ライフサイエンスコーパス: ribose

1 c efficiency for protein-conjugated poly(ADP-ribose).

2 a monomer or in polymeric chains as poly(ADP-ribose).

3 ase IV is dependent upon ATP not NAD+ or ADP-ribose.

4 of a single hydroxyl group from the terminal ribose.

5 l tool to investigate different forms of ADP-ribose.

6 acids, glycogen-bound glucose, and RNA-bound ribose.

7 y of NrtR is antagonized by the effector ADP-ribose.

8 ansesterification to yield 2'-OH RNA and ADP-ribose-1",2"-cyclic phosphate products.

9 f Tpt1 in a product-mimetic complex with ADP-ribose-1"-phosphate in the NAD(+) site and pAp in the RN

10 P1 in ligand-free and in complex with uracil/ribose-1-phosphate, 2'-deoxyuridine/phosphate and thymid

11 lytically cleaves adenosine into adenine and ribose-1-phosphate.

12 upling as building blocks suitably protected ribose 12 with l-(+)-3-O-trifluoromethylsulfonyl-6-O-p-m

13 Decaprenylphosphoryl-beta-d-ribose 2'-epimerase (DprE1) is an essential enzyme in My

14 ctories of the MD simulation indicate that a ribose 2'-hydroxyl group destabilizes the pai-pai stacki

15 hich facilitates and precedes the subsequent ribose 2'-O methylation by the nsp16-nsp10 complex.

16 ve with a DNA one revealed the importance of ribose 2'-OH groups for the complex formation.

17 E1, a subunit of decaprenylphosphoryl-beta-d-ribose-2'-epimerase.

18 of a crystal structure of MtbPYK with bound ribose 5-phosphate (R5P), combined with biochemical anal

19 Here we use TEM to show that ribose-5-phosphate (R5P) glycation of collagen fibrils -

20 e OPPP, ribulose-5-phosphate is converted to ribose-5-phosphate (R5P)-required for purine nucleotide

21 nd therefore activates the PPP for NADPH and ribose-5-phosphate, which consequently detoxifies intrac

22 size and structure, for example, glucose or ribose-6-phosphate.

23 Poly(ADP-ribose) a dynamic and reversible posttranslational modif

24 ctroscopies led to the assignment of the two ribose adducts being the constitutional isomers of an S-

25 nnel activation requires binding of both ADP-ribose (ADPR) and Ca(2+).

26 It is activated by cytosolic ADP ribose (ADPR) and contains a nudix-type motif 9 (NUDT9)-

27 lated cation channel hTRPM2, is gated by ADP-ribose (ADPR) independently of the C-terminal NUDT9H dom

28 members covalently link either a single ADP-ribose (ADPR) or a chain of ADPR units to proteins using

29 al roles, as well as the activity of the ADP-ribose (ADPR) transferase enzymes (PARP family members)

30 TRPM2's activation by Ca(2+) and ADP ribose (ADPR), an NAD(+)-metabolite produced under oxida

31 N(6)-Dicyclobutylmethyl ribose agonist (9, MRS7469, >2000-fold selective for A(1

32 ymatic synthesis of an active azido-modified ribose analog, 5-azidoribose (5-AR), as well as the synt

33 te (PS) backbone modifications and different ribose and base modifications to improve pharmacological

34 Heterolytic phosphate release from ribose and deoxyribose nucleotide C4' radicals was also

35 we synthesized a variety of C4'-methylated d-ribose and l-lyxose-configured uridine derivatives by a

36 The JGS4143 LTA also had a terminal ribose and ManNAc instead of ManN in the core region, su

37 s, we identified, and characterized in vivo, ribose and methanocarba nucleosides, including with A(1)

38 The crystal structures of ribose and NADP(+) (the oxidized form of nicotinamide ad

39 s of nucleotides-either via the synthesis of ribose and the canonical nucleobases and then joining th

40 of an S- and an O-adduct of bisulfite to the ribose, and these are the final products after heating.

41 distinct ligands, fructose (anti-FruR) or D-ribose (anti-RbsR); and were complemented by 14 addition

42 fy a variant of cyclic adenosine diphosphate ribose as a biomarker of TIR enzymatic activity.

43 DNA ligase IV cannot use either NAD+ or ADP-ribose as adenylation donor for ligation.

44 lso utilize NAD+ and, to a lesser extent ADP-ribose, as the source of the adenylate group and that NA

45 on of miRNAs at the 2'-hydroxyl group on the ribose at 3'-end (2'-O-methylation, 2'Ome) is critical f

46 Ribose binding induces the RBP "closed" conformation, wh

47 , we show that an optimal site exists within ribose binding protein (RBP) that, when disrupted, resul

48 et and small carbocyclic rings accessing the ribose-binding pocket.

49 the highly specific recognition of ribose by ribose-binding protein (RBP) to develop a single-protein

50 We demonstrate that RBP, with a tunable ribose-binding site and further engineered to bind xenon

51 und with all hydroxyl groups of the terminal ribose blocked as its 1"-beta- O-methyl-2",3"- O-isoprop

52 ability against protein-conjugated mono(ADP-ribose), but improved catalytic efficiency for protein-c

53 e utilize the highly specific recognition of ribose by ribose-binding protein (RBP) to develop a sing

54 lcium-mobilizing second messenger cyclic ADP-ribose (cADPR), CD157, a sister protein of CD38, has bee

55 h an IL-13-CD38-cyclic adenosine diphosphate ribose (cADPR)-dependent process.

56 ADP-ribose can be conjugated to proteins singly as a monomer

57 r, we attempted to confirm that NAD+ and ADP-ribose can be used as co-factors by human DNA ligase IV.

58 s, beyond its enzymatic activity in poly(ADP-ribose) catabolism.

59 ectuated by associated reduction in poly-ADP-ribose chain formation.

60 er in ZBTB24 binds PARP1-associated poly(ADP-ribose) chains and mediates the PARP1-dependent recruitm

61 eover, through its association with poly(ADP-ribose) chains, ZBTB24 protects them from degradation by

62 dicate that ARH3 can act as an eraser of ADP-ribose chromatin scars at sites of PARP activity during

63 We demonstrate that the ADP-ribose chromatin scars result in reduced endogenous leve

64 in CSB-deficient cells using ADPr-ChAP (ADP ribose-chromatin affinity purification), and the results

65 ethods are currently limited for quantifying ribose concentration in complex biological samples.

66 Ribose concentration was measured for mammalian cell lys

67 vage those forces act through control of the ribose conformation and are transmitted to the sulfur vi

68 of the cleaved S-C bond correlates with SAM ribose conformation but not with positioning and orienta

69 restricted glucose availability, restricted ribose/deoxyribose flow and NADPH production, an accumul

70 This facilitates the poly(ADP-ribose)-dependent assembly of the LIG4/XRCC4 complex at

71 ose) polymerases (PARPs) using NAD(+) as ADP-ribose donor.

72 imidine nucleosides from small molecules and ribose, driven solely by wet-dry cycles.

73 s or for generating C(5) precursors (such as ribose) during growth on other (non-C(5)) substrates, th

74 We measured eNAD and its metabolites eADP-ribose (eADPR), eAMP and e-adenosine (eADO) from tissues

75 hat (1) in tissues, eNAD is degraded to eADP-ribose, eAMP and e-adenosine (eADO) by CD38, ENPP1 and N

76 adenine ring (PKA) and position 2'-OH of the ribose (Epac) have been used to produce target-selective

77 otides, suggesting a guanosine nucleoside or ribose-first mechanism for nucleotide association.

78 and guanine base positions while leaving the ribose flexible, and a transition state stabilization th

79 med ELTA (enzymatic labeling of terminal ADP-ribose) for labeling free or protein-conjugated ADP-ribo

80 tes and appear to have diversified to access ribose from a variety of substrates.

81 ns, 16 of which catalyze the transfer of ADP-ribose from NAD(+) to macromolecular targets (namely, pr

82 aomicron can also extract the monosaccharide ribose from nucleosides and characterize proteins necess

83 he ARH3 (ADPRHL2) hydrolase that removes ADP-ribose from proteins have been associated with neurodege

84 enzymatic synthesis of NAD(+) analogues with ribose functionalized by terminal alkyne and azido group

85 cells, supporting the dynamic regulation of ribose glycation as well as validating the probe as a ne

86 t, similar to methylglyoxal (MGO) glycation, ribose glycation specifically accumulates on histones.

87 emonstrate this probe's utilities to uncover ribose-glycation and deglycation events as well as track

88 eir application toward understanding protein ribose-glycation in vitro and in cellulo.

89 We recently identified that poly (ADP) ribose glycohydrolase (PARG) is a strong candidate targe

90 y(ADP-ribose) polymerase (PARP) and poly(ADP-ribose) glycohydrolase (PARG) are key enzymes in BER tha

91 1 (PARP1) and PARylation removal by poly(ADP-ribose) glycohydrolase (PARG) critically regulate DNA da

92 patient biopsies are sensitive to a poly(ADP-ribose) glycohydrolase (PARG) inhibitor.

93 PAR degradation by poly(ADP-ribose) glycohydrolase (PARG) is essential for progressi

94 -ribose transferases and removed by poly(ADP-ribose) glycohydrolase (PARG), which plays important rol

95 4 protects them from degradation by poly(ADP-ribose) glycohydrolase (PARG).

96 show increased resistance to human poly(ADP-ribose) glycohydrolase-mediated degradation.

97 on refers to the addition of one or more ADP-ribose groups onto proteins.

98 Blocking poly-ADP-ribose gylcohydrolase also enhanced this association.

99 Moreover, IDP-ribose (IDPR) induced currents both in hTRPM2 and NvTRPM

100 and serum, which led to estimates of low-mM ribose in a HeLa cell line.

101 16 in complex with monomeric and dimeric ADP-ribose in identifying the active site for binding and pr

102 hment at 2'- or 3'-hydroxyls of the terminal ribose in oligoribonucleotides, we have performed an ext

103 SCA7 patients displayed increased poly(ADP-ribose) in cerebellar neurons, supporting poly(ADP-ribos

104 eading to elevated DNA breakage and poly(ADP-ribose) induction that cannot be rescued by catalytic or

105 d processing free and protein-conjugated ADP-ribose into phosphoribose forms.

106 When a base is lost from RNA, the remaining ribose is found as a closed-ring or an open-ring sugar w

107 in milk from OB women and included: mannose, ribose, lyxose, lyxitol (0.5 mo); mannose, ribitol, glyc

108 of the available rNMP sequencing techniques, Ribose-Map can increase the reproducibility of rNMP sequ

109 Here, by using ribose-seq and Ribose-Map techniques, we built and analyzed high-throug

110 Through a series of analytical modules, Ribose-Map transforms raw sequencing data into summary d

111 of rNMP sequencing experiments, we developed Ribose-Map.

112 reak repair; a process regulated by poly(ADP-ribose) metabolism.

113 e channel activated by adenosine diphosphate ribose metabolites and oxidative stress.

114 In the adenine series, most ribose modifications and 1-deaza and 3-deaza were detrim

115 centre is essential for the addition of ADP-ribose moieties after DNA damage in human cells.

116 PARP catalytic domains transfer the ADP-ribose moiety from NAD(+) to amino acid residues of targ

117 while in Rossmanns it binds the nucleotide's ribose moiety.

118 for labeling free or protein-conjugated ADP-ribose monomers and polymers at their 2'-OH termini usin

119 actor to transfer monomer or polymers of ADP-ribose nucleotide onto macromolecular targets such as pr

120 This study underscores the selection of ribose nucleotides as second messengers and finds its ro

121 ional design of modulators, but the terminal ribose of ADPR is known to be essential for activation.

122 uanosine and a unique 2'O-methylation on the ribose of the penultimate nucleotide.

123 Recently, the ribose operon repressor, RbsR, was also defined as a ple

124 his activity of TNT was not inhibited by ADP-ribose or nicotinamide, indicating low affinity of TNT f

125 d to bind xenon, enables the quantitation of ribose over a wide concentration range (nM to mM).

126 e ZnF domain of SIRT1 interact with poly-ADP ribose (PAR) in response to DNA damage, and are responsi

127 and activate PARP1/2, which deposit poly-ADP-ribose (PAR) to recruit XRCC1-Ligase3 and other repair f

128 expressed alone, it associates with poly(ADP-ribose) (PAR) chains and is recruited to DNA damage site

129 ges including the complexity of the poly(ADP-ribose) (PAR) chains, low abundance of the modification

130 ugh its ability to bind the ends of poly(ADP-ribose) (PAR) chains, the function of the histone varian

131 mutated in human cancers, binds to poly(ADP-ribose) (PAR) immediately following DNA damage and media

132 Poly(ADP-ribose) (PAR) is a nucleic acid-like protein modificatio

133 Poly(ADP-ribose) (PAR) is rapidly synthesized from NAD(+) at site

134 The synthesis of poly(ADP-ribose) (PAR) reconfigures the local chromatin environme

135 lar RNAs (snoRNAs) as activators of poly(ADP-ribose) (PAR) synthesis, demonstrating that this snoRNA-

136 Here, the distribution of poly (ADP ribose) (PAR) was determined in CSB-deficient cells usin

137 s through the addition of mono- and poly(ADP-ribose) (PAR)(1-5).

138 nal modification by the addition of poly(ADP-ribose) (PAR), which promotes protein recruitment and lo

139 mpartments at DNA damage sites in a poly(ADP ribose) (PAR)-dependent manner.

140 d that NOCT recognizes the chemically unique ribose-phosphate backbone of the metabolite, placing the

141 his effect, presumably because they generate ribose-phosphate derivatives from products of an unlinke

142 on to low folAmix by rerouting the 2-Deoxy-D-ribose-phosphate metabolism from glycolysis towards synt

143 selectivity: Optimization of the lipophilic ribose pocket-targeting substituent was followed by the

144 tive, rotated binding mode upon changing the ribose-pocket binding moiety from a pyrrolidinyl to an a

145 ng domain and, at least in part, on poly-ADP ribose polymerase (PARP) activity.

146 ctivity and accompanied full-length poly ADP ribose polymerase (PARP) cleavage.

147 AD5-depleted cells are sensitive to poly(ADP)ribose polymerase (PARP) inhibitors and that the process

148 A repair targeted therapies such as poly-ADP ribose polymerase (PARP) inhibitors.

149 ax, TNFalpha, cleaved Caspase-3 and poly ADP-ribose polymerase (PARP).

150 Inhibition of polyADP-ribose polymerase 1 (PARP-1) suppressed the nuclease-med

151 otein PARylation catalyzed by human poly-ADP-ribose polymerase 1 (PARP1) and PARP2.

152 alpha exhibited lower expression of poly-ADP-ribose polymerase 1 (PARP1) gene, leading to a higher in

153 Mechanistically, poly-ADP-ribose polymerase 1 (PARP1) represses expression of NKG2

154 Inhibitors of poly-ADP-ribose polymerase 1 (PARPi) are highly effective in kill

155 Alcohol feeding induced apoptosis (poly ADP-ribose polymerase [PARP] and caspase-3 [CASP-3] cleavage

156 n-1-associated protein to attenuate poly ADP-ribose polymerase activation and mitochondrial DNA damag

157 tivity to DNA damaging agents and poly-(ADP)-ribose polymerase inhibitors (PARPis).

158 The success of poly-ADP ribose polymerase inhibitors in the treatment of breast

159 ologs) and SIRT1 is an inhibitor of poly-ADP-ribose polymerase-1 (PARP1).

160 Poly(ADP-ribose) polymerase (PARP) and poly(ADP-ribose) glycohydr

161 e that concurrent administration of poly(ADP-ribose) polymerase (PARP) and WEE1 inhibitors is effecti

162 induction of autophagy, and robust poly(ADP-ribose) polymerase (PARP) cleavage indicative of DNA dam

163 Inhibitors of poly(ADP-ribose) polymerase (PARP) have demonstrated efficacy in

164 Synthetic lethality between poly(ADP-ribose) polymerase (PARP) inhibition and BRCA deficiency

165 with response to poly(adenosine diphosphate-ribose) polymerase (PARP) inhibition in patients with pr

166 Olaparib, a poly (ADP-ribose) polymerase (PARP) inhibitor (PARPi), is approved

167 the automated radiosynthesis of the poly(ADP-ribose) polymerase (PARP) inhibitor [(18)F]olaparib.

168 sed a radiolabled poly(adenosine diphosphate ribose) polymerase (PARP) inhibitor called (125)I-KX1 to

169 n cancer (EOC) to poly(adenosine diphosphate-ribose) polymerase (PARP) inhibitor in a CARM1-dependent

170 synergistic cytotoxicity with the poly (ADP-ribose) polymerase (PARP) inhibitor olaparib against TNB

171 The poly (ADP-ribose) polymerase (PARP) inhibitor olaparib is FDA appr

172 M-mutant cells to topotecan or the poly-(ADP-ribose) polymerase (PARP) inhibitor olaparib reflects de

173 CA2, could help select patients for poly(ADP-ribose) polymerase (PARP) inhibitor or platinum chemothe

174 ge, BRCA1 localization to DSBs, and poly(ADP-ribose) polymerase (PARP) inhibitor resistance.

175 Methods: Using a radiolabeled poly(ADP-ribose) polymerase (PARP) inhibitor, (125)I-KX1, we deli

176 d GLS(high) cells vulnerable to the poly(ADP-ribose) polymerase (PARP) inhibitor, olaparib, and prolo

177 at elicits therapeutic response to poly (ADP-Ribose) polymerase (PARP) inhibitor.

178 Poly (ADP-ribose) polymerase (PARP) inhibitors (olaparib and talaz

179 , besides direct cytotoxic effects, poly(ADP ribose) polymerase (PARP) inhibitors (PARPis) exhibit an

180 tations that confer sensitivity to poly (ADP-ribose) polymerase (PARP) inhibitors (PARPis), but the r

181 nding acquired tumour resistance to poly(ADP-ribose) polymerase (PARP) inhibitors and other therapeut

182 ted breast cancers are sensitive to poly(ADP-ribose) polymerase (PARP) inhibitors and platinum agents

183 Poly(adenosine 5'-diphosphate-ribose) polymerase (PARP) inhibitors are a class of anti

184 Poly(ADP-ribose) polymerase (PARP) inhibitors are increasingly be

185 Bevacizumab and maintenance poly(ADP-ribose) polymerase (PARP) inhibitors both significantly

186 Targeted therapies such as poly (ADP-ribose) polymerase (PARP) inhibitors have emerged as one

187 Poly(ADP-ribose) polymerase (PARP) inhibitors have shown efficacy

188 h immune checkpoint inhibitors and poly (ADP-ribose) polymerase (PARP) inhibitors in a variety of sol

189 nd renders cells hypersensitive to poly (ADP-ribose) polymerase (PARP) inhibitors used to treat BRCA1

190 work, we found that combination of poly (ADP-ribose) polymerase (PARP) inhibitors with drugs that inh

191 evels show increased sensitivity to poly(ADP-ribose) polymerase (PARP) inhibitors, especially when co

192 n important structural motif of new poly(ADP-ribose) polymerase (PARP) inhibitors, playing a useful r

193 r but also creates vulnerability to poly(ADP-ribose) polymerase (PARP) inhibitors.

194 cells exhibit a high sensitivity to poly(ADP-ribose) polymerase (PARP) inhibitors.

195 ent show a significant response to poly (ADP-ribose) polymerase (PARP) inhibitors; patients with ovar

196 Poly(ADP-ribose) Polymerase (PARP) is a family of enzymes, which

197 In CSB-deficient cells, poly (ADP ribose) polymerase (PARP) is persistently activated by u

198 Poly (ADP-ribose) polymerase (PARP) is the best-known element of t

199 Poly (ADP-ribose) polymerase (PARP) plays a significant role in DN

200 Poly(ADP-ribose) polymerase (PARP) superfamily members covalently

201 nkyrase-1 (TNKS) is a member of the poly(ADP-ribose) polymerase (PARP) superfamily of proteins that p

202 isite sensitivity to inhibitors of poly (ADP-ribose) polymerase (PARP) that are being tested in clini

203 olecular targets available such as poly (ADP-ribose) polymerase (PARP), epidermal growth factor recep

204 nhibitor of poly(adenosine diphosphate [ADP]-ribose) polymerase (PARP), has been associated with sign

205 ir C termini: ZAPL (long) encodes a poly(ADP-ribose) polymerase (PARP)-like domain that is missing in

206 y inhibiting the DNA repair protein poly(ADP-ribose) polymerase (PARP).

207 base excision repair (BER) protein poly (ADP-ribose) polymerase (PARP).

208 downstream effector TCDD-inducible poly(ADP-ribose) polymerase (TiPARP) during infection.

209 sociates with the DNA damage sensor poly(ADP-ribose) polymerase 1 (PARP-1) and that the association r

210 NEDD8 in regulating the activity of poly(ADP-ribose) polymerase 1 (PARP-1) in response to oxidative s

211 The success of poly(ADP-ribose) polymerase 1 (PARP-1) inhibitors in cancers with

212 Poly(ADP-ribose) polymerase 1 (PARP-1) is a multidomain multifunc

213 Poly(ADP-ribose) polymerase 1 (PARP-1) is a nuclear enzyme involv

214 romote the rapid proteolysis of the poly(ADP-ribose) polymerase 1 (PARP-1), but the mechanism of reco

215 f E4orf4 with the DNA damage sensor poly(ADP-ribose) polymerase 1 (PARP-1).

216 e central DNA damage sensor protein poly(ADP-ribose) polymerase 1 (PARP1) and activates caspase-3 to

217 The anti-cancer drug target poly(ADP-ribose) polymerase 1 (PARP1) and its close homologue, PA

218 e found that ZBTB24 associates with poly(ADP-ribose) polymerase 1 (PARP1) and stimulates its auto-pol

219 inhibitor of the DNA repair enzyme poly(ADP-ribose) polymerase 1 (PARP1) for the detection of cancer

220 Poly (ADP-ribose) polymerase 1 (PARP1) has emerged as an attractiv

221 to a variety of cellular stresses, poly(ADP-ribose) polymerase 1 (PARP1) has vital roles in orchestr

222 hermore, inhibition or silencing of poly(ADP-ribose) polymerase 1 (PARP1) inhibits PAR-mediated recru

223 we have found that a host protein, poly(ADP-ribose) polymerase 1 (PARP1), facilitates IFNAR degradat

224 ntain other factors, including PML, poly(ADP-ribose) polymerase 1 (PARP1), ligase IIIalpha, and origi

225 we report that a cellular protein, poly(ADP-ribose) polymerase 1 (PARP1), plays a critical role in m

226 nzyme that catalyses this reaction, poly(ADP-ribose) polymerase 1 (PARP1), were discovered more than

227 replication forks from stalling at poly(ADP-ribose) polymerase 1 (PARP1)-DNA complexes trapped by PA

228 reversibly inhibits the activity of poly(ADP-ribose) polymerase 1, an important anticancer target in

229 CXCL9, CXCL10, CXCL5, ENRAGE, and poly (ADP-ribose) polymerase 1.

230 nsitizers such as poly(adenosine diphosphate ribose) polymerase and mammalian-target-of-rapamycin inh

231 es elevated CD38 NADase and reduced poly(ADP-ribose) polymerase and SIRT1 activities, respectively, a

232 uisitely sensitive to inhibition of poly(ADP-ribose) polymerase has ushered in a new era of research

233 ree steps to produce veliparib 1, a poly(ADP-ribose) polymerase inhibitor.

234 Poly(ADP ribose) polymerase inhibitors (PARPi) have efficacy in t

235 Poly-(ADP-ribose) polymerase inhibitors (PARPi) selectively kill b

236 Poly(ADP-ribose) polymerase inhibitors (PARPi) selectively target

237 form HDR, conferring sensitivity to poly(ADP-ribose) polymerase inhibitors (PARPi).

238 , RITA, AF, and Onc-1 sensitized to poly(ADP-ribose) polymerase inhibitors both in vitro and ex vivo

239 Poly (ADP-ribose) polymerase inhibitors combined with immunotherap

240 e disease, bone stabilizing agents, poly(ADP-ribose) polymerase inhibitors for BRCA mutation carriers

241 ion of the treatment indication for poly(ADP-ribose) polymerase inhibitors to include patients with H

242 s 4 and 6, angiogenesis inhibitors, poly(ADP-ribose) polymerase inhibitors, as well as chemotherapy a

243 tizes cells to DNA crosslinkers and poly(ADP-ribose) polymerase inhibitors.

244 required for HR and resistance to poly (ADP-ribose) polymerase inhibitors.

245 CRPC) and may confer sensitivity to poly(ADP-ribose) polymerase inhibitors.

246 ld change (suppression) of cleaved poly (ADP-ribose) polymerase was greater with palbociclib plus let

247 s is a prominent mechanism of PARP (Poly(ADP-ribose) Polymerase) inhibitor (PARPi) resistance in BRCA

248 e was associated with activation of poly(ADP-ribose) polymerase, which led to consumption of NAD(+).

249 on of LuTate and the small molecule Poly(ADP-ribose) polymerase-1 (PARP) inhibitor, talazoparib led t

250 The success of poly(ADP-ribose) polymerase-1 (PARP-1) inhibitors (PARPi) to trea

251 toxicity in a process dependent on poly (ADP-ribose) polymerase-1 (PARP-1); a NAD(+)-consuming enzyme

252 amage, neuroinflammation, increased poly(ADP-ribose) polymerase-1 (PARP1) activity, single-cell somat

253 ) in cerebellar neurons, supporting poly(ADP-ribose) polymerase-1 upregulation.

254 and the cleavage of caspase-3 and poly (ADP-ribose) polymerase.

255 involve the catalytic activity of poly (ADP-ribose) polymerase.

256 ved CASP8/3 [caspase-8/3] and PARP [poly(ADP-ribose) polymerase] formation).

257 ntaining therapy and inhibitors of poly-(ADP-ribose)-polymerase (PARP)(14,15).

258 Poly(ADP-ribose)-polymerase (PARP)-1 and PARP-2 play an essential

259 age-repair-targeting agents such as poly(ADP-ribose)-polymerase inhibitors.

260 otein kinase, and poly[adenosine diphosphate ribose] polymerase (PARP) 1/2.

261 oxidative stress via regulation of poly [ADP-ribose] polymerase 1 (PARP1).

262 cent inhibitor of poly[adenosine diphosphate-ribose]polymerase 1 (PARP1), which is a nuclear enzyme t

263 Poly-adenosine diphosphate-ribose polymerases (PARPs) promote ADP-ribosylation, a h

264 ccumulation of three test proteins, poly-ADP-ribose polymerases 1 and 2 (PARP1/2) and histone PARylat

265 irtuins and poly-adenosine diphosphate [ADP] ribose polymerases [PARPs]) consumes considerable amount

266 )-converting enzymes, such as CD38, poly-ADP-ribose polymerases, and sirtuins (SIRTs).

267 ) through mechanisms that depend on poly(ADP-ribose) polymerases (PARP) and the catalytic subunit of

268 rms DNA adducts, thereby activating poly(ADP-ribose) polymerases (PARPs) to initiate DNA repair.

269 slational modification catalyzed by poly(ADP-ribose) polymerases (PARPs) using NAD(+) as ADP-ribose d

270 gets in anticancer therapy, are the poly(ADP-ribose) polymerases (PARPs).

271 en suggested to be a target of the poly (ADP-ribose) polymerases Tankyrase 1, and we have found that

272 several NAD-consuming enzymes (e.g. poly(ADP-ribose) polymerases, sirtuins, and others).

273 zymes, including sirtuins, CD38 and poly(ADP-ribose) polymerases.

274 ncluding a subset commonly known as poly(ADP-ribose) polymerases.

275 +) consumers in mammalian cells are poly-ADP-ribose-polymerases (PARPs).

276 And its derived poly-ADP-ribose polymers show increased resistance to human poly(

277 he enzymatic conversion of NAD+ to ADPR (ADP Ribose) products by the SARM1's TIR domain.

278 nd modifications to the 2'-carbon of the UTP ribose ring further decreased rates of excision to an un

279 es Psi-monobisulfite adduction, heat-induced ribose ring opening, and Mg(2+)-assisted reorientation,

280 1' carbon, which resulted in opening of the ribose ring.

281 plane, placing a C5'-H antiperiplanar to the ribose-ring oxygen, which helps stabilize the radical ag

282 Moreover, we show that the mono(ADP-ribose) scars are lost from the chromatin of ARH3-defect

283 H3-mutated patient cells accumulate mono(ADP-ribose) scars on core histones that are a molecular memo

284 ng protein (RBP) to develop a single-protein ribose sensor detectable via a sensitive NMR technique k

285 Here, by using ribose-seq and Ribose-Map techniques, we built and analy

286 fy numerous proteins with mono- and poly(ADP-ribose) signals that are important for the subsequent de

287 and F61S) have reduced activity for free ADP-ribose, similar processing ability against protein-conju

288 ptured in the act of 2'-O methylation of the ribose sugar of the first nucleotide of SARS-CoV-2 mRNA.

289 biological activities of RNAs by biasing the ribose sugar pucker equilibrium toward the C3'-endo conf

290 Ribose sugars that promoted or accommodated A-form helic

291 dify themselves and target proteins with ADP-ribose (termed PARylation).

292 cks and are produced de novo by reduction of ribose to deoxyribose.

293 ranslational modification synthetized by ADP-ribose transferases and removed by poly(ADP-ribose) glyc

294 ose), three pentoses (xylose, arabinose, and ribose), two deoxyhexoses (fucose and rhamnose), and two

295 structurally complex polymer composed of ADP-ribose units that facilitates local chromatin relaxation

296 Dysregulation of cellular ribose uptake can be indicative of metabolic abnormaliti

297 We describe several ribose-utilization systems (RUSs) that are broadly repre

298 Such detection is remarkably specific for ribose, with the minimal background signal from endogeno

299 Poly(ADP-ribose)ylation (PARylation) by PAR polymerase 1 (PARP1)

300 t a compact pseudoknot, dock via an extended ribose zipper and jointly create a binding groove specif