ライフサイエンスコーパス: HAT

1 HAT-7 cells formed epithelial layers with measureable tr

2 HAT-7 cells were seeded onto Transwell permeable filters

3 HAT-B is a multisubunit complex composed of the histone

4 HAT-L4 knockout mice were viable and fertile.

5 The excited-state quenching of [Ru(TAP)2(HAT)](2+) (TAP = 1,4,5,8-tetraazaphenanthrene, HAT= 1,4,

6 Human airway trypsin-like protease 4 (HAT-L4) is a type II transmembrane serine protease.

7 nger than that for 1-H, which decays via 1,5-HAT (tau1/2 = 48 s, DeltaH(double dagger) = 10.0 +/- 0.3

8 ermore, this allows for a chemoselective 1,5-HAT over competing direct cyclizations and beta-fragment

9 tramolecular 1,5-hydrogen atom transfer (1,5-HAT) in the decay of a PEGylated carbazyl (aminyl) radic

10 tramolecular 1,5-hydrogen atom transfer (1,5-HAT) that was observed in its constitutional isomer 1-H

11 chemoselective 1,6-HAT over a competing 1,5-HAT.

12 This has enabled a chemoselective 1,6-HAT over a competing 1,5-HAT.

13 ng mostly compounds originating from two 1,8-HAT consecutive processes.

14 tone rings within the CD framework via a 1,8-HAT-beta-scission tandem mechanism.

15 the high rate of hydrogen atom abstraction (HAT) from dihydroanthracene (DHA) by the complex LCuOH (

16 d kinetics of its hydrogen-atom abstraction (HAT) reactions.

17 Loss of the histone acetyltransferase (HAT) activity blocks oogenesis, while loss of the H2B de

18 A alters HDAC and histone acetyltransferase (HAT) activity, which suggests a role for HAT/HDAC homeos

19 ules, which house histone acetyltransferase (HAT) and deubiquitinase (DUB) activities.

20 emodeling through histone acetyltransferase (HAT) and histone deactylase (HDAC) enzymes affects funda

21 sing steady-state histone acetyltransferase (HAT) assays, we show that an RNA binding region in the H

22 recruits the MOF histone acetyltransferase (HAT) complex to ERalpha target gene promoters to deposit

23 ubunit of the MOZ histone acetyltransferase (HAT) complex, critical for normal developmental programs

24 nsferase 6 (KAT6) histone acetyltransferase (HAT) complexes are highly conserved from yeast to higher

25 onent of specific histone acetyltransferase (HAT) complexes.

26 co-activator and histone acetyltransferase (HAT) complexes.

27 as a modulator of histone acetyltransferase (HAT) in plants.

28 The histone acetyltransferase (HAT) inhibitor garcinol or vehicle was injected followin

29 Several histone acetyltransferase (HAT) inhibitors with these liabilities are now routinely

30 plex known as the histone acetyltransferase (HAT) module that contains the HAT, Gcn5, bound to Sgf29,

31 covered the H4K16 histone acetyltransferase (HAT) MOF to be important for leukemia cell growth.

32 s, controlled by histone acetyltransferases (HATs) and deacetylases (HDACs), profoundly affects DNA t

33 Histone acetyltransferases (HATs) and histone deacetylases (HDACs) compete to modula

34 odifying enzymes histone acetyltransferases (HATs) and histone deacetylases (HDACs) shapes chromatin

35 ns, catalysed by histone acetyltransferases (HATs) and histone deacetylases (HDACs), is a major epige

36 KAT6 histone acetyltransferases (HATs) are highly conserved in eukaryotes and are involve

37 KAT6 histone acetyltransferases (HATs) are highly conserved in eukaryotes and have been s

38 ases (HDACs) and histone acetyltransferases (HATs) are involved in MSH2 deacetylation/acetylation is

39 Although histone acetyltransferases (HATs) have been well characterized both structurally and

40 closely related histone acetyltransferases (HATs) that play a key role in the regulation of gene tra

41 ability of seven histone acetyltransferases (HATs) to catalyze acylations on histones in vitro using

42 1 as a lead for development of drugs against HAT.

43 lly adiabatic, corresponding primarily to an HAT mechanism.

44 In Western analysis, HAT-L4 expressed in transfected CHO cells appeared as a

45 The MS-CPET and HAT oxidations of TEMPOH at the same driving force occur

46 ing) analysis revealed that both the DUB and HAT modules bind most SAGA target genes even though many

47 erence was observed between the SERO/HAT and HAT groups.

48 ysine and histone acetyltransferase (KAT and HAT) and deacetylase (KDAC and HDAC) activities.

49 ts, organized into two subdomains, HAT-N and HAT-C.

50 ntal insights regarding the relative OAT and HAT reactivity of valence tautomers such as M(V)(O)(porp

51 The BRD, PHD, and HAT domains form an integral structural unit to which th

52 thine, which is antagonistic to another anti-HAT drug, suramin.

53 The pyrrolopyrimidine AEE788 (a hit for anti-HAT drug discovery) associates with three trypanosome pr

54 f which affect sensitivity to important anti-HAT drugs.

55 nce of coordinated actions of its associated HATs, GCN5, PCAF, and p300, and a new partner that we de

56 , a single molecular system can exhibit both HAT and EPT character.

57 gated reacted with hydroxyl radical via both HAT and SPLET in the solvents investigated.

58 In summary, we provide evidence that both HATs are bona fide tumor suppressors that control MHCII

59 RAF pathways are faster, but HAT yields thermodynamically more stable radical product

60 tioxidant and it can be better understood by HAT and TMC mechanisms as it has low BDE, DeltaHacidity

61 The structure of the apo-CBP HAT domain is similar to that of acyl-CoA-bound p300 HAT

62 kynurenine pathway is activated in clinical HAT and associated with CNS inflammatory responses.

63 that both reactions proceed through a common HAT mechanism.

64 Flow cytometry confirmed HAT-L4 expression on the cell surface with the expected

65 y subunits of the ADA2a- or ADA2b-containing HAT modules and is further increased by incorporation of

66 Given the key importance of ADA3-containing HAT complexes in the regulation of various biological pr

67 Compared with wild-type controls, HAT-L4-deficient newborn mice had greater body fluid los

68 Twenty-one (3.2%) patients developed HAT.

69 With N,N-dialkylformamides HAT preferentially occurs from the formyl C-H bond, whil

70 regulated in the two related, but different, HAT complexes we carried out in vitro HAT assays.

71 Collectively, 2-dimensional HAT-7 cell cultures on permeable supports 1) form tight

72 r increased by incorporation of the distinct HAT modules in the ATAC or SAGA holo-complexes.

73 on via its histone acetyltransferase domain (HAT) and, as a result, activates gene expression by alte

74 n redox potentials, which appear to dominate HAT reactivity.

75 the same electronic-structure changes during HAT.

76 kynurenine pathway activation occurs during HAT, including cases prior to the current diagnostic cut

77 MA of 65 mm or greater went on to develop E-HAT (hazard ratio, 5.28; 95% confidence interval, 2.10-1

78 f recipients at greater risk of developing E-HAT, and intense surveillance and anticoagulation prophy

79 patients with increased risk of developing E-HAT.

80 nts with an MA less than 65 mm experienced E-HAT.

81 risk factors, to identify risk factors for E-HAT.

82 tation (LT) are multifactorial, early HAT (E-HAT) remains pertinent complication impacting on graft a

83 erall, 79 (9.5%) patients experienced HAT, E-HAT was diagnosed in 23, and in the remainder this was "

84 the curve of 0.750 (P < 0.001) predicting E-HAT with a sensitivity of 70%.

85 ficantly higher in patients diagnosed with E-HAT compared with those who did not (71.2 mm vs 57.9 mm;

86 ansplantation (LT) are multifactorial, early HAT (E-HAT) remains pertinent complication impacting on

87 cidic and neutral media 5CQA can take either HAT or RAF pathways.

88 ce by disrupting the Tmprss11f gene encoding HAT-L4.

89 onstruct the VB diagrams and how to estimate HAT barriers from raw data, starting with the simplest r

90 Here we examined HAT-L4 expression and function in vitro and in vivo.

91 udy of the transiting Neptune-mass exoplanet HAT-P-26b.

92 Overall, 79 (9.5%) patients experienced HAT, E-HAT was diagnosed in 23, and in the remainder thi

93 tion that proline residues represent favored HAT sites in the reactions of peptides and proteins with

94 Current drugs for HAT are difficult to administer and have severe side eff

95 2-yl)amino)benzamide] as potential drugs for HAT.

96 This article describes the risk factors for HAT and outcomes after LT.

97 The identification of risk factors for HAT may aid transplant teams in the development of strat

98 Based on these data, we propose a model for HAT-B/histone chaperone assembly and acetylation of H3-H

99 se (HAT) activity, which suggests a role for HAT/HDAC homeostasis in neuroprotection.

100 a polarized 2-dimensional culture system for HAT-7 cells, a rat cell line of ameloblast origin.

101 t 1 order of magnitude higher than those for HAT from the corresponding tertiary axial C-H bonds (kH(

102 kH values for HAT from tertiary equatorial C-H bonds were found to be

103 ormyl C-H bond, while in N-formylpyrrolidine HAT mostly occurs from the ring alpha-C-H bonds.

104 nt for the catastrophic epidemics of Gambian HAT (gHAT) seen over the past century.

105 core is structurally homologous to the Gcn5 HAT, but contains unique additional features including a

106 We generated HAT-L4 knockout mice by disrupting the Tmprss11f gene en

107 ibitory scaffolds within the GlaxoSmithKline HAT (Human African Trypanosomiasis) and Chagas chemical

108 ical approaches, such as a facile remote C-H HAT step, with that of transition-metal-catalyzed chemis

109 CAG expansions in the absence of H4 HATs NuA4 and Hat1 and HDACs Sir2, Hos2, and Hst1 depend

110 found in any of these BRM-regulating HDACs, HATs or TFs.

111 ain is required for the MOZ-BRPF1-ING5-hEaf6 HAT complex to be recruited to chromatin and to acetylat

112 o known as 1,4,5,8,9,12-hexaazatriphenylene (HAT) is an electron deficient, rigid, planar, aromatic d

113 part of purified recombinant hATAC or hSAGA HAT modules or endogenous hATAC or hSAGA complexes using

114 With DMF, a solvent-induced change in HAT selectivity was observed, suggesting that solvent ef

115 s of the Hif1 and Asf1 histone chaperones in HAT-B histone binding and acetyltransferase activity, we

116 No defects were found in HAT-L4 knockout mice in hair growth, wound healing, wate

117 strongly suggest the involvement of HLA-G in HAT disease progression.

118 s and evidence implicating human genetics in HAT epidemiology.

119 a sHLA-G levels were significantly higher in HAT (P = 6 x 10(-7)) and SERO/HAT (P = .007) than SERO p

120 viding evidence for early CNS involvement in HAT.

121 overn reactivity and selectivity patterns in HAT reactions from amino acid C-H bonds.

122 maturation ameloblasts were also present in HAT-7 cells.

123 lly distinct African populations residing in HAT endemic regions identified eight single nucleotide p

124 loyed to control the reaction selectivity in HAT-based procedures for the functionalization of C-H bo

125 We find that the variability in HAT is significantly correlated with sea-level variabili

126 stabilizing role of the ancillary protein in HATs.

127 Mechanistic experiments indicate HAT is rate-limiting, whereas intramolecular amination i

128 Instead, initial HAT from a metal hydride to directly generate a carbon-c

129 Intraoperative HAT (odds ratio, 62.63; 95% confidence interval, 12.64-3

130 ght ratio of 1.1% or less and intraoperative HAT were independently associated with HAT.

131 rate that all subunits are important for its HAT activity.

132 lpha gene, and inactivating mutations in its HAT domain abolished its ability to regulate ERalpha, su

133 In addition, the human KAT6 HATs are recurrently mutated in leukemia and solid tumor

134 mechanisms underlying the regulation of KAT6 HATs and their roles in cell cycle progression.

135 ovides novel insights into the roles of KAT6 HATs in cell cycle regulation through modulating PCNA le

136 We further focus on the roles of KAT6 HATs in regulating cell proliferation and stem cell main

137 in 23, and in the remainder this was "late" HAT.

138 lanine, valine, norvaline, and tert-leucine, HAT occurs from the alpha-C-H bonds, and the stability o

139 With leucine, HAT from the alpha- and gamma-C-H bonds was observed.

140 ance as a proxy for metallicity, we measured HAT-P-26b's atmospheric heavy element content ([Formula:

141 ation of the major antioxidative mechanisms: HAT (Hydrogen Atom Transfer), SPLET (Sequential Proton-L

142 catalysis, there are currently no molecular HAT catalysts that are capable of homolysing the strong

143 G5 and hEaf6 subunits, thereby promoting MOZ HAT activity.

144 of free radical scavenging activity, namely HAT, SET-PT and SPLET.

145 of this binding on the enzymatic activity of HAT-B.

146 nteracting with HATs and other components of HAT complexes but are deficient in their ability to rest

147 ysis revealed a decrease in the incidence of HAT (P = 0.008) and an increase in the use of 2-arterial

148 a significant reduction in the incidence of HAT over time, as well as the increased use of 2 hepatic

149 ties, full cures in a stage 1 mouse model of HAT, and a partial cure in a stage 2 mouse model of HAT.

150 In a murine model of HAT, oral administration of compound 1 cured the disease

151 d a partial cure in a stage 2 mouse model of HAT.

152 n vivo curative activity in a mouse model of HAT.

153 re further probed by evaluating the rates of HAT by the corresponding Cu(III)-hydroxide complexes fro

154 microstructures will reveal the relevance of HAT as a basic scaffold in the areas of organic material

155 RT3 dimerizes through the concave surface of HAT-C, whereas the HAT-C convex surface binds USP15 in a

156 mising druggable target for the treatment of HAT in both stages 1 and 2 of the disease.

157 (Gcn5-related N-acetyltransferase) family of HATs.

158 ions between the heavy and light subunits of HATs is scarce.

159 he almost three decades of research based on HAT from the synthetic, theoretical and application poin

160 in the SERO (n = 65), SERO/HAT (n = 14), or HAT (n = 268) group and in cerebrospinal fluid for patie

161 in is similar to that of acyl-CoA-bound p300 HAT complexes and shows that the acetyl-CoA binding site

162 onal change and significantly increases p300 HAT activity on histone H3K18 residues, which, in turn,

163 to-apical bicarbonate transport in polarized HAT-7 cells.

164 Preferential HAT from proline was also observed in the reactions of C

165 development of strategies aimed at reducing HAT.

166 ponent reactions are compared with a related HAT reaction of TEMPOH, with the 2,4,6-tri-tert-butylphe

167 in the epidemiologies of gHAT and Rhodesian HAT (rHAT) impact on strategies for disease control.

168 domain (BRD), CH2 (comprising PHD and RING), HAT, and ZZ domains at 2.4-A resolution.

169 ue to CBP/p300-allows RNA to stimulate CBP's HAT activity.

170 ADA2a, ADA3, and SGF29, whereas in the SAGA HAT module ADA2b is present instead of ADA2a.

171 We find that the SAGA HAT module preferentially acetylates H3K4me3 nucleosomes

172 asma for patients in the SERO (n = 65), SERO/HAT (n = 14), or HAT (n = 268) group and in cerebrospina

173 ntly higher in HAT (P = 6 x 10(-7)) and SERO/HAT (P = .007) than SERO patients.

174 nths following their initial diagnosis (SERO/HAT), others remain parasitologically negative for long

175 No difference was observed between the SERO/HAT and HAT groups.

176 In the skin, HAT-L4 expression was abundant in keratinocytes and seba

177 the inflammatory pathogenesis of late-stage HAT.

178 mity, and the DUB module modestly stimulates HAT function.

179 In metabolic studies, HAT-L4-deficient adult mice drank water more frequently

180 HAT) repeats, organized into two subdomains, HAT-N and HAT-C.

181 Unexpectedly, subsequent HAT from the hydroxy moiety to the vinyl radical leads t

182 T)](2+) (TAP = 1,4,5,8-tetraazaphenanthrene, HAT= 1,4,5,8,9,12-hexaazatriphenylene) by hydroquinone (

183 es a member of the Half-A-Tetratricopeptide (HAT) family of super-helical repeat proteins, some of wh

184 SART3 contains 12 half-a-tetratricopeptide (HAT) repeats, organized into two subdomains, HAT-N and H

185 At 1/2 [TFA] < [substrate] </= [TFA], HAT occurs from the C-H bonds that are alpha to the nonp

186 Mutational studies further demonstrate that HAT-B binding to the histone tail regions is not suffici

187 We also demonstrate that HAT-B is significantly more active against an intact H3-

188 The results indicate that HAT is strongly influenced by structural and medium effe

189 These results indicate that HAT-L4 is important in epidermal barrier function to pre

190 nd immunostaining experiments indicated that HAT-L4 was expressed in epithelial cells and exocrine gl

191 This likely indicates that HAT-P-26b's atmosphere is primordial and obtained its ga

192 It was suggested that HAT may be the predominant mechanism in nonpolar solvent

193 The HAT and DUB modules are in close proximity, and the DUB

194 The HAT at unactivated C(sp(3))-H sites is enabled by the ea

195 The HAT module of ATAC is composed of GCN5, ADA2a, ADA3, and

196 The HAT rate constants are significantly higher than those o

197 The HAT-B enzyme complex is responsible for acetylating newl

198 After the HAT-selection and cloning, we established nine hybridoma

199 ally disordered AL are autoacetylated by the HAT domain.

200 Consequently, the HAT process performed by 1 occurs on the triplet surface

201 yltransferase (HAT) module that contains the HAT, Gcn5, bound to Sgf29, Ada2, and Ada3.

202 proteins contain a bromodomain flanking the HAT catalytic domain that is important for the targeting

203 nontoxic inhibitor of proliferation for the HAT pathogen (Trypanosoma brucei), we have now tested th

204 s, we show that an RNA binding region in the HAT domain of CBP-a regulatory motif unique to CBP/p300-

205 nes was not changed when incorporated in the HAT modules of ATAC or SAGA complexes.

206 From large to very large increases in the HAT rate constant (kH) were measured on going from MeOH

207 nced by the 10(4)-10(7)-fold decrease in the HAT rate constants in acetonitrile following addition of

208 An increase in the HAT reactivity of QINO was observed in the presence of 0

209 a redox-active beta-diketonate ligand in the HAT step.

210 Increase in torsional strain in the HAT transition state accounts instead for tertiary axial

211 n terms of 1,3-diaxial strain release in the HAT transition state.

212 ected silane solvolysis distributions in the HAT-initiated hydrogenation of alkenes reveal that pheny

213 nd order (NEVPT2), provided insight into the HAT trajectories of 1 and A.

214 enes by interfering with the function of the HAT complex during infection.

215 PsAvh23 binds to the ADA2 subunit of the HAT complex SAGA and disrupts its assembly by interferin

216 nstrated that the subunit environment of the HAT complexes into which GCN5 incorporates determines th

217 etylation, a small-molecule inhibitor of the HAT component MYST blocked the growth of both murine and

218 Partial deletion of the HAT domain in the CBP gene, blocked these effects.

219 regulate transcription independently of the HAT module.

220 nt and allowing for careful control over the HAT reactivity of amide substrates.

221 ken together, our results establish that the HAT activity of MOF is required to sustain MLL-AF9 leuke

222 dicals with toluene, which indicate that the HAT process is characterized by a significant degree of

223 We therefore propose that the HAT-7 cell line is a useful functional model for studyin

224 Microfluorometry showed that the HAT-7 cells were polarized with a high apical membrane C

225 gh the concave surface of HAT-C, whereas the HAT-C convex surface binds USP15 in a novel bipartite mo

226 ain, the autoregulatory loop (AL) within the HAT domain, and the ZZ domain do not directly influence

227 Within the HAT group, specific haplotypes (HG010102 and HG0103) dis

228 Whilst causes of hepatic artery thrombosis (HAT) after liver transplantation (LT) are multifactorial

229 Hepatic artery thrombosis (HAT) increases morbidity and mortality after liver trans

230 dant capacity of GA can be explained through HAT rather than the SET-PT mechanism.

231 , a proxy for the highest astronomical tide (HAT), changes over seasonal and interannual time scales.

232 Moreover, the Tip60/HAT inhibitor, NU9056, was able to block EtOH-induced H4

233 TSP), e.g., TMPRSS2, TMPRSS4, and TMPRSS11d (HAT), have been shown to cleave influenza virus HA for v

234 iometry and binding mode of Hif1 and Asf1 to HAT-B and the effect of this binding on the enzymatic ac

235 through different modes and independently to HAT-B, whereby Hif1 binds directly to Hat2, and Asf1 is

236 These results point to HAT as implausible for the reaction with nitric oxide ra

237 est reaction H + H2 and going all the way to HAT in the enzyme cytochrome P450.

238 eactivation of the C-H bond of amides toward HAT.

239 e C-H bonds, deactivating these bonds toward HAT to an electrophilic radical such as CumO(*), indicat

240 ide, leading to C-H bond deactivation toward HAT to the electrophilic radical CumO(*).

241 on of the C-H bonds alpha to nitrogen toward HAT to PINO as evidenced by the 10(4)-10(7)-fold decreas

242 ) complex is moderately more reactive toward HAT with substituted phenol and shows superior activity

243 tes the C-H bonds of these substrates toward HAT to CumO(*), providing a powerful method for selectiv

244 principles and synthetic strategies towards HAT derivatives will be established and their use in n-t

245 energetically inaccessible using traditional HAT-based approaches.

246 are associated with hydrogen atom transfer (HAT) and electron-proton transfer (EPT) mechanisms, resp

247 ionalization via 1,5-hydrogen atom transfer (HAT) and enables net incorporation of ammonia at the bet

248 photoredox-mediated hydrogen atom transfer (HAT) and nickel catalysis, we have developed a highly se

249 We found that second hydrogen atom transfer (HAT) and second sequential proton loss electron transfer

250 Despite advances in hydrogen atom transfer (HAT) catalysis, there are currently no molecular HAT cat

251 toredox, enamine and hydrogen-atom transfer (HAT) catalysis-enables an enantioselective alpha-aldehyd

252 nolinium salts under hydrogen atom transfer (HAT) conditions, and an expanded scope for the coupling

253 y observed rate increase of H-atom transfer (HAT) for Mn(IV)(O)(TBP8Cz(*+)):LA with phenols.

254 e rate constants for hydrogen atom transfer (HAT) from cycloalkanes and decalins to the cumyloxyl rad

255 Here we show that in hydrogen atom transfer (HAT) from the aliphatic C-H bonds of alkane, ether, alco

256 f solvent effects on hydrogen atom transfer (HAT) from the C-H bonds of N,N-dimethylformamide (DMF),

257 e rate constants for hydrogen atom transfer (HAT) from the C-H bonds of N-Boc-protected amino acids t

258 he rate constant for hydrogen atom transfer (HAT) from the C-H bonds of these substrates (kH) was mea

259 are consistent with hydrogen atom transfer (HAT) generation of a carbon-centered radical that leads

260 celerate the desired hydrogen atom transfer (HAT) over competing pathways.

261 radicals mediate 1,6-hydrogen-atom transfer (HAT) processes to guide gamma-C(sp(3) )-H chlorination.

262 e intramolecular 1,8-hydrogen atom transfer (HAT) promoted by the 6(I)-O-yl radical, which abstracts

263 been observed in the hydrogen atom transfer (HAT) reactions from 4-alkyl-N,N-dimethylbenzylamines (al

264 kinetic study of the hydrogen atom transfer (HAT) reactions from a series of organic compounds to the

265 kinetic study of the hydrogen atom transfer (HAT) reactions from a series of secondary N-(4-X-benzyl)

266 kinetic study on the hydrogen atom transfer (HAT) reactions from the aliphatic C-H bonds of a series

267 ctivity of TEMPOH by hydrogen atom transfer (HAT) to a single e(-)/H(+) acceptor.

268 hree reaction types: hydrogen atom transfer (HAT), electron transfer (ET), and oxygen atom transfer (

269 nvestigations of the hydrogen atom transfer (HAT), radical adduct formation (RAF), sequential proton

270 f substrates via C-H hydrogen atom transfer (HAT), reducing 1 to [(PyPz)Fe(II)(OH2)2](4+) (2).

271 lable ethers through hydrogen atom transfer (HAT), were coupled with a range of electron-deficient he

272 mplex (4) after the initial H atom transfer (HAT).

273 Histone acetyl transferases (HATs) play a crucial role in eukaryotes by regulating ch

274 es encoding the histone acetyl-transferases (HATs) CREB binding protein (CREBBP) and EP300 are recurr

275 of care medications currently used to treat HAT have severe limitations, and there is a need to find

276 n the form of human African trypanosomiasis (HAT) and Chagas disease.

277 both forms of human African trypanosomiasis (HAT) are confined to spatially stable foci in Sub-Sahara

278 Human African trypanosomiasis (HAT) caused by Trypanosoma brucei gambiense can be diagn

279 ive agent for human African trypanosomiasis (HAT) or sleeping sickness.

280 n particular (human African trypanosomiasis (HAT), Chagas disease, cutaneous leishmaniasis, and malar

281 es that cause human African trypanosomiasis (HAT), depend on ornithine uptake and metabolism by ornit

282 brucei causes Human African trypanosomiasis (HAT), which threatens millions of people in sub-Saharan

283 fatal illness human African trypanosomiasis (HAT).

284 cond stage of human African trypanosomiasis (HAT).

285 otection from human African trypanosomiasis (HAT).

286 tic) stage of human African trypanosomiasis (HAT).

287 brucei causes human African trypanosomiasis (HAT).

288 ing sickness (Human African Trypanosomiasis, HAT), contains a kinetoplast with the mitochondrial DNA

289 s mild approach takes advantage of a tunable HAT catalyst that exhibits predictable reactivity patter

290 We profile the most commonly used HAT inhibitors and confirm that the majority of them are

291 In vitro HAT assays suggest that the RING domain, the autoregulat

292 erent, HAT complexes we carried out in vitro HAT assays.

293 minant mechanism in nonpolar solvents, while HAT and SPLET are competitive pathways in polar media.

294 ative HAT were independently associated with HAT.

295 ivals were significantly worse in cases with HAT.

296 N, indicative of alpha-CH2 deactivation with HAT that predominantly occurs from the most remote methy

297 as explained in terms of polar effects, with HAT that predominantly occurs from the delta-C-H bonds,

298 n of the strongly activating NH2 group, with HAT that shifts to the C-H bonds that are adjacent to th

299 nd Asf1 is only capable of interactions with HAT-B through contacts with histones H3-H4.

300 tive mutants are capable of interacting with HATs and other components of HAT complexes but are defic