2.02); NPH 0.77 (0.32, 1.86) after three OGLDs.

15 atization to their 2-nitrophenylhydrazide (2-NPH) derivatives, fatty acid (FA) abundances have been e

16 pment of the chromatographic separation of 2-NPH FAs may lead to greater utility of this HPLC approac

17 sus basal: pre-mix 1.08 (95% CI 0.73, 1.59); NPH 1.00 (0.63, 1.58) after two OGLDs, and pre-mix 0.97

18 Furthermore, preincubation of a NPH I minus cell extract with NPH I prior to antibody ad

19 Inhibition is overcome by adding NPH I, demonstrating that oligonucleotide inhibition is

20 y weight remained lower after DET than after NPH after 48 h.

21 longer after intraperitoneal DET than after NPH.

22 The observed sequence bias allows NPH-II to efficiently unwind a DNA x RNA hybrid containi

23 circulatory failure, with features of AD and NPH.

24 DET and NPH had comparable saturable, receptor-mediated transpor

25 Transport of DET and NPH insulin into the cerebrospinal fluid (CSF) was compa

26 nto the 3rd cerebral ventricle, both DET and NPH insulin reduced food intake and body weight at 24 h,

27 ), metabolites 1 (M1) and 2 (M2), IGF-I, and NPH insulin to activate the insulin receptor (IR)-A and

28 estibular nuclei and the MVN, DVN, Psol, and NPH.

29 y a helical segment of E. coli 23S rRNA, and NPH-II unwinds RNAs by directional translocation.

30 d IGF-IR autophosphorylation (activation) as NPH insulin.

31 Here, we identify factor X as NPH-I (nucleoside triphosphate phosphohydrolase-I), a vi

32 rase; A18 DNA helicase; DNA-dependent ATPase NPH-I; and DNA topoisomerase.

33 viding evidence that the interaction between NPH I and H4L is required for termination.

34 irement for an essential interaction between NPH I and H4L provides an explanation for the observed r

35 (i) Unwinding of duplex nucleic acids by NPH-II is optimal when the polynucleotide strand of the

36 nistic framework for unwinding initiation by NPH-II and suggest that the various stages of the ATP hy

37 ducts (NPHP) function at the primary cilium, NPH is classified as a ciliopathy.

38 rsal thalamus cells in animals with complete NPH lesions.

39 type virus-infected cell extracts containing NPH I.

40 M were initially stabilized with twice-daily NPH and regular insulin.

41 anscription bubble is required for efficient NPH I-mediated transcript release.

42 For NPH-II from vaccinia virus, unwinding initiation is rate

43 rm that the source of the ssDNA cofactor for NPH I is the upstream portion of the non-template strand

44 es to explore the molecular determinants for NPH-II specificity on RNA and to determine if there are

45 Comparison of our findings for NPH-I with those of mutational studies of other DExH and

46 modynamic aspects of this reaction phase for NPH-II in vitro, using biochemical and single molecule f

47 strands in this region is also required for NPH I-mediated transcript release.

48 hown to bind glutathione S-transferase (GST)-NPH I.

49 polymerase specifically co-purified with GST-NPH I, consistent with a physical interaction.

50 ine, detemir) or neutral protamine Hagedorn (NPH) insulin between 2002 and 2012, was formed using the

51 the conventional neutral protamine Hagedorn (NPH) insulin for diabetic control.

52 mplexes, such as neutral protamine Hagedorn (NPH) insulin, have been hampered by high crystal solvent

53 asal, pre-mix or Neutral Protamine Hagedorn, NPH) while ANCOVAs compared haemoglobin A(1c) (HbA(1c))

54 well-studied relative, the Vaccinia helicase NPH-II.

55 Vaccinia virus RNA helicase (NPH-II) catalyzes nucleoside triphosphate-dependent unwi

56 Idiopathic normal pressure hydrocephalus (NPH) remains both oversuspected on clinical grounds and

57 o be lower in normal pressure hydrocephalus (NPH) than in normal controls.

58 se (AD) or as normal-pressure hydrocephalus (NPH).

59 patients with normal-pressure hydrocephalus (NPH; mean age, 75 years; age range, 58-87 years; 26 men,

60 eus (SGN) and nucleus prepositus hypoglossi (NPH), are known to project to the HD network and are tho

61 ocated in the nucleus prepositus hypoglossi (NPH), spinal vestibular nucleus, cochlear complex, and g

62 sol), and the nucleus prepositus hypoglossi (NPH).

63 Nucleoside triphosphate phosphohydrolase I (NPH I) is a single-stranded DNA-dependent ATPase.

64 Nucleoside triphosphate phosphohydrolase I (NPH I) is an essential component of the early gene trans

65 nucleoside triphosphate phosphohydrolase I (NPH I) serves as the ATPase activity employed in early g

66 nucleoside triphosphate phosphohydrolase I (NPH I), an ATPase that is employed in early gene transcr

67 nucleoside triphosphate phosphohydrolase I (NPH I), and ATP.

68 nucleoside triphosphate phosphohydrolase I (NPH-I) is a DNA-dependent ATPase that serves as a transc

69 In an attempt to identify NPH I-related protein/protein interactions involved in t

70 atients with initial diagnosis of idiopathic NPH persist in only 32% of patients at 36 months, with k

71 Twelve patients with idiopathic NPH (mean age 69 years) underwent a CSF infusion study.

72 nucleoside triphosphate phosphohydrolase II (NPH-II) result in the production of noninfectious progen

73 nucleoside triphosphate phosphohydrolase-II (NPH-II) exhibits robust RNA helicase activity but typica

74 In NPH, raised CSF pressure causes lower CSF production and

75 paraventricular white matter CBF (WM CBF) in NPH at baseline and during a controlled rise in intracra

76 n increased risk of microvascular disease in NPH versus basal after 3 OGLDs, adjusted hazard ratio 1.

77 The WM CBF is reduced in NPH, with an abnormal gradient from the lateral ventricl

78 etiology of periventricular CBF reduction in NPH.

79 juvenile or late-onset and cilia-independent NPH.

80 h this conclusion we also show that isolated NPH I acts as a 5' to 3' translocase on single-stranded

81 analysis indicate that these particles lack NPH-II, whereas other enzymatic components of the virus

82 y using virus-infected cell extracts lacking NPH I, but antibodies raised against H4L amino acids 568

83 Like NPH-II, NS3 translocates along the loading strand (the s

84 Since most NPH gene products (NPHP) function at the primary cilium,

85 Wild-type and mutant NPH-II-Ala genes were tested for the ability to rescue t

86 Nephronophthisis (NPH) is an autosomal-recessive cystic kidney disease and

87 Nephronophthisis (NPH), an autosomal-recessive tubulointerstitial nephriti

88 recessive PKD (ARPKD) and nephronophthisis (NPH), are characterized by collecting-duct cysts.

89 ts from five families with nephronophthisis (NPH) and retinal degeneration, two of the most common ma

90 Viral RNA helicases of the NS3/NPH-II group unwind RNA duplexes by processive, directio

91 ternary complexes prepared in the absence of NPH I, prevented antibody inhibition of transcription te

92 phosphohydrolase and helicase activities of NPH-II are essential for virus replication.

93 The ATPase activity of NPH I requires single-stranded (ss) DNA as a cofactor; h

94 important role in modulating the behavior of NPH-II.

95 e mutations analyzed affected the binding of NPH-II to RNA.

96 e of these mutations affected the binding of NPH-II to single-strand RNA or to the tailed duplex RNA

97 hology is often seen in cortical biopsies of NPH patients.

98 e cilium, contributing to the development of NPH-related ciliopathies.

99 The COOH-terminal end of NPH I was also shown to be required for transcript relea

100 sight into potential biological functions of NPH-II and the role of sequence in targeting NPH-II to a

101 In an aged animal model of NPH, we quantify Abeta and pTau accumulation and describ

102 length bind one, two, and three molecules of NPH I maximally, respectively, indicating that the NPH I

103 A mutation (K61A) in the GxGKT motif of NPH-I abolishes ATP hydrolysis and eliminates the termin

104 hermore, COOH-terminal deletion mutations of NPH I failed to bind the NH(2)-terminal region of H4L, e

105 Carboxyl-terminal deletion mutations of NPH I lose both the ability to mediate transcription ter

106 COOH-terminal deletion mutations of NPH I retain both ATPase and DNA binding activities but

107 xes on the P4(1)2(1)2 (110) crystal plane of NPH, based on a low-resolution x-ray diffraction structu

108 ycle dictate distinct binding preferences of NPH-II for duplex versus single-stranded RNA.

109 prior to antibody addition, or readdition of NPH I to isolated ternary complexes prepared in the abse

110 odel posits that the COOH-terminal region of NPH I binds to one or more components in the termination

111 ow-resolution x-ray diffraction structure of NPH, arguing that the NPH and NPL insulins are isostruct

112 tiate detailed structure-function studies of NPH I, we undertook combined kinetic and binding analyse

113 Ten mutated versions of NPH-II were expressed in vaccinia virus-infected BSC-40

114 and diminished postoperative improvement on NPH symptom severity scales, gait measures, and cognitiv

115 The H4L binding site on NPH I was mapped to the COOH-terminal region between 457

116 important oligonucleotide activation site on NPH I. ssDNA inhibits transcription termination in vitro

117 als from five families presenting late-onset NPH with massive renal fibrosis.

118 ents who carry the diagnosis of either AD or NPH.

119 Serum from patients treated with GLA or NPH insulin induced similar IR-A and IR-B activation.

120 .1% [mean +/- SE]) were randomized to GLA or NPH insulin therapy for 36 weeks.

121 d by serum from patients treated with GLA or NPH insulin.

122 had reduced less in basal versus pre-mix or NPH at 6-8 and at 9-11 months, and versus pre-mix at 12-

123 hen basal insulin was compared to pre-mix or NPH, adjusted hazard ratio versus basal: pre-mix 1.08 (9

124 rovided either with human ultralente (UL) or NPH insulins.

125 eeks of therapy with RHI plus UL or RHI plus NPH, 50% of patients were randomly assigned to begin ins

126 , if resistance to CSF outflow predominates, NPH results.

127 DbpA and the vaccinia virus DExH-box protein NPH-II gave little, if any, group I or group II intron s

128 We demonstrate that the DExH protein NPH-II from vaccinia virus can displace the protein U1A

129 Here we show that the DExH protein NPH-II unwinds RNA duplexes in a processive, unidirectio

130 We postulate that previously reported NPH cases with "dual" pathology (ie, developing a "secon

131 regulated by the primary cilium and several NPH proteins, although the mechanism remains unclear.

132 virus, vNPHINGST, that expresses GST-tagged NPH I.

133 NPH-II and the role of sequence in targeting NPH-II to appropriate substrates.

134 We conclude that NPH-II is required for early mRNA synthesis uniquely in

135 In this study, we demonstrate that NPH I also uses forward translocation to catalyze transc

136 h previous mutational studies, indicate that NPH-II motifs I, Ia, II, and VI (QRxGRxGRxxxG) are essen

137 We report that NPH-I serves two roles in transcription (1) it acts in c

138 These data show that NPH I and the inhibitory antibodies compete for a bindin

139 Moreover, we show that NPH I-mediated release can occur at a stalled RNAP in th

140 Our data show that NPH-II functions as a monomer and that different stages

141 yperbolic kinetics are seen, suggesting that NPH I may adopt two conformational states.

142 atial tuning in downstream HD cells, but the NPH has historically been defined as an oculomotor nucle

143 OH-terminal truncation mutations of H4L, the NPH I interaction site was localized to the NH(2)-termin

144 single, stage-specific conformations in the NPH-II-RNA complex but primarily control transitions bet

145 th significant but incomplete lesions of the NPH had HD cells that were stable under normal condition

146 er neurotoxic or electrolytic lesions of the NPH.

147 We critically review the NPH literature, highlighting the near universal lack of

148 ffraction structure of NPH, arguing that the NPH and NPL insulins are isostructural.

149 maximally, respectively, indicating that the NPH I binding site is no more than 12 bases in length.

150 hese results support the hypothesis that the NPH, beyond its traditional oculomotor function, plays a

151 We further find that the NPH-II-RNA complex does not adopt a single conformation

152 The cocrystal is analogous to the NPH (neutral protamine Hagedorn) crystalline complex for

153 cs appears to impair Abeta clearance in this NPH model.

154 igonucleotide inhibition is mediated through NPH I.

155 Prior studies have shown that ssRNA binds to NPH I, but it does not activate ATPase activity.

156 oth RNA and DNA can be photo-cross-linked to NPH I by UV light.

157 A cross-compete in UV photo-cross-linking to NPH I, indicating that both oligonucleotides share a com

158 However, unlike NPH-II, NS3 readily unwinds RNA duplexes that contain lo

159 bind VETF and core subunits of RPO, and (v) NPH I and VETF bind independently and possibly simultane

160 Vaccinia virus NPH-II is an essential nucleic acid-dependent nucleoside

161 Vaccinia virus NPH-II is the prototypal RNA helicase of the DExH box pr

162 uires the vaccinia termination factor (VTF), NPH I, a single stranded DNA-dependent ATPase, the virio

163 ation of premature termination required VTF, NPH I, Rap 94, and ATP, demonstrating that the normal te

164 Whereas NPH-II efficiently unwound double-stranded RNA substrate

165 , comparing long-acting insulin analogs with NPH overall, as well as by duration and cumulative dose.

166 arent effect on any activity associated with NPH-II, whereas a mutation at the weakly conserved posit

167 ines, a phenotype previously associated with NPH.

168 mediates GLA effects and that compared with NPH insulin, GLA does not increase IGF-IR signaling duri

169 Compared with NPH insulin, insulin glargine was associated with an inc

170 increased risk of microvascular events with NPH warrants further study.

171 ncubation of a NPH I minus cell extract with NPH I prior to antibody addition, or readdition of NPH I

172 interaction of linear oligonucleotides with NPH I.

173 rve of 0.96 in differentiating patients with NPH from patients without NPH (ie, Alzheimer disease and

174 the radiologist differentiate patients with NPH from patients without NPH, which would allow for des

175 is useful in the selection of patients with NPH to undergo shunt formation.

176 The direct association of RAP94 with NPH I, a DNA-dependent ATPase required for transcription

177 Eighteen patients (mean age, 73 years) with NPH underwent routine MR imaging and CSF velocity MR ima

178 ting patients with NPH from patients without NPH (ie, Alzheimer disease and healthy control).

179 iate patients with NPH from patients without NPH, which would allow for designation of patients for f