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 derivatization by 3-nitrophenylhydrazine (3-NPH) and glycidyltrimethylammonium chloride (GTMA) to en

18 s performed on CT head examinations from 305 NPH patients and 294 controls.

19 ncing of extracellular vesicles in CSF of 42 NPH patients, and we identify genes and pathways whose e

20 A total of 118,526 NPH diagnoses were recorded, with 29,662 surgical interv

21 55 NPH patients and 55 age-matched healthy subjects underwe

22 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

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

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

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

26 longer after intraperitoneal DET than after NPH.

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

28 circulatory failure, with features of AD and NPH.

29 VETF, the mRNA processing factors VTF/CE and NPH-I, the viral core protein E11, and host tRNA(Gln).

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

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

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

33 Insulin glargine, insulin detemir, and NPH insulin.

34 association between Alzheimer's disease and NPH changes, supporting the recently suggested dichotomy

35 oglobin A1c, general diabetes education, and NPH or L insulins.

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

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

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

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

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

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

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

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

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

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

46 The characterization .NPH-CO and .PNH-CO with matrix-isolation IR spectroscopy

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

48 rsal thalamus cells in animals with complete NPH lesions.

49 type virus-infected cell extracts containing NPH I.

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

51 t to most other neurodegenerative disorders, NPH symptoms can be improved by the placement of a ventr

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

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

54 for glargine, 1693 for detemir, and 460 for NPH insulin, with a median follow-up across the 3 cohort

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

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

57 large brain size itself is a risk factor for NPH and may help account for increased NPH risk among ma

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

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

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

61 evaluate surgical management strategies for NPH in Germany.

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

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

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

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

66 ulin analogs and neutral protamine Hagedorn (NPH) insulin in patients with type 2 diabetes.

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

68 n glulisine, and Neutral Protamine Hagedorn (NPH) insulin.

69 nsulins regular, neutral protamine Hagedorn [NPH], lispro, glulisine, glargine, detemir, degludec, an

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

71 iting some form of non-proportional hazards (NPH), these methods could lead to an under- or over-esti

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

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

74 eproduced the histological features of human NPH in murine models.

75 extrarenal phenotypes associated with human NPH, including renal cyst development, tubular basement

76 Normal pressure hydrocephalus (NPH) is a neurological disorder characterized by progres

77 Normal pressure hydrocephalus (NPH) is a poorly understood neurodegenerative condition

78 Normal pressure hydrocephalus (NPH) is a reversible cause of gait disturbances and deme

79 in idiopathic normal pressure hydrocephalus (NPH) patients from the gait decline in the elderly popul

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

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

82 ith suspected normal pressure hydrocephalus (NPH) who respond to CSF drainage from patients who do no

83 rodynamics in normal pressure hydrocephalus (NPH), Chiari type I malformations (CMI), syringomyelia,

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

85 , n = 23), or Normal Pressure Hydrocephalus (NPH, n = 57).

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

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

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

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

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

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

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

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

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

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

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

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

98 neurodegenerative NPH and a true idiopathic NPH, with the latter appearing to be rare.

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

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

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

102 ay have important implications for improving NPH diagnosis and treatment and for understanding diseas

103 In NPH precisely performed PC-MRI provides reliable clinica

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

105 01) and ~ 2.5% larger in males (p = .003) in NPH compared with controls and ICV was ~ 5.2% larger in

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

107 A major challenge in NPH management is the identification of patients who ben

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

109 conclusion, the hypokinetic gait disorder in NPH can be quantitatively differentiated from gait patte

110 hich we hypothesize will also be elevated in NPH and account for the increase in ICV.

111 mmatory mediators, whereas their presence in NPH was accompanied by anti-inflammatory mediators.

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

113 etiology of periventricular CBF reduction in NPH.

114 The study highlights a 48% rise in NPH incidence in Germany from 2005 to 2022, particularly

115 io of brain volume to intracranial volume in NPH versus controls was not significantly different for

116 r for NPH and may help account for increased NPH risk among males.

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

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

119 l as a first therapeutic option for juvenile NPH-associated ciliopathies.

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

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

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

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

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

125 al ear canal (EEC) lavages, and nasopharynx (NPH) samples from children with OME.

126 Nephronophthisis (NPH) is an autosomal recessive tubulointerstitial nephro

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

128 Nephronophthisis (NPH) is the most prevalent monogenetic disorder leading

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

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

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

132 y suggested dichotomy of a neurodegenerative NPH and a true idiopathic NPH, with the latter appearing

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

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

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

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

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

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

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

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

141 If BEH is a major cause of NPH this would then require that it also results in pers

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

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

144 selection by accommodating various forms of NPH.

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

146 The population-adjusted incidence of NPH increased by 48%, from 5.4 to 8.0 cases per 100,000

147 etic resonance imaging changes indicative of NPH were studied with regard to cognitive and gait funct

148 ed methods successfully address the issue of NPH in genomic feature selection and outperform existing

149 calized protein, account for the majority of NPH cases.

150 the epidemiology and surgical management of NPH are not well understood.

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

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

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

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

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

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

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

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

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

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

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

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

163 pective nationwide population-based study of NPH cases in Germany from 2005 to 2022 was conducted usi

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

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

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

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

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

169 407 018), insulin detemir (n = 141 588), or NPH insulin (n = 26 402) from January 1, 2007, to July 3

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

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

172 .1% [mean +/- SE]) were randomized to GLA or NPH insulin therapy for 36 weeks.

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

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

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

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

177 mproved ciliary and kidney phenotypes in our NPH zebrafish and Nphp1 knockout mouse models.

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

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

180 ions, underscoring the need for prioritising NPH in national healthcare research agendas.

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

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

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

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

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

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

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

188 the Pol II elongation factor TFIIS, and that NPH-I resembles chromatin remodeling enzymes.

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

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

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

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

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

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

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

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

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

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

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

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

201 er neurotoxic or electrolytic lesions of the NPH.

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

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

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

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

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

207 nt in MEE, whereas their presence in the the NPH was accompanied by a proinflammatory profile.

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

209 The .NPH-CO complex is extremely unstable, as it undergoes sp

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

211 igonucleotide inhibition is mediated through NPH I.

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

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

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

215 54 nm, the reverse conversion of .PNH-CO to .NPH-CO along with dehydrogenation to yield PN was observ

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

217 rgine, 141 588 used detemir, and 26 402 used NPH insulin.

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

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

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

221 lin, 0.71; 95% CI, 0.63-0.80; HR, detemir vs NPH insulin, 0.72; 95% CI, 0.63-0.82).

222 red with NPH insulin use (HR for glargine vs NPH insulin, 0.71; 95% CI, 0.63-0.80; HR, detemir vs NPH

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

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

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

226 ) and ~ 3.7% larger in males (p < .001) with NPH compared with controls.

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

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

229 ines, a phenotype previously associated with NPH.

230 pitalizations for hypoglycemia compared with NPH insulin in older patients with type 2 diabetes in Me

231 a reduced risk of hypoglycemia compared with NPH insulin use (HR for glargine vs NPH insulin, 0.71; 9

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

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

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

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

236 interaction of linear oligonucleotides with NPH I.

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

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

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

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

241 r intracranial volume (ICV) among those with NPH which has been taken to establish a link to Benign e

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

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

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