ライフサイエンスコーパス: HAT

1 HAT administration increased from 0.03% of patients (95%

2 HAT-L4 knockout mice were viable and fertile.

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

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

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

6 Relying on 1,5-HAT reactivity, these methods are limited to beta - or d

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

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

9 fer (HAT) catalysis and intramolecular [1,5] HAT was observed through precise manipulation of the pro

10 It first serves as a HAT initiator and subsequently functions as a silyl radi

11 en a pendant phenol is present, it follows a HAT pathway with a pendant quinol.

12 rinsic kinase and histone acetyltransferase (HAT) activities that activates transcription of key prot

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

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

15 highly conserved histone acetyltransferase (HAT) and histone deacetylase (HDAC) enzymes that were fi

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

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

18 onent of specific histone acetyltransferase (HAT) complexes.

19 n of MAML1 to the histone acetyltransferase (HAT) domain of p300 rescues expression of HES4 but not D

20 The histone acetyltransferase (HAT) family of proteins performs histone acetylation.

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

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

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

24 core module, the histone acetyltransferase (HAT) module and the histone deubiquitination (DUB) modul

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

26 Histone acetyltransferase (HAT) p300 and its paralog CBP acetylate histone lysine s

27 a fork-associated histone acetyltransferase (HAT) that regulates the stability of stalled forks and t

28 onse factor (ARF)-histone acetyltransferase (HAT).

29 onse factor (ARF)-histone acetyltransferase (HAT).

30 ely regulated by histone acetyltransferases (HAT) and histone deacetylases, have been recognized as m

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

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

33 stic activity of histone acetyltransferases (HATs) and histone deacetylases (HDACs), is necessary for

34 nes encoding the histone acetyltransferases (HATs) CREBB-binding protein (CREBBP) and EP300 are commo

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

36 is controlled by histone acetyltransferases (HATs/KATs) found in multiprotein complexes that are recr

37 ATs, also termed histone acetyltransferases, HATs) catalyze the acetylation of substrate lysine resid

38 d aerotolerance, such as hyper-aerotolerant (HAT) and aerotolerant (AT) strains, were more tolerant t

39 in the strength of the O-H bond formed after HAT by the oxoiron unit, the O-H bond derived from 3 bei

40 experimentally demonstrate a 40-kHz airborne HAT system implemented using two 256-emitter phased arra

41 dermal barrier formation is unique among all HAT/DESC proteases.

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

43 f aerotolerance in C. jejuni and that AT and HAT strains of C. jejuni are more tolerant to oxidants a

44 The AT and HAT strains that were tolerant to stresses, particularly

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 f MQ and ADN, photo-generated through ET and HAT.

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

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

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

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

52 sited that tyrosine (Tyr or Y) 224 serves as HAT intermediary to separate the C21 radical (C21*) and

53 P on the MQ-ADN complex ((Au)MQ-ADN) assists HAT by limiting the ET channel, on the other hand, FeNP

54 the current policy not to treat asymptomatic HAT should be reconsidered.

55 (H(+)) travel "together" as a true H atom, (HAT), or whether the H(+) and e(-) are transferred in co

56 g agent, LiAlH(4), to completely reduce both HAT and PRA-derived products and the relative quantitati

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 * peroxyl adduct to olefinic C27 followed by HAT to the C26* from a Tyr.

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

62 C6 HAT exhibits a half-life of 789 years in solution.

63 nd that the thermal isomerization rate of C6 HAT drastically increases on metal surfaces, the thermal

64 tion mechanism to explain the behavior of C6 HAT on these different metal surfaces.

65 onalized with a C6 alkyl thiolate spacer (C6 HAT) was characterized on a number of metal surfaces.

66 It was found that C6 HAT switches on Au and Cu surfaces when irradiated with

67 ed to study the photoisomerization of the C6 HAT self-assembled monolayers (SAMs) on Au, Ag, and Cu s

68 ally expressed in a squamous cell carcinoma (HAT/DESC) cluster of membrane-anchored serine proteases.

69 electivity and reactivity in metal-catalyzed HAT alkene coupling, and create a firm basis for elucida

70 nd shows the intersection of metal-catalyzed HAT and thiol radical trapping HAT catalytic cycles to b

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

72 ful probe for biological studies of p300/CBP HAT but also a pharmacological lead for further drug dev

73 In summary, we identified the p300/CBP HAT domain as a putative therapeutic target in highly th

74 Consortium (SGC) and identified the p300/CBP HAT inhibitor A-485, in addition to the well-known BET i

75 inal chemistry, novel inhibitors of p300/CBP HAT with their IC(50) values as low as 620 nM were disco

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

77 that both reactions proceed through a common HAT mechanism.

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

79 tion step pertains to a diffusion-controlled HAT by (3)O(2) from the 10-OH-9-anthroxyl radical.

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

81 elieve that this reaction undergoes a direct HAT mechanism catalyzed by eosin Y.

82 e FtmOx1 mechanism revealed, instead, direct HAT from C21 to the ferryl complex and surprisingly comp

83 documentation of an unusual form of directed HAT and are of crucial importance for defining the neces

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

85 the same electronic-structure changes during HAT.

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

87 shock, we compared the association of early HAT therapy (within 2 d of hospitalization) with hospita

88 Receipt of early HAT was associated with higher hospital mortality (28.2%

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

90 ission paradox is key to finally eliminating HAT.

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

92 The enhanced HAT and PET have been confirmed by the escape yields of

93 ectron affinity (EA) of NACs and established HAT- and EA-based LFERs for six hydroquinone species.

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

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

96 2-yl)amino)benzamide] as potential drugs for HAT.

97 We computed the gas-phase energies for HAT and electron affinity (EA) of NACs and established H

98 , and the subsequent in vivo experiments for HAT.

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

100 me-infected mice; it is an advanced lead for HAT drug development.

101 Different pathways have been discerned for HATs involving OH or CH moieties.

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

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

104 F6L, components or co-activators of the GNAT-HAT complexes for the mouse ESC (mESC) state.

105 High-grade HAT was considered as definite DRT.

106 tected 2 (1.4%) cases with DRT or high-grade HAT, respectively.

107 nd cardiac CT 6 (2.4%) cases with high-grade HAT.

108 High-grade HAT/DRT was associated with thromboembolism in 2 cases,

109 Cardiac CT demonstrated low-grade HAT in 9 (3.6%) cases at 8 weeks; and 13 cases (9.4%) at

110 Low-grade HAT resolved spontaneously over time.

111 hromboembolism in 2 cases, whereas low-grade HAT was not related to embolic events.

112 cardiac CT demonstrates cases with low-grade HAT, not visualized by TEE.

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

114 the mechanisms of the photoredox-nickel-HAT (HAT: hydrogen atom transfer) catalyzed arylation and alk

115 tate density function theory revealed a high HAT character, yet multiconfigurational nature in the tr

116 polar effects in the HAT reaction, i.e., in HAT promoted by N-oxyl radicals containing electron-with

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

118 viding evidence for early CNS involvement in HAT.

119 with that of 2,6-dimethyl-3-methoxyphenol in HAT promoted by a series of radicals (cumyloxyl, galvino

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

121 ssion analyses to examine temporal trends in HAT administration.

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

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

124 g Lewis base-catalysed, complexation-induced HAT (LBCI-HAT).

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

126 entered radical that forms after the initial HAT by the high valent oxoiron complex depends on the ox

127 /mol) Fe-H bond, which performs irreversible HAT to alkenes in contrast to previous studies on isolab

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

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

130 The catalytic LBCI-HAT is capable of accessing both branch-specific hydrosi

131 se-catalysed, complexation-induced HAT (LBCI-HAT).

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

133 ical precursor facilitates catalyst-mediated HAT stereoselectivity, enabling the synthesis of several

134 The approach to 1 features an Fe-mediated HAT reaction of the intermediate olefin 2, effecting a t

135 t a metal hydride hydrogen atom transfer (MH-HAT) to generate a C-centered radical that undergoes add

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

137 we describe a sustainable, net redox-neutral HAT process involving hydrosilanes and alkali metal Lewi

138 In an effort to develop new HAT therapeutics, we report the structure-activity relat

139 s of the mechanisms of the photoredox-nickel-HAT (HAT: hydrogen atom transfer) catalyzed arylation an

140 study aims to describe the administration of HAT therapy among U.S. adults with septic shock before a

141 th significantly increased administration of HAT.

142 dation of mechanisms in the growing class of HAT alkene cross-coupling reactions.

143 ngenic mouse strains lacking combinations of HAT/DESC proteases, including a mouse strain deficient i

144 been used to determine the rate constants of HAT reactions (k(H)), but no radical clock is available

145 this study, we evaluated the feasibility of HAT energy for predicting NAC reduction rate constants.

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

147 18 cured 60% of mice in a systemic model of HAT, the compound was unable to clear parasitemia in a C

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

149 e iron center modulates not only the rate of HAT but also the rate of ligand rebound.

150 In line with our predictions, the ratio of HAT rate constants ( k(H) (mOMe)/ k(H)(H)) is larger in

151 The primary outcome was receipt of HAT at least once during hospitalization.

152 patients with early septic shock, receipt of HAT was not associated with mortality benefit.

153 new congenic mouse strains for the study of HAT/DESC proteases in physiological and in pathophysiolo

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

155 xamples shown here suggest the future use of HAT for novel forms of displays in which the objects are

156 irst independent, experimental validation of HAT-based LFER, a new approach that enables rate predict

157 Mutation, malfunction, and dysregulation of HATs are associated with a wide range of pathologies or

158 , MOF (hMOF), a member of the MYST family of HATs, acetylates histone H4 at lysine 16 (H4K16ac).

159 parate the C21 radical (C21*) and Fe(III)-OH HAT products and prevent rebound.

160 in organic solutions, can be either PCET or HAT and is governed by the thermodynamics of these inter

161 indicate that leptin, acting via an AKT-p300 HAT epigenetic cascade, induces exon-specific Bdnf expre

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

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

164 esponse to small-molecule inhibition of p300 HAT activity.

165 tivates histone acetyltransferase p300 (p300 HAT), leading to changes in histone H3 acetylation and m

166 reased interest in new strategies to perform HAT in a sustainable manner.

167 P and MQ molecules with FeNP, a preferential HAT and PET process is eased.

168 en patients who received and did not receive HAT therapy.Methods: We performed a retrospective cohort

169 mong 338,597 patients, 3,574 (1.1%) received HAT therapy, 98.7% in the postpublication period.

170 development of strategies aimed at reducing HAT.

171 This regioselective HAT was also rendered enantioselective by harnessing ene

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

173 n-coupled electron transfer-mediated reverse HAT cycle of eosin Y.

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

175 Conversely, MYC inhibits BRD4's HAT activity, suggesting that MYC regulates its own tran

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

177 n of the metal catalyst by O(2) and a second HAT to form the unprotected saturated N-heterocycle appe

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

179 ect and atom-economical, enabled by a Shenvi-HAT hydrogenation.

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

181 the inflammatory pathogenesis of late-stage HAT.

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

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

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

185 Using this library, we demonstrate that HAT/DESC proteases are dispensable for term development,

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

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

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

189 The results suggest that HAT energy is a reliable predictor of NAC reduction rate

190 The HAT and AT strains of C. jejuni exhibited significantly

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

192 The HAT domain of p300/CBP is a potential drug target for ca

193 The HAT rate constants are significantly higher than those o

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

195 ht, can be either reduced or oxidized by the HAT and nickel catalysts, respectively, indicating that

196 ally disordered AL are autoacetylated by the HAT domain.

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

198 Consistently, the HAT and AT strains were highly tolerant to oxidants, suc

199 inding of a nucleosome to SAGA displaces the HAT and DUB modules from the core-module surface, allowi

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

201 t tunneling underlies the preference for the HAT pathway.

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

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

204 greater contribution of polar effects in the HAT reaction, i.e., in HAT promoted by N-oxyl radicals c

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

206 into the origin of enantioselectivity in the HAT step.

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

208 coupling, an important representative of the HAT alkene reactions.

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

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

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

212 Our analysis of the HAT cycle indicated that activation of a alpha-amino C(s

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

214 regulate transcription independently of the HAT module.

215 that the recently described function of the HAT-like 4 protease in epidermal barrier formation is un

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

217 A kinetic analysis shows that the HAT by chain-carrying HO(2)(*) occurs with a high rate c

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

219 ith HO, anionic forms of 5CQA conform to the HAT, radical adduct formation, sequential proton loss el

220 recent advances, the mechanism by which the HAT and transcriptional coactivator p300 mediates tumori

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

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

223 sone, high-dose ascorbic acid, and thiamine (HAT therapy) was published online.Objectives: This study

224 d for presence of hypoattenuated thickening (HAT) on the device, which was subclassified as low grade

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

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

227 ote transcription through SAGA DUB and Tip60 HAT activity.

228 Increasing Tip60 HAT levels specifically in the mushroom body learning an

229 We show that like AD, disruption of Tip60 HAT/HDAC2 balance with concomitant epigenetic repression

230 weakened rhythmicity, whereas reducing Tip60 HAT expression drastically weakened rhythmicity.

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

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

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

234 energetically inaccessible using traditional HAT-based approaches.

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

236 mbination of thermal hydrogen-atom transfer (HAT) and proton-coupled electron transfer (PCET) process

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

238 d photocatalytic and hydrogen atom transfer (HAT) approach for the light-mediated epimerization of re

239 Hydrogen atom transfer (HAT) by (3)O(2) and HO(2)(*) from arenols (ArOH), arylox

240 tween intermolecular hydrogen-atom transfer (HAT) catalysis and intramolecular [1,5] HAT was observed

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

242 with azide ion as a hydrogen atom transfer (HAT) catalyst, provides a direct synthesis of alpha-tert

243 n Y, which acts as a hydrogen atom transfer (HAT) catalyst.

244 gests intermolecular hydrogen atom transfer (HAT) chemistry is at play, rather than classical Norrish

245 base catalyst, and a hydrogen-atom transfer (HAT) co-catalyst.

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

247 o enantiodetermining hydrogen-atom transfer (HAT) during the C-H amination event.

248 reactions occur: (a) hydrogen-atom transfer (HAT) from a donor to the peroxyl radical; (b) peroxyl ra

249 ng reactions involve hydrogen atom transfer (HAT) from a metal-hydride species to an alkene to form a

250 Hydrogen-atom transfer (HAT) from a substrate carbon to an iron(IV)-oxo (ferryl)

251 ude slower than 3 in hydrogen atom transfer (HAT) from C-H bonds.

252 ing ability of S via hydrogen atom transfer (HAT) from TEMPO-H (2,2,6,6-tetramethylpiperdine-N-hydrox

253 posed to operate via hydrogen atom transfer (HAT) from the substrate to the photoexcited TAC radical

254 at utilizes computed hydrogen atom transfer (HAT) Gibbs free energy instead of E(H)(1) as a predictor

255 of the importance of hydrogen atom transfer (HAT) in biology and chemistry, there is increased intere

256 suppresses autoxidation by H-atom transfer (HAT) in favor of addition, such that the epoxides are th

257 c forms undergo only hydrogen atom transfer (HAT) mechanism with CH(3)OO.

258 3.5), implicating a hydrogen atom transfer (HAT) mechanism.

259 cterized as either a hydrogen-atom transfer (HAT) or a concerted proton-coupled electron transfer (cP

260 on transfer (ET) and hydrogen atom transfer (HAT) pathways between an anti-tumor drug vitamin-K3 (MQ)

261 of polar effects in hydrogen atom transfer (HAT) processes is made difficult by the fact that in mos

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

263 is dictated by a 1,5-hydrogen atom transfer (HAT) reaction by a pendent amide.

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

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

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

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

268 n transfer (SET) and hydrogen atom transfer (HAT) reactions, thus covering all the physiologically re

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

270 al hydrogenation via hydrogen atom transfer (HAT) to alkenes is an increasingly important transformat

271 irecting its regioselective H atom transfer (HAT) to the beta carbon of an alcohol.

272 sformations, notably hydrogen atom transfer (HAT) triggered processes, which can be promoted through

273 H iodination via 1,5-hydrogen atom transfer (HAT), (ii) desaturation via I(2) complexation, and (iii)

274 processes, including hydrogen atom transfer (HAT), a Povarov-type reaction, and atom-transfer radical

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

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

277 nlisting late-stage, hydrogen atom transfer (HAT)-mediated free radical bond formations (C20-C2 and C

278 or subtraction, as well as H-atom transfer (HAT).

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

280 ocess as well as via hydrogen atom transfer (HAT).

281 at underwent intramolecular H-atom transfer (HAT).

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

283 ough two successive hydrogen atom transfers (HAT) to 2 equiv of phenoxyl that are generated transient

284 Heteromeric amino acid transporters (HATs) comprise a group of membrane proteins that belong

285 tal-catalyzed HAT and thiol radical trapping HAT catalytic cycles to be essential for effective catal

286 Human African trypanosomiasis (HAT) is a neglected tropical disease caused by infection

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

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

289 Human African trypanosomiasis (HAT), or African sleeping sickness, is a fatal disease f

290 Human African trypanosomiasis (HAT), or sleeping sickness, is caused by the protozoan p

291 brucei causes human African trypanosomiasis (HAT).

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

293 tive agent of human African trypanosomiasis (HAT).

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

295 ealization of holographic acoustic tweezers (HAT).

296 usly uncharacterized interaction between two HAT units is mediated via dimerization of the heavy chai

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

298 n, that Fe(III)-OOH species being formed via HAT reactivity of the partner ferric heme superoxide com

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

300 hen considered on the scale of a wavelength, HAT provides similar manipulation capabilities as HOT wh

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