ライフサイエンスコーパス: Ac

1 Ac measurements conducted on a polycrystalline sample of

2 Ac susceptibility data indicates a 100 s blocking temper

3 Ac-d-Trp-PheNH(2) appeared to be the minimal binding seq

4 Ac-induced mutations range from small footprints of host

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

20 particle emitters (211)At, (213)Bi, and (225)Ac.

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

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

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

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

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

26 ance of lanthanide phosphate to contain (225)Ac and its radioactive decay daughters, the magnetic pro

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

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

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

30 labelled with alpha-particle-generating (225)Ac were found to clear rapidly, thus mitigating radioiso

31 oaded with the alpha-particle generator (225)Ac to selectively kill prostate-specific membrane antige

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

33 e involves the loss of 90% of the input (225)Ac.

34 Historic obstacles to the use of (225)Ac have been the difficulty in finding suitable chelator

35 The loading efficiency of (225)Ac into preformed liposomes ranged from 58.0% +/- 4.6% t

36 s the possible clinical applications of (225)Ac monoclonal antibodies.

37 ions and contain the decay daughters of (225)Ac while targeting biologically relevant receptors in a

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

39 3+) ions show 2 distinct populations of (225)Ac(3+) ions: one rapidly lost in human serum and one tha

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

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

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

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

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

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

46 150 (n = 2), and 200 kBq/kg (n = 4) of (225)Ac-PSMA-617 were evaluated retrospectively regarding tox

47 o facilitate the more widespread use of (225)Ac.

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

49 , (177)Lu, (90)Y, (212/213)Bi, (212)Pb, (225)Ac, (186/188)Re).

50 rticle radiation using the radioisotope (225)Ac is a promising form of therapy for various types of c

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

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

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

54 The recoil energy of the (225)Ac daughters following alpha decay will sever any metal-

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

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

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

58 y, PEGylated liposomes were loaded with (225)Ac and labeled with the mouse antihuman PSMA J591 antibo

59 ly active conjugates of antibodies with (225)Ac at high specific activity.

60 nti-PSMA-targeted liposomes loaded with (225)Ac selectively bind, become internalized, and kill PSMA-

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

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

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

64 d conditions, 0.1% formic acid (FA) and NH(4)Ac at different pH, are far from the optimum for untarge

65 2], 1 [Ac-His-Arg-(pI)DPhe-Tic-NH2], and 41 [Ac-Arg-Arg-(pI)DPhe-DNal(2')-NH2] were more potent (EC50

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

67 r of an acetyl group from acetyl-coenzyme A (Ac-CoA) to the amine of a wide range of substrates, incl

68 (Nor-Ep), Ascorbic Acid (AA), Acetaminophen (Ac) and Uric Acid (UA).

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

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

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

72 imuthal repositioning of Tm along the actin (Ac):Tm:troponin (Tn) thin filament to block or expose my

73 the transposon-tagging construct Activator (Ac)/Dissociator (Ds)-ATag-Bar_gosGFP to produce activati

74 The autonomous transposon Activator (Ac) is a powerful mutagen.

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

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

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

78 emization catalyst with the acylating agent (Ac(2)O) used in the kinetic resolution.

79 -LVE and Ac-YYD formed fibrillar aggregates, Ac-VIE and Ac-MYD formed hydrogels, and Ac-YLD crystalli

80 r [1(3)2](2), where 1 is a D-Pro-X (X = Aib, Ac(4)c, Ac(6)c, L-4-Cl-PhGly)-derived monomer and 2 is a

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

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

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

84 ted COG complex, is also shown to contain an Ac/N-degron.

85 t of the APC/C ubiquitin ligase, contains an Ac/N-degron that is repressed by Cut9, another APC/C sub

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

87 and its dimannosides (PIM(2), AcPIM(2), and Ac(2)PIM(2)) that all possess the predominant natural 19

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

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

90 ex formation between the Grb2 SH2 domain and Ac-pTyr-Xaa-Asn derived tripeptides in which the Xaa res

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

92 tes, Ac-VIE and Ac-MYD formed hydrogels, and Ac-YLD crystallized under ambient conditions.

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

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

95 formed bead-like microstructures, Ac-LVE and Ac-YYD formed fibrillar aggregates, Ac-VIE and Ac-MYD fo

96 the hydrogel-forming sequences of Ac-MYD and Ac-VIE were shuffled.

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

98 e-NH2, Ac-His-(pCl)DPhe-Arg-(pI)Phe-NH2, and Ac-Arg-(pCl)DPhe-Tic-(pNO2)DPhe-NH2, revealing new ligan

99 ng complementarity of the Arg/N-end rule and Ac/N-end rule pathways enables the elimination of protei

100 -YYD formed fibrillar aggregates, Ac-VIE and Ac-MYD formed hydrogels, and Ac-YLD crystallized under a

101 entatives, including McClintock's archetypal Ac mobile genetic element, in many eukaryotic species.

102 ived parameters with model peptides, such as Ac-R-W-V-W-V-N-G-Orn-K(Me)(n)-I-L-Q-NH(2), where n = 0,

103 partic acid is substituted by an asparagine (Ac-LPFFN-NH2).

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

105 Kinetic studies demonstrate that the B(Ac)2 mechanistic pathway is followed.

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

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

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

109 cies of host and self-mutations generated by Ac, we used an allele harboring Ac in the 5' untranslate

110 nisms of the double-strand break produced by Ac excision: footprints by nonhomologous end joining and

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

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

113 ](2), where 1 is a D-Pro-X (X = Aib, Ac(4)c, Ac(6)c, L-4-Cl-PhGly)-derived monomer and 2 is an L-Pro'

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

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

116 ific inhibitor N-Acetyl-Tyr-Val-Ala-Asp-CHO (Ac-YVAD-CHO).

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

118 structure of TAT in complex with acetyl-CoA (Ac-CoA) at 2.7 A resolution.

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

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

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

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

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

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

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

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

127 CQ and zinc/copper chloride led to decreased Ac-H3.

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

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

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

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

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

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

134 molecular recognition of a target dipeptide (Ac-EY-OH) mimicking a biologically relevant sequence by

135 experiment using the Activator/Dissociation (Ac/Ds) system in a W22 background.

136 this research, an Affibody analog, anti-EGFR Ac-Cys-Z(EGFR:1907), was successfully site-specifically

137 Dsg requires the autonomous element Ac for transposition.

138 cardiac and gizzard muscle Tm on filamentous Ac in the position that corresponds to the closed state.

139 s establishes the molecular determinants for Ac-CoA and tubulin substrate recognition.

140 acterized MR1 ligand, acetyl-6-formylpterin (Ac-6-FP), markedly stabilized MR1, potently up-regulated

141 at both contain an intact Ac and a fractured Ac (fAc) structure at the maize p1 locus.

142 All nine terminal deletions or fractured Ac (fAc) elements had rearrangements of adjacent host se

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

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

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

146 hree-stranded coiled coils (TRI-H)3 [TRI-H = Ac-G WKALEEK LKALEEK LKALEEK HKALEEK G-NH2].

147 ysine 9 (H3K9me2) and increased acetyl H3K9 (Ac-H3K9) and p65 at the retinal MMP-9 promoter.

148 generated by Ac, we used an allele harboring Ac in the 5' untranslated region bronze (bz).

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

150 so synthesized Nalpha-acetyl-Ser26-iAbeta42 (Ac-iAbeta42), which cannot undergo O-->N acyl chemistry,

151 ced stability of the Pro-cisPro conformer in Ac-Pro-Pro-Xaa-NH(2) when Xaa is aromatic.

152 ng the stability of Pro-cisPro population in Ac-Pro-Pro-Aro-NH(2).

153 nt compounds at all these hMC4R SNPs include Ac-His-(pI)DPhe-Tic-(pNO2)DPhe-NH2, Ac-His-(pCl)DPhe-Tic

154 Increased Ac-H3K9 facilitates the recruitment of p65, resulting in

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

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

157 ), and in mice given the caspase 1 inhibitor Ac-YVAD-CMK.

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

159 Furthermore, a peptide-based inhibitor (Ac-GSL-AOMK) was found to block the cytotoxicity of TcdB

160 y the use of a specific caspase-1 inhibitor, Ac-YVAD-CMK.

161 parental alleles that both contain an intact Ac and a fractured Ac (fAc) structure at the maize p1 lo

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

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

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

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

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

167 edicted tripeptides (Ac-LVE, Ac-YYD, Ac-LLE, Ac-YLD, Ac-MYD, Ac-VIE) were chosen for experimental val

168 20) < CHO (250) < CO2Me (850) < NO2 (4300) < Ac (7300) < CO2H (150 000).

169 mputationally predicted tripeptides (Ac-LVE, Ac-YYD, Ac-LLE, Ac-YLD, Ac-MYD, Ac-VIE) were chosen for

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

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

172 hat Ac-LLE formed bead-like microstructures, Ac-LVE and Ac-YYD formed fibrillar aggregates, Ac-VIE an

173 des (Ac-LVE, Ac-YYD, Ac-LLE, Ac-YLD, Ac-MYD, Ac-VIE) were chosen for experimental validation in order

174 Timely administration of N-acetylcysteine (N-Ac) prevents the progression of serious liver injury and

175 and disease, whereas failure to administer N-Ac within a critical time frame allows disease progressi

176 S domains and low sulfate domains known as N-Ac domains.

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

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

179 se and the time to first administration of N-Ac.

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

181 gG binding cyclic depsipeptide cyclo[(Nalpha-Ac)-S(A)-RWHYFK-Lact-E] is presented to demonstrate the

182 acid (Lact) and the dipeptide ester (Nalpha-Ac)-Ser(Ala)- as linkers for dilactonization.

183 d three kinds of beta-sheet breakers, namely Ac-LPFFD-NH2 and two variants thereof, one obtained by s

184 transitions that shield and unshield natural Ac/N-degrons.

185 measurements with cationic (KALP), neutral (Ac-KALP), and pH-sensitive (HALP) transmembrane peptides

186 ism provide consistent evidence that the new Ac-LPFFN-NH2 beta-sheet breaker is more effective than t

187 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

188 he-NH2, Ac-His-(pCl)DPhe-Tic-(pNO2)DPhe-NH2, Ac-His-(pCl)DPhe-Arg-(pI)Phe-NH2, and Ac-Arg-(pCl)DPhe-T

189 include Ac-His-(pI)DPhe-Tic-(pNO2)DPhe-NH2, Ac-His-(pCl)DPhe-Tic-(pNO2)DPhe-NH2, Ac-His-(pCl)DPhe-Ar

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

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

192 3, for which 9-O-acetylated sialic acid (9-O-Ac-Sia) serves as a receptor determinant, HKU1-S1 bound

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

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

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

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

197 ranscription was supported by the absence of Ac-Lys-14-histone H3 in dendritic cells treated with zym

198 of H(+), and the high gas-phase basicity of Ac(-) and (ii) a reproducible LC separation due to an ac

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

200 an employ the demonstrated conditionality of Ac/N-degrons to regulate subunit stoichiometries and oth

201 study was carried out on a single crystal of Ac-YLD, which revealed that each molecule adopts a beta-

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

203 Internal and terminal deletions of Ac predominated among the 72 bz-s derivatives.

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

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

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

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

208 ontrast, whereas coinjection with 500 mug of Ac-Cys-Z(EGFR:1907) successfully blocked the tumor uptak

209 coinjection of the PET probe with 45 mug of Ac-Cys-Z(EGFR:1907) was able to improve the tumor uptake

210 A rank order of Ac-iAbeta42>iAbeta42>Abeta42 was observed.

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

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

213 These enhanced properties of Ac-6-FP were attributable to structural alterations in M

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

215 approach, the hydrogel-forming sequences of Ac-MYD and Ac-VIE were shuffled.

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

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

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

219 upy the blocked, closed, or open position on Ac.

220 t to block or expose myosin binding sites on Ac.

221 Transcripts originating within Ds or Ac accumulated to lower levels than the wild-type Ps1 al

222 ther the sequence Ac-(LSLLLSL)3-NH2 (LS2) or Ac-(LSSLLSL)3-NH2 (LS3).

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

224 in a cell-permeable FRET substrate SM-P124 (Ac-GRRRK(Dabcyl)-GGAANC(MeOBn)RMGG-fluorescein).

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

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

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

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

229 gregation of the tau-protein-derived peptide Ac-VQIVYK-NH2 (AcPHF6).

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

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

232 e for the acetylated version of the peptide (Ac-HWRGWV) supported on alkanethiol SAM was 5.8x10(-7)M

233 We have designed a cyclic peptide, Ac-c[CVDINNNC]-NH2, containing the key sequence motif me

234 lity of a host-guest collagen model peptide, Ac-GPOGPOGPYGXOGPOGPO-NH2, substituting KGE, KGD, EGK, a

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

236 the activity profiles of the linear peptides Ac-Xaa-Phe-Yaa (Xaa = l/d-Trp, d-His/Lys/Arg; Yaa = H, G

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

238 tor bradykinin and N-acetyl-Ser-Asp-Lys-Pro (Ac-SDKP), a physiological modulator of hematopoiesis.

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

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

241 ptide N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP).

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

243 ted N-acetylated cysteine sulfinyl radicals (Ac-(SO*)Cys); instead, charge-directed H2O loss followed

244 -A-resolution structure of the reconstituted Ac:Tm filament formed with gizzard-derived Tm, we discus

245 ced by alternative transposition of reversed Ac/Ds termini in maize.

246 earrangements elicited by a pair of reversed Ac/Ds termini, we isolated and analyzed 100 new mutant a

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

248 n a peptide series with the general sequence Ac-Pro-Pro-Xaa-NH(2).

249 hetic alpha-helices with either the sequence Ac-(LSLLLSL)3-NH2 (LS2) or Ac-(LSSLLSL)3-NH2 (LS3).

250 PPII using a host-guest system with sequence Ac-GPPXPPGY-NH(2), where X represents any amino acid.

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

252 tor major transcript X054214.1 on the stable Ac element, along with a 35S enhancer tetramer and glufo

253 ve phosphonate inhibitors with the structure Ac-peptidyl(P)(O-C6H4-4-Cl)2.

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

255 e engineered KATs in junction with synthetic Ac-CoA surrogates to effectively label KAT substrates ev

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

257 o create specific degradation signals termed Ac/N-degrons and targeted by the Ac/N-end rule pathway.

258 < 73 nM) than the melanocortin tetrapeptide Ac-His-DPhe-Arg-Trp-NH2.

259 In a model tetrapeptide (Ac-TYPN-NH2), 4R-Hyp was stereospecifically converted to

260 .5- to 6.2-fold more strongly attracted than Ac workers were.

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

262 nd electron microscopy studies revealed that Ac-LLE formed bead-like microstructures, Ac-LVE and Ac-Y

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

264 e interaction region between peptide and the Ac-LPFFN-NH2 beta-sheet breaker.

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

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

267 nals termed Ac/N-degrons and targeted by the Ac/N-end rule pathway.

268 We name these families the Ac and Buster families after the first identified transp

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

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

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

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

273 everal that began within the terminus of the Ac and Ds elements.

274 onalized and transferable acyl moiety of the Ac-CoA analogs further allowed the labeled substrates to

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

276 nal methionine residue are substrates of the Ac/N-end rule pathway, the resulting complementarity of

277 c unacetylated N-terminal residues while the Ac/N-end rule pathway targets proteins through their N(a

278 rice EPSPS marker gene was inserted with the Ac transposon 5' end, which provided a splice donor site

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

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

281 yl] maleimide ((18)F-FBEM) was conjugated to Ac-Cys-Z(EGFR:1907) under mild conditions (pH 7) to prod

282 utility because of restricted transposition (Ac/Ds: soybean) or the requirement for tissue culture ac

283 The noncationizable tripeptide Ac-D-Trp-Phe-GlyNH2 was recently proposed as a novel min

284 using the known self-associating tripeptide, Ac-IVD, as a structural template.

285 Six computationally predicted tripeptides (Ac-LVE, Ac-YYD, Ac-LLE, Ac-YLD, Ac-MYD, Ac-VIE) were cho

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

287 07) with or without coinjection of unlabeled Ac-Cys-Z(EGFR:1907) for up to 3 h after injection.

288 and destroyed via its activated (unshielded) Ac/N-degron if the total level of Cog1 increased in a ce

289 Prep expression, increased plasma and urine Ac-SDKP, and attenuated renal fibrosis.

290 rep in both glomeruli and tubules, low urine Ac-SDKP, and increased deposition of collagen.

291 ein and the specific activity, assayed using Ac-Ala-p-nitroanilide substrate, was >1 unit.

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

293 ed to be the minimal binding sequence, while Ac-d-Trp-Phe-GlyNH(2) emerged as the first noncationizab

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

295 of PA4794 in the apo-form, in complexes with Ac-CoA, CoA, several antibiotics and other small molecul

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

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

298 tripeptides (Ac-LVE, Ac-YYD, Ac-LLE, Ac-YLD, Ac-MYD, Ac-VIE) were chosen for experimental validation

299 nally predicted tripeptides (Ac-LVE, Ac-YYD, Ac-LLE, Ac-YLD, Ac-MYD, Ac-VIE) were chosen for experime

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