ライフサイエンスコーパス: Ac

1 Ac(4)C is markedly induced in response to increases in t

2 Ac-PHF6 interactions with the membrane were also accompa

3 onists, 18 [Ac-Arg-Arg-(pI)DPhe-Tic-NH2], 1 [Ac-His-Arg-(pI)DPhe-Tic-NH2], and 41 [Ac-Arg-Arg-(pI)DPh

4 The three most potent MC3R agonists, 18 [Ac-Arg-Arg-(pI)DPhe-Tic-NH2], 1 [Ac-His-Arg-(pI)DPhe-Tic

5 Treatment with anti-IL-1beta, Ac-YVAD-cho, and MCC950 suppressed IL-1beta responses an

6 [(225) Ac(macropa)](+) remained intact over 7 to 8 days when ch

7 icromolar concentration, complexed all (225) Ac (26 kBq) in 5 min at RT.

8 ocycle H2 macropa was investigated for (225) Ac chelation in targeted alpha therapy (TAT).

9 pa to be a highly promising ligand for (225) Ac chelation that will facilitate the clinical developme

10 ted to tumors and did not release free (225) Ac over 96 h.

11 and macropa-Tmab retained >99 % of its (225) Ac in human serum after 7 days.

12 In LNCaP xenograft mice, (225) Ac-macropa-RPS-070 was selectively targeted to tumors an

13 facilitate the clinical development of (225) Ac TAT for the treatment of soft-tissue metastases.

14 Both constructs rapidly radiolabeled (225) Ac in just minutes at RT, and macropa-Tmab retained >99

15 (225)Ac was received with trace amounts of (227)Ac, (227)Th a

16 (225)Ac(3+) is a generator of alpha-particle-emitting radionu

17 (225)Ac-E4G10 was found to accumulate in tissues expressing t

18 (225)Ac-L1 also showed an increased survival benefit in the m

19 (225)Ac-L1 is a promising therapeutic for further clinical ev

20 [(225)Ac]hu11B6-IgG(3) was a functionally enhanced alternative

21 s, Actinium-225-labeled hu11B6-IgG(1) ([(225)Ac]hu11B6-IgG(1)) has shown promising treatment efficacy

22 Actinium-225 ((225)Ac) can be produced from a Thorium-229/Radium-225 ((229)

23 d progression-free survival (PFS) after (225)Ac-PSMA-617 treatment.

24 treatment of disease-is identifying an (225)Ac chelator that is compatible with in vivo applications

25 tep separation that could be used in an (225)Ac generator from (225)Ra and/or (229)Th.

26 l data of antibody-mediated (213)Bi and (225)Ac delivery in a metastatic transgenic breast cancer mod

27 pended on cosequestration of Gd(3+) and (225)Ac(3+) ions.

28 Results: (213)Bi- and (225)Ac-L1 demonstrated specific cell uptake and cell kill in

29 The biodistribution of (213)Bi-L1 and (225)Ac-L1 revealed specific uptake of radioactivity within P

30 , and biodistribution of (213)Bi-L1 and (225)Ac-L1 were evaluated.

31 -emitting analogs of L1, (213)Bi-L1 and (225)Ac-L1, to evaluate their safety and cell kill effect in

32 the comparison of the (132)La-NM600 and (225)Ac-NM600 tissue distributions revealed a similar biodist

33 omising alpha-emitting isotopes such as (225)Ac and (227)Th are incompatible with PET imaging.

34 )Ho, (161)Tb, (149)Tb, (212)Pb/(212)Bi, (225)Ac, and (213)Bi-have been produced and evaluated (pre)cl

35 US-tubes internally loaded with both (225)Ac(3+) ions and Gd(3+) ions show 2 distinct populations

36 Aqueous loading of both (225)Ac(3+) ions and Gd(3+) ions via bath sonication was used

37 morphology and functionality caused by (225)Ac-E4G10.

38 Conclusion: (225)Ac-L1 demonstrated activity-dependent efficacy with mini

39 a bath sonication was used to construct (225)Ac@gadonanotubes ((225)Ac@GNTs).

40 CC49 was labeled with the alpha-emitter (225)Ac to target tumor-associated glycoprotein 72-positive x

41 as labeled with alpha-particle-emitting (225)Ac.

42 (132)La as a PET imaging surrogate for (225)Ac using a DOTA-based, tumor-targeting alkylphosphocholi

43 be used as a PET imaging candidate for (225)Ac(III) (with reduced (134)Ce(III)) or (227)Th(IV) (with

44 after administration were evaluated for (225)Ac-L1.

45 was to develop a treatment protocol for (225)Ac-PSMA-617 alpha-radiation therapy in advanced-stage, m

46 nd absorbed alpha-emission dosages from (225)Ac and its daughters.

47 sed to construct (225)Ac@gadonanotubes ((225)Ac@GNTs).

48 olecules, also successfully incorporate (225)Ac(3+).

49 Methods: (225)Ac-PSMA-617 was administered to patients who had metasta

50 Methods: (225)Ac-RPS-074 was evaluated in male BALB/c mice bearing LNC

51 xample, two administrations of 200 nCi, (225)Ac-labeled antibody, separated by 30 days, resulted in a

52 ical challenge facing implementation of (225)Ac in targeted alpha therapy-an emerging technology that

53 to probe the in vivo biodistribution of (225)Ac radiotherapeutics.

54 for radioimmunotherapy for delivery of (225)Ac(3+) ions at higher concentrations than is currently p

55 3+) ions show 2 distinct populations of (225)Ac(3+) ions: one rapidly lost in human serum and one tha

56 unctional chelates limits the amount of (225)Ac(3+) that can be delivered.

57 trapolated to the physical half-life of (225)Ac, assuming instant decay of unstable daughter nuclides

58 tential for the clinical translation of (225)Ac-DOTA-MC1RL as a novel therapy for metastatic uveal me

59 burden after a single administration of (225)Ac-DOTA-MC1RL in treated mice relative to controls.

60 ice using a therapeutic 7.4-kBq dose of (225)Ac-E4G10.

61 Treatment studies of (225)Ac-L1 demonstrated activity-dependent, specific inhibiti

62 alpha-Camera imaging of (225)Ac-L1 revealed high renal cortical accumulation at 2 h f

63 d acute and chronic toxicity studies of (225)Ac-L1 revealed off-target radiotoxicity, mainly in kidne

64 The efficacy of (225)Ac-L1 was determined in human PSMA+ subcutaneous and mic

65 The absorbed radiation dose of (225)Ac-L1 was determined using the biodistribution data and

66 rmined at 4 and 24 h after injection of (225)Ac-NM600.

67 Dosimetry estimates for 1 MBq of (225)Ac-PSMA-617 assuming a relative biologic effectiveness o

68 , a treatment activity of 100 kBq/kg of (225)Ac-PSMA-617 per cycle repeated every 8 wk presents a rea

69 A 100-kBq activity of (225)Ac-PSMA-617 per kilogram of body weight was administered

70 150 (n = 2), and 200 kBq/kg (n = 4) of (225)Ac-PSMA-617 were evaluated retrospectively regarding tox

71 rcinoma were treated with 210 cycles of (225)Ac-PSMA-617.

72 Results: Thirty-four cycles of (225)Ac-PSMA-I&T were applied (median dose, 7.8 MBq; range, 6

73 of 7 mice using 37, 74, and 148 kBq of (225)Ac-RPS-074 and compared with positive and negative contr

74 Conclusion: A single dose of 148 kBq of (225)Ac-RPS-074 induced a complete response in 86% of tumors,

75 nger were evaluated for purification of (225)Ac.

76 diopurity was >99% (calculated based on (225)Ac, (227)Th, and (223)Ra).

77 esults are highly comparable to data on (225)Ac-PSMA-617 TAT.

78 igated options to enhance and optimize [(225)Ac]hu11B6 treatment.

79 (68)Ga for diagnosis or with (177)Lu or (225)Ac for therapy.

80 Methods: Fourteen patients receiving (225)Ac-PSMA-I&T were included in this retrospective analysis

81 fter a human serum challenge, rendering (225)Ac@GNTs candidates for radioimmunotherapy for delivery o

82 Results: (225)Ac-labeled DOTAylated-huCC49 radioimmunotherapy signific

83 or volume exceeded 1,500 mm(3) Results: (225)Ac-RPS-074 was labeled in greater than 98% radiochemical

84 PCST ion exchanger could separate (225)Ac from isotopes of Ra and Th, and the process represent

85 ndicated PCST could be used to separate (225)Ac produced on small (226)Ra targets (0.3-1 g), but PCST

86 , demonstrating efficacy of sequential [(225)Ac]hu11B6 in a mouse model.

87 US-tubes successfully sequester (225)Ac(3+) ions in the presence of Gd(3+) ions and retain th

88 Targeting (225)Ac(3+) by use of ligands conjugated to traditional bifun

89 Over 90% of the (225)Ac was recovered from PCST, and the radiopurity was >99%

90 Methods: The (225)Ac-DOTA-MC1RL conjugate was synthesized in high radioche

91 distribution and blood clearance of the (225)Ac-E4G10 radioimmunoconstruct in a transgenic Nestin-tum

92 The (225)Ac@GNTs were subsequently challenged with heat, time, an

93 Promising biochemical responses to (225)Ac-prostate-specific membrane antigen (PSMA) 617, even i

94 tions who showed a complete response to (225)Ac-PSMA-617 therapy.

95 a functionally enhanced alternative to [(225)Ac]hu11B6-IgG(1) but offered no improvement of therapeut

96 PSMA-targeted alpha-therapy (TAT) using (225)Ac-PSMA imaging and therapy (I&T).

97 : Our first clinical data for TAT using (225)Ac-PSMA-I&T showed a promising antitumor effect in advan

98 ed targeted alpha-particle therapy with (225)Ac-E4G10 as an antivascular approach and showed increase

99 Radioimmunotherapy with (225)Ac-E4G10 was performed in Ntva mice to assess overall su

100 an or equal to 50% after treatment with (225)Ac-PSMA-617 was proven by multivariate analyses to be si

101 Targeted alpha-therapy with (225)Ac-PSMA-617, although still experimental, obviously has

102 rostate carcinoma patients treated with (225)Ac-PSMA-617, identifying variables predictive for overal

103 Methods: Of 60 patients treated with (225)Ac-PSMA-617, we identified 10 patients who presented wit

104 eneic RM1-PGLS tumors were treated with (225)Ac-PSMA617, an anti-PD-1 antibody, or both.

105 5)Ac was received with trace amounts of (227)Ac, (227)Th and (223)Ra, and the solution was used to ev

106 agents using small quantities (mug) of (227)Ac.

107 pectrometry (ESI-MS), a BGE composed of NH(4)Ac, 1.0 mM, pH 4.0, in 70.0% (v/v) acetonitrile was used

108 2], 1 [Ac-His-Arg-(pI)DPhe-Tic-NH2], and 41 [Ac-Arg-Arg-(pI)DPhe-DNal(2')-NH2] were more potent (EC50

109 dy resulted in the discovery of compound 42 (Ac-Val-Gln-(pI)DPhe-DTic-NH(2)), a full MC3R agonist tha

110 ence analysis showed that V. anguillarum 531 Ac and 531Ad differ in the hmgA gene mutation and 23 mut

111 (hNaa60) in complex with Acetyl-Coenzyme A (Ac-CoA) or Coenzyme A (CoA).

112 own to be involved in acetylated coenzyme A (Ac-CoA) synthesis and is primarily expressed in the brai

113 h simple protecting groups such as acetates (Ac, Piv) and carbamates (Boc, Fmoc), respectively.

114 ty profiles against benzoyl (Bz) and acetyl (Ac) were synthesized, and KHSO(5)/AcCl in methanol was i

115 essed the effects of K326Q and K328Q acetyl (Ac)-mimetic actin on Ca(2+)-dependent, in vitro motility

116 Thus, the Nt-acetylated Ac-MX-Rgs2 (X = Arg, Gln, Leu) proteins are specific sub

117 structures of three N-terminally acetylated (Ac) alpha-syn constructs, Ac1-140, Ac1-122, and Ac1-103,

118 rowth assays that the MnSOD-K68 acetylation (Ac) mimic mutant (MnSOD(K68Q)) functions as a tumor prom

119 tion-prone PHF6 with N-terminal acetylation (Ac-PHF6) and the non-aggregation prone PHF6 with a stand

120 y to 1,3,4-O-acetylated N-acetylmannosamine (Ac(3)ManNAc) to deliver ManNAc-6-phosphate (ManNAc-6-P),

121 C in complex with Aplysia californica AChBP (Ac-AChBP) at a resolution of 2.1 A.

122 In addition, Ac-DEX has been used to encapsulate small molecules, del

123 ptide substrates acetyl-Lys-Lys-Cha-Gly-AFC (Ac-KKChaG-AFC) and acetyl-Lys-Thr-Cha-Gly-AFC (Ac-KTChaG

124 -KKChaG-AFC) and acetyl-Lys-Thr-Cha-Gly-AFC (Ac-KTChaG-AFC).

125 -derived macrophages, using a C5aR2 agonist (Ac-RHYPYWR-OH; P32) to selectively activate the receptor

126 anied by stabilizing the expression of alpha-Ac-Tub in vivo and in vitro, which is related with deace

127 Our data suggest that alpha-Ac-Tub regulation by Ac-SDKP may potentially be a new an

128 mechanism of acetylated alpha-tubulin (alpha-Ac-Tub) regulation by Ac-SDKP.

129 nut1 is caused by an Ac transposon insertion into the coding region of a uniq

130 using a cell-permeable sialic acid analogue (Ac(5)Neu5Ac) boosted GD2 expression without or with mino

131 One among the synthesized analogue, Ac-Arg-Ala-[d-Cys-Arg-Phe-His-Pen]-COOH (19), displayed

132 tion and invasion stimulated by Hp(2-20) and Ac(2-26), two well-characterized ligands for FPR2 in GC

133 iently modulated the expression of p-AKT and Ac-H3, arrested the cell cycle, and induced apoptosis in

134 d simultaneous deprotecting of OPAc, Bz, and Ac.

135 The Ac-Cl and Ac-OH2O distances are measured to be 2.95(3) and 2.59(3)

136 histone H4 acetylated at K16 (Ac-H4K16) and Ac-alpha-tubulin.

137 should help design novel ACE inhibitors and Ac-SDKP analogues that could be used in the treatment of

138 I) + H2O2 --> Active catalyst (Ac) (kI), and Ac + Substrate (S) --> Fe(III) + Product (kII).

139 the linear fragments Ac-tTG(553-564)-NH2 and Ac-alpha2-Glia(63-71)-NH2 and the corresponding cross-li

140 opioid receptor selective antagonist arodyn (Ac[Phe(1,2,3),Arg(4),d-Ala(8)]dynorphin A(1-11)-NH(2)) b

141 and delocalization indices) and the average Ac-He distances, and also with the incremental He bindin

142 to tailor a chelator for Ac binding because Ac coordination chemistry is poorly defined.

143 itivity differences to QMP compounds because Ac workers have higher levels of ovarian activation than

144 Beta-Ac alone increased lung compliance and surfactant concen

145 ate (Beta-P) and betamethasone-acetate (Beta-Ac) - the clinical drug.

146 opmental pathways were less affected by Beta-Ac than the clinical drug.

147 pus compared to control, while low dose Beta-Ac alone did not.

148 ither the clinical drug (0.25 mg/kg) or Beta-Ac (0.125 mg/kg).

149 model the efficacy of the slow release Beta-Ac alone for enhancing fetal lung maturation and to redu

150 A low dose ANS treatment with Beta-Ac should be assessed for efficacy in human trials.

151 her ligand currently employed: 10(6) between Ac and relevant metal impurities, and over 10(8) for red

152 absorption spectroscopy comparisons between Ac(III) and Am(III) in HCl solutions indicate Ac(III) co

153 doped tin oxide (FTO) substrate using [BMIM][Ac] ionic liquid at 90 degrees C.

154 crystal structure of the complex with bound Ac-CoA allows first insight, to our knowledge, into the

155 data suggest that alpha-Ac-Tub regulation by Ac-SDKP may potentially be a new anti-fibrosis mechanism

156 d alpha-tubulin (alpha-Ac-Tub) regulation by Ac-SDKP.

157 Angiostrongylus cantonensis (Ac), or the rat lungworm, is a major cause of eosinophil

158 chanism: Fe(III) + H2O2 --> Active catalyst (Ac) (kI), and Ac + Substrate (S) --> Fe(III) + Product (

159 udy, smooth muscle-specific acid ceramidase (Ac) gene knockout mice (Asah1(fl/fl)/SM(Cre)) were used

160 Lysosomal acid ceramidase (Ac) has been shown to be critical for ceramide hydrolysi

161 Both Apis cerana (Ac) and Apis mellifera (Am) share an evolutionarily cons

162 e have developed a method for characterizing Ac complexes that contain highly complex chelating agent

163 or lipid biosynthesis, cytosolic acetyl CoA (Ac-CoA), is produced by ATP-citrate lyase (ACLY) from mi

164 ntification of the beta2c selective compound Ac-LAE-ep represents a promising starting point for the

165 (3) The compound Ac-LAA-ep was found to favor subunit beta5c over beta5i

166 rgo inactivation under catalytic conditions: Ac --> Inactive catalyst (ki).

167 The peptide II, containing Ac-tTG(553-564)-NH2 sequence cross-linked with deamidate

168 pper salts, i.e. (Cu(acac)2, Cu(OH)2, and Cu(Ac)2.H2O).

169 primary enzyme involved in making cytosolic Ac-CoA in cells with abundant nutrients.

170 cetate is being used to synthesize cytosolic Ac-CoA by ACSS2.

171 4)-NH2 sequence cross-linked with deamidated Ac-alpha2-Glia(63-71)-NH2, was able to identify specific

172 DEX-Ac treatment led to increased expression of fibronectin,

173 njections of a dexamethasone-21-acetate (DEX-Ac) formulation.

174 creased myocilin expression in the TM on DEX-Ac treatment.

175 lent and significantly elevated IOP with DEX-Ac treatment every week.

176 ted no systemic toxicity associated with DEX-Ac treatment.

177 Acetalated dextran (Ac-DEX) is a tunable acid-labile biopolymer with facile

178 Acetylated eEF1A1 (Ac-eEF1A1) translocates into the nucleus of myelinating

179 Dsg requires the autonomous element Ac for transposition.

180 Of the few Ac compounds that have been characterized spectroscopica

181 It is unclear how to tailor a chelator for Ac binding because Ac coordination chemistry is poorly d

182 ability as a One Health detection method for Ac and Am.

183 tion strategy on three distinct systems, for Ac, Pu, and Bk purification.

184 ctural conformations of the linear fragments Ac-tTG(553-564)-NH2 and Ac-alpha2-Glia(63-71)-NH2 and th

185 des (Ln, from La to Lu), actinides (An, from Ac to Lr), Ti, and Zr is initially introduced.

186 h a clinical syndrome indistinguishable from Ac.

187 geting and gamma-GCT-targeting) but not from Ac-alpha-Glu-gamma-secretase inhibitor prodrug 15a (APA-

188 nondiseased mice, the cleavage product from Ac-gamma-Glu-gamma-secretase inhibitor prodrug 13a (gamm

189 l-2-N-azidoacetyl-2-deoxy-d-galactopyranose (Ac(4)GalNAz).

190 on (pCORA), that introduces 4-N(3)-Bn-GalNAc(Ac)(3) as a novel precursor in large-scale cell cultures

191 present a versatile acetyl-alanine-glycine (Ac-AG) tag that conceals quantitative information in iso

192 erium (H(dAc)) and cognate protium heroin (H(Ac)) haptens were compared head to head in an inclusive

193 n murine behavioral models compared to the H(Ac) vaccine.

194 ChIPseq analysis shows enrichment of H3K27-Ac, a mark for active enhancers, in the 5' region of the

195 Hence, Ac(III) reactivity is often inferred from the lanthanide

196 Acetylated HMGB1 (Ac-HMGB1) secreted by geminin-overexpressing cells activ

197 Toward advancing understanding in Ac chelation chemistry, we have developed a method for c

198 c(III) and Am(III) in HCl solutions indicate Ac(III) coordinates more inner-sphere Cl(1-) ligands (3.

199 or, MCC950; the specific caspase-1 inhibitor Ac-YVAD-cho; and neutralizing anti-IL-1beta antibody.

200 D-fmk or a more specific caspase 3 inhibitor Ac-DEVD-CHO in lymphocytes reduced kirenol induced apopt

201 gh formation of an acyl-enzyme intermediate, Ac-Ser-216, by a double displacement bi-bi mechanism inv

202 nopyranosyloxy-benzyl glucosinolate isomers (Ac-Isomers-GS) during HPLC analysis.

203 Upon autoacetylation, acetyl-K1596 (Ac-K1596) binds intramolecularly to the BRD, competing w

204 ular levels of histone H4 acetylated at K16 (Ac-H4K16) and Ac-alpha-tubulin.

205 d for Tam resistance exhibited increased K68-Ac and monomeric MnSOD.

206 These results suggest a MnSOD-K68-Ac metabolic pathway for Tam resistance, carcinogenesis

207 8Q Ac-mimic, or physically K68-Ac (MnSOD-K68-Ac), suggest that these monomers function as a peroxidas

208 g the MnSOD-K68Q Ac-mimic, or physically K68-Ac (MnSOD-K68-Ac), suggest that these monomers function

209 Biochemical experiments using the MnSOD-K68Q Ac-mimic, or physically K68-Ac (MnSOD-K68-Ac), suggest t

210 alogs of the model amphipathic peptide KFE8 (Ac-FKFEFKFE-NH(2)), composed of two FKFE repeat motifs w

211 -obese sedentary (Ob/Sed) and lean active (L/Ac) individuals through dynamic, static, and ST (31)P-MR

212 Using a fluorogenic tripeptide library (Ac-X3X2X1-aminomethylcoumarin) and by determining specif

213 Lysosomal Ac in SMCs controls sEV release by regulating lysosomal

214 hese results strongly suggest that lysosomal Ac in podocytes is essential for the maintenance of the

215 We discovered that all M(3+) cations (M = Ac, Am, Cm, La) were completely encapsulated within the

216 combination with earlier findings for maize Ac elements, these results give insight into transposase

217 ins are specific substrates of the mammalian Ac/N-end rule pathway.

218 ked with the fluorinated sialic acid mimetic Ac(5)3F(ax)Neu5Ac.

219 Most Ac chemistry is inferred from radiochemical experiments

220 d a dipeptide, N-acetyl-l-valyl-l-leucine (N-Ac-VL), were studied via one- and two-dimensional solid-

221 Through-space hydrogen bonding of N-Ac-VL was investigated by a two-dimensional (1)H-detecte

222 by hydroquinone (H2Q), N-acetyl-tyrosine (N-Ac-Tyr) or guanosine-5'-monophosphate (GMP) was investig

223 mpatible with reaction conditions, whereas N-Ac and N-Tf failed to undergo this reaction.

224 htho[1,2-b]furan-3-ones is described via NaH/Ac(2)O-mediated dearylacetylative dimerization of 2-aryl

225 Ac-Nle-c[Asp-His-D-Nal(2')-Arg-Trp-Lys]-NH2 (Ac-Nle(4)-c[Asp(5),D-Nal(2')(7),Lys(10)]-NH2), a nonsele

226 ify the mutations underlying the 9-O- to 4-O-Ac-Sia substrate switch.

227 group of coronaviruses switched to using 4-O-Ac-Sias instead (type II).

228 3, for which 9-O-acetylated sialic acid (9-O-Ac-Sia) serves as a receptor determinant, HKU1-S1 bound

229 ors carrying 9-O-acetylated sialic acid (9-O-Ac-Sia).

230 a1CoV S RBS, using the general design of 9-O-Ac-Sia-binding sites as blueprint, backed-up by automate

231 determinant, HKU1-S1 bound with neither 9-O-Ac-Sia-containing glycoprotein(s) nor rat and mouse eryt

232 e I) target 9-O-acetylated sialic acids (9-O-Ac-Sias), but one group of coronaviruses switched to usi

233 esults demonstrate that hCoV-HKU1 exploits O-Ac-Sia as a cellular attachment receptor determinant to

234 ficity; (ii) in consequence, the switch in O-Ac-Sia specificity could be readily accomplished via con

235 trate acetylation and argues that binding of Ac-CoA to hMOF likely drives Lys-274 autoacetylation for

236 successfully characterized the chelation of Ac(3+) by DOTP(8-) using EXAFS, NMR, and DFT techniques.

237 ily controlled by changing concentrations of Ac(4)ManNAz and DBCO-Cy5.5 in cultured cells.

238 Furthermore, the Ac/N-degron of Ac-MQ-Rgs2 was conditional, and Teb4, an endoplasmic ret

239 Systematic N-methylated derivatives of Ac-Nle(4)-c[Asp(5),D-Nal(2')(7),Lys(10)]-NH2, with all p

240 of silicosis and the anti-fibrotic effect of Ac-SDKP.

241 t study finds that 1) the lost expression of Ac-Tub-alpha may be a new mechanism in rat silicosis; 2)

242 Genomic DNA (gDNA) of Ac were used to determine the analytical sensitivity and

243 say targeting the ITS1 rDNA region (ITS1) of Ac.

244 The levels of Ac-H3(K9/18) and H3K4me2, two active gene markers, at FS

245 thods were developed to provide a library of Ac(3)ManNAc-6-phosphoramidates that were evaluated in a

246 tructural basis for the domain preference of Ac-SDKP.

247 the AcanR3990 qPCR detected the presence of Ac in 49/49 ITS1 confirmed angiostrongyliasis patients a

248 CE in complex with the dipeptide products of Ac-SDKP cleavage were obtained and offered a template to

249 e we highlight the properties and results of Ac-DEX nano-/microparticles as well as the use of the po

250 A comprehensive kinetic study of Ac-SDKP and domain co-operation was performed and indica

251 he alpha subunit (main catalytic subunit) of Ac.

252 solid state structure of the mixed oligomer Ac-(tBu)2-(s1tbe)4-(tBu)2-COOtBu, the longest to be solv

253 applied a backbone N-methylation approach on Ac-Nle-c[Asp-His-D-Nal(2')-Arg-Trp-Lys]-NH2 (Ac-Nle(4)-c

254 adeno-associated virus, Tol2 transposons or Ac/Ds transposons, and can be adapted for other inserted

255 l2, ZnSO4, NiCl2, HgSO4, HgCl2, PbI2, and Pb(Ac)2.

256 structural analogue of the existing {Pd84 }(Ac) wheel with glycolate ligands, {Pd84 }(Gly) , and the

257 The {Pd84 }(Ac) wheel, initially discovered serendipitously, is the

258 A new modular route to {Pd84 }(Ac) is described, allowing incorporation of other ligand

259 We previously described the peptide Ac-LLLLRVK-Amba that displays potent inhibitory effects

260 ts: AnxA1Ac2-26 [Annexin A1 mimetic peptide (Ac-AMVSEFLKQAWFIENEEQEYVQTVK), 2.5 mug/kg] and 15-epimer

261 otent, selective, and plasma stable peptide, Ac-Arg-Ala-[d-Cys-Arg-Phe-Phe-Cys]-COOH (3).

262 y, the tetrapetide N-acetyl-Ser-Asp-Lys-Pro (Ac-SDKP) has emerged as a potent antifibrotic agent and

263 with N-acetyl-Seryl-Aspartyl-Lysyl-Proline (Ac-SDKP) inhibits myofibroblast differentiation and coll

264 ct of N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) using proteomic profile analysis.

265 the alpha-ImI dendrimers to binding protein Ac-AChBP was measured by surface plasmon resonance and r

266 Inactive SaAcs(Ac) was deacetylated (hence reactivated) by the NAD(+) -

267 Herein, a novel tetrapeptide scaffold [Ac-Xaa(1)-Arg-(pI)DPhe-Xaa(4)-NH2] is reported.

268 tin peptides derived from the W4A9 sequence (Ac-ICVWQDWGAHRCT-NH2, cyclized between C2 and C12), base

269 e-conformation spectroscopy is used to study Ac-Gln-Gln-NHBn in order to probe the interplay between

270 found that the Pt{100}-specific peptide T7 (Ac-TLTTLTN-CONH2) adopts ST-turn secondary structure, pr

271 to regulate G protein signaling by targeting Ac-MX-Rgs2 proteins for degradation through their N(alph

272 h N-azidoacetyl-D-mannosamine-tetraacylated (Ac(4)ManNAz) for incorporating azide (N(3)) groups on th

273 < 73 nM) than the melanocortin tetrapeptide Ac-His-DPhe-Arg-Trp-NH2.

274 .5- to 6.2-fold more strongly attracted than Ac workers were.

275 As predicted, Am was more sensitive than Ac in all cases (1.3- to 2.7- fold higher responses).

276 Mechanistic studies revealed that Ac(5)Neu5Ac supplementation increased intracellular CMP-

277 The Ac-Cl and Ac-OH2O distances are measured to be 2.95(3) a

278 The Ac. species Cas12a (AsCas12a) enzyme, widely used for ge

279 ed mutant, ML-Rgs2, was targeted by both the Ac/N-end rule and Arg/N-end rule pathways.

280 d its mutant, MR-Rgs2, were destroyed by the Ac/N-end rule pathway, which recognizes N(alpha)-termina

281 processes were especially determined for the Ac-Isomers-GS III.

282 smit an activated phosphoryl moiety from the Ac-CoA binding site (within the alpha subunit) to the ND

283 Furthermore, the Ac/N-degron of Ac-MQ-Rgs2 was conditional, and Teb4, an

284 fferent labeling channels are identical, the Ac-AG tag is compatible with both DDA and DIA.

285 To develop confidence and credibility in the Ac results, comparisons with +3 cations (Am, Cm, and La)

286 s caused by a loss of MyoD expression in the Ac-mut-expressing cells prior to and after induction of

287 he proteome quantification capability of the Ac-AG tag was demonstrated by triplex labeling of a yeas

288 ese new findings show that expression of the Ac-mut form of H2A.Z resulted in a dominant phenotype th

289 ively down-regulated upon treatment with the Ac-gamma-Glu-gamma-secretase-inhibitor 13a.

290 Thus, Ac workers responded less strongly to QMP than Am worker

291 ides and highlight the unexpected and unique Ac(III) chemical behaviour.

292 between Ubc9 and its K65 acetylated variant (Ac-Ubc9K65) with three NDSMs derived from Elk1, CBP, and

293 illation after 6 days of incubation, whereas Ac-PHF6 adopted a beta-sheet conformation at the surface

294 Serpin-3 associated with Ac-SVAFS-COO(-) had an altered circular dichroism spectr

295 sponsible for its high affinity binding with Ac-AChBP and alpha3beta2 nAChR were identified, our stud

296 Pharmacologic inhibition with Ac-YVAD-cmk of caspase 1, a critical component of the NL

297 detected contacts for GIC interactions with Ac-AChBP and alpha3beta2 nAChR subtypes.

298 urthermore, sialic acid supplementation with Ac(5)Neu5Ac combined with various histone deacetylase (H

299 l and silicosis rats treated with or without Ac-SDKP.

300 of the H2A.Z non-acetylatable mutant (H2A.Z-Ac-mut) resulted in a complete block of myoblast differe