ライフサイエンスコーパス: GAPDH

1 GAPDH and PGK have been shown to interact weakly, but th

2 GAPDH binds to numerous adenine-uridine rich elements (A

3 GAPDH bound Ape1 in the SMC nucleus, and blocking (or ox

4 GAPDH colocalizes with alpha-synuclein in amyloid aggreg

5 GAPDH content was 64, 54, 160, and 138% more abundant in

6 GAPDH down-regulation potentiated H2O2-induced DNA damag

7 GAPDH forms the unstable organoarsenical 1-arseno-3-phos

8 GAPDH is thus a pivotal and central regulator of autopha

9 GAPDH levels were reduced in atherosclerotic plaque SMCs

10 GAPDH nitrosylation was assessed in normal and cholestat

11 GAPDH normally exists in a soluble form; however, follow

12 GAPDH up-regulated Ape1 via a transcription factor homeo

13 GAPDH, a target of NleB during infection, bound to TRAF3

14 GAPDH, by engaging/disengaging glycolysis and through fl

15 cular mass differences of just 4 kDa or 12% (GAPDH, 36 kDa; PS6, 32 kDa) in each of 129 single cells.

16 iver, excess levels of bile salts activate a GAPDH-mediated transnitrosylation cascade that provides

17 Taken together, we identified a GAPDH/PKCdelta signaling switch, which is activated duri

18 trASADH, revealing a tetrameric ASADH with a GAPDH-like fold.

19 PJ34 reduced PARP activity, GAPDH ribosylation, and GAPDH translocation; ameliorated

20 In addition, GAPDH-C1q complexes were observed by transmission electr

21 t the mutation does not significantly affect GAPDH tetramerization as previously proposed.

22 itor of the interaction between deltaPKC and GAPDH and of the resulting phosphorylation of GAPDH by d

23 y during gestation in the mammary gland, and GAPDH binding was nucleotide-specific for the SNAT2 ERE.

24 lated EPRS, Ser(77)-phosphorylated L13a, and GAPDH forms a functional GAIT complex that inhibits tran

25 LDH and GAPDH are part of a complex that promotes H2B synthesis

26 terplay between L1, ANT proteins, MMP14, and GAPDH at the plasma membrane mediates L1-induced neurite

27 d selectively blocks GAPDH nitrosylation and GAPDH-Siah binding, prevents these actions as well as be

28 duced PARP activity, GAPDH ribosylation, and GAPDH translocation; ameliorated muscle fiber injury; an

29 d and identified as elongation factor Tu and GAPDH.

30 Arabidopsis GAPDH activity was reversibly inhibited by nitrosylation

31 Arabidopsis GAPDH was found to be denitrosylated by GSH but not by p

32 properties for the regulation of Arabidopsis GAPDH functions in vivo is discussed.

33 The membrane-associated GAPDH on HeLa cells bound the globular regions of C1q as

34 osphorylating the mitochondrially associated GAPDH at threonine 246 following I/R.

35 sed to analyze 15 candidate HKGs (ACTB, B2M, GAPDH, HPRT1, LDHB, PGK1, RPL4, RPL8, RPL18, RPS9, RPS18

36 ity of C1q to sense both human and bacterial GAPDHs sheds new insights on the role of this important

37 Because GAPDH can be secreted outside the cell where glycosamino

38 tein levels, induced the association between GAPDH and Siah1, and led to GAPDH nuclear translocation.

39 ts demonstrated a strong correlation between GAPDH upregulation and the proto-oncogene c-jun expressi

40 antitatively examine the interaction between GAPDH and PGK, two sequential enzymes in the glycolysis

41 our data reveal important interplay between GAPDH and TRAF3 and suggest a mechanism by which the Nle

42 r Siah1-directed peptides were used to block GAPDH and Siah1 interaction.

43 3466B, which potently and selectively blocks GAPDH nitrosylation and GAPDH-Siah binding, prevents the

44 substantial and selective reduction of both GAPDH activity and expression was achieved using pH resp

45 GSNO was found to trigger both GAPDH nitrosylation and glutathionylation, although nitr

46 osttranscriptional repression of TNF mRNA by GAPDH binding to the TNF 3' untranslated region.

47 ding the C-terminal disulfide is selected by GAPDH.

48 Experiments utilizing C152S GAPDH confirmed that the NO effects are all linked to S-

49 This causes GAPDH to redistribute into the nucleus.

50 vity index of >5000 with respect to cellular GAPDH.

51 eversibly oxidized, functionally compromised GAPDH identifies enhanced vesiculation as a self-protect

52 Concurrent GAPDH nuclear accumulation and ERK inhibition were requi

53 ontrol and an internal manufacturer control, GAPDH (glyceraldehyde-3-phosphate dehydrogenase).

54 Conversely, GAPDH overexpression decreased DNA damage and protected

55 , but not amino acid starvation, cytoplasmic GAPDH is phosphorylated on Ser122 by activated AMPK.

56 (+) T cells also had more abundant cytosolic GAPDH and increased glycolytic reserve.

57 enerating a catalytic advantage in cytosolic GAPDH.

58 Arabidopsis (Arabidopsis thaliana) cytosolic GAPDH isoenzymes GAPC1 and GAPC2 to cadmium-induced stre

59 d with increase in GAPDH activity, decreased GAPDH poly-ADP-ribosylation, and nuclear translocation o

60 osphorylation of GAPDH by deltaPKC decreased GAPDH tetramerization, which corresponded to reduced GAP

61 Conversely, active glycolysis with decreased GAPDH availability in TEM resulted in elevated HIF1alpha

62 or expression of a phosphorylation-defective GAPDH mutant during I/R promotes a reduction in mitochon

63 of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and a major facilitator superfamily protein (ArsJ

64 th glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and phosphoribulokinase, two enzymes of the carbo

65 th glyceraldehyde 3-phosphate dehydrogenase (GAPDH) and phosphoribulokinase.

66 ng glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and Rpa1177, a putative 4-oxalocrotonate tautomer

67 en glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and the E3 ubiquitin ligase, seven in absentia ho

68 he glyceraldehyde-3-phosphate dehydrogenase (GAPDH) as a C1q partner when exposed at the surface of h

69 me glyceraldehyde 3-phosphate dehydrogenase (GAPDH) as an NleB-interacting protein.

70 es glyceraldehyde-3-phosphate dehydrogenase (GAPDH) association with mitochondria and promotes direct

71 it glyceraldehyde 3-phosphate dehydrogenase (GAPDH) by forming a reduction reversible active site dis

72 Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) from human pathogens Staphylococcus aureus and Ps

73 Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) has been found down-regulated or dysfunctional in

74 of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) in human hepatocellular carcinoma (HCC) by using

75 Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is a multifunctional enzyme that has been associa

76 Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is a ubiquitous and abundant protein that partici

77 nt glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is a ubiquitous enzyme involved in the glycolytic

78 Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is an enzyme best known for its role in glycolysi

79 Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is often used as a stable housekeeping marker for

80 nd glyceraldehyde-3-phosphate dehydrogenase (GAPDH) mediates cocaine's transcriptional and behavioral

81 of glyceraldehyde 3-phosphate dehydrogenase (GAPDH) on the sporozoite surface and that GAPDH directly

82 Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) plays a key regulatory function in glucose oxidat

83 nd glyceraldehyde 3-phosphate dehydrogenase (GAPDH) proteins and that the silencing of each of these

84 ng glyceraldehyde-3-phosphate dehydrogenase (GAPDH) silencing with small interfering RNAs (siRNAs) fo

85 nd glyceraldehyde 3-phosphate dehydrogenase (GAPDH) were determined as the important allergens in mus

86 in glyceraldehyde-3-phosphate dehydrogenase (GAPDH) were examined.

87 ar glyceraldehyde-3-phosphate dehydrogenase (GAPDH) with apurinic/apyrimidinic endonuclease 1 (Ape1),

88 at glyceraldehyde 3-phosphate dehydrogenase (GAPDH), a conventional glycolytic enzyme, is a critical

89 ng glyceraldehyde-3-phosphate dehydrogenase (GAPDH), a cytoplasmic enzyme that appears on the cell su

90 Glyceraldehyde-3-phosphate dehydrogenase (GAPDH), an important glycolytic enzyme, has a non-cataly

91 e, glyceraldehyde-3-phosphate dehydrogenase (GAPDH), and enolase, all of which are responsible for en

92 y, glyceraldehyde 3-phosphate dehydrogenase (GAPDH), citrate synthase (CS), and total p38 content.

93 li glyceraldehyde-3-phosphate dehydrogenase (GAPDH), which is not known to bind ATP under native cond

94 of glyceraldehyde-3-phosphate dehydrogenase (GAPDH), which participates in intracellular propagation

95 nd glyceraldehyde-3-phosphate dehydrogenase (GAPDH).

96 me glyceraldehyde-3-phosphate dehydrogenase (GAPDH).

97 er glyceraldehyde-3-phosphate dehydrogenase (GAPDH).

98 es glyceraldehyde-3-phosphate dehydrogenase (GAPDH).

99 te glyceraldehyde 3-phosphate dehydrogenase (GAPDH).

100 rmed the efficacy of DOTAP-SES in delivering GAPDH-siRNA into skin.

101 e identified genes are cell cycle-dependent (GAPDH Associated Cell Cycle, or GACC).

102 sociated autophagy is abolished by depleting GAPDH via shRNA; by the drug CGP3466B, which prevents GA

103 tive inhibition of inappropriately dispersed GAPDH rescues antioxidant capacity.

104 per CTC basis and two statistically distinct GAPDH subpopulations within the patient-derived CTCs.

105 his binding can be reversed by knocking down GAPDH expression or by increasing glycolysis.

106 to mediate specific silencing of endogenous GAPDH gene activity in MCF-7 and A549 cells and compared

107 sequestration/inactivation of the EMP enzyme GAPDH.

108 ated by the binding of the glycolysis enzyme GAPDH to AU-rich elements within the 3' UTR of IFN-gamma

109 hnRNPA1 and PABP1 and the glycolysis enzyme GAPDH.

110 ults in acetylation of the glycolytic enzyme GAPDH and improves the recall function of memory CD8(+)

111 We determined that the glycolytic enzyme GAPDH negatively regulates HIF1A expression by binding t

112 y determined the concentration of the enzyme GAPDH in single U937 cells and HEK 293 cells, and found

113 dependent on the presence of surface-exposed GAPDH.

114 TAT-FLAG GAPDH and/or Siah1-directed peptides were used to block

115 roved by the Institutional Review Board, for GAPDH expression analysis.

116 d that these two residues were essential for GAPDH-mediated activation of TNF receptor-associated fac

117 ich indicated that Ape1 is indispensable for GAPDH-dependent protective effects.

118 olysis by generating NAD(+), a substrate for GAPDH-mediated glycolytic reaction, promoting PDAC cell

119 hich was significantly higher than that from GAPDH-siRNA PBS (p<0.05).

120 Furthermore, GAPDH overexpression reduced HIF1alpha expression and im

121 is reversal only occurs for some genes (e.g. GAPDH and LDH) but not others (e.g. Hsp90 and cyclophili

122 fication of CRX; only the housekeeping gene (GAPDH) demonstrated amplification.

123 enzyme, without forming any glutathionylated GAPDH.

124 In this study, we have employed glycolytic GAPDH from Arabidopsis thaliana as a tool to investigate

125 ther the interplay among glycosaminoglycans, GAPDH, and alpha-synuclein has a role in pathological st

126 leB, EHEC NleB1, and SseK1 glycosylated host GAPDH.

127 How GAPDH binds to these AREs is still unknown.

128 ere transfected with a vector encoding human GAPDH or a control vector.

129 These data identify GAPDH as a TRAF2 signaling cofactor and reveal a virulen

130 un, ERCC1, XPD, XRCC1, Gli1, Gli2, SHH, IHH, GAPDH and alpha-tubulin.

131 e T cell responses to hypoxia and implicates GAPDH as a potential mechanism for controlling T cell fu

132 which temporally correlated with increase in GAPDH activity, decreased GAPDH poly-ADP-ribosylation, a

133 useful in predicting their reaction rates in GAPDH.

134 rk, we showed that glycosaminoglycan-induced GAPDH prefibrillar species accelerate the conversion of

135 that AKT inhibition alone maximally induced GAPDH nuclear accumulation, whereas MEK/ERK inhibition a

136 er injury, metabolic activity, inflammation, GAPDH activity/intracellular localization, and poly-ADP-

137 NleB glycosyltransferase activity inhibited GAPDH-TRAF3 binding, resulting in reduced TRAF3 ubiquiti

138 The 3-BrPA treatment primarily inhibited GAPDH activity (74.5%) compared with its expression (34.

139 oxidative stress, suggesting that inhibiting GAPDH phosphorylation should decrease cell injury.

140 t protein kinase C delta (PKCdelta) inhibits GAPDH-driven mitophagy by phosphorylating the mitochondr

141 poly(ADP-ribose) polymerase, which inhibits GAPDH, shunting early glycolytic intermediates into path

142 he (1)O2 accessibility of residues in intact GAPDH has a profound effect on their photodegradation ki

143 ing rebinding and photoactivation of labeled GAPDH, aldolase, lactate dehydrogenase, and pyruvate kin

144 through overexpression of nuclear-localized GAPDH, increases Sirt1 activation and autophagy.

145 has been widely demonstrated that mammalian GAPDH, in addition to its role in glycolysis, fulfills a

146 vasion without cross-reacting with mammalian GAPDH.

147 ) peptide, an inhibitor of deltaPKC-mediated GAPDH phosphorylation that does not inhibit the phosphor

148 NleB-mediated GAPDH O-GlcNAcylation disrupts the TRAF2-GAPDH interacti

149 H2S modifies GAPDH essentially via sulfhydration in dendrites, which

150 osamine (O-GlcNAc) transferase that modifies GAPDH.

151 in the context of the high resolution native GAPDH structure suggested that oxidation of methionine 4

152 ecause methionine 46 is irrelevant to native GAPDH function, mutation of methionine 46 in models of d

153 a soluble form; however, following necrosis, GAPDH and numerous other intracellular proteins convert

154 le NOS (iNOS) causes buildup of S-nitrosated GAPDH (SNO-GAPDH) in cells, which then inhibits further

155 Nitrosylated GAPDH complexes with the ubiquitin-E3-ligase Siah1 and R

156 GSH fully converted nitrosylated GAPDH to the reduced, active enzyme, without forming any

157 Levels of nitrosylated GAPDH and nitrosylated HDAC2 were increased in cholestat

158 d blocking nuclear transport of nitrosylated GAPDH reduced cholate-induced nitrosylation of HDAC2 and

159 he DISC1 mice, a major hallmark of a nuclear GAPDH cascade that is activated in response to oxidative

160 e stress-associated cascade (e.g., a nuclear GAPDH cascade) points to an underlying condition that ma

161 e pathways synergistically induces a nuclear GAPDH-dependent cell death.

162 n of SMC apoptosis by maintenance of nuclear GAPDH/Ape1 interactions may be a novel therapy to increa

163 Instead, cell death requires nuclear GAPDH accumulation.

164 Thus, we demonstrated that nuclear GAPDH/Ape1 interaction preserved Ape1 activity, reduced

165 Inside the nucleus, GAPDH interacts directly with Sirt1, displacing Sirt1's

166 trosylation; and by mutating cysteine-150 of GAPDH, its site of nitrosylation.

167 SES on mice skin resulted in 63.2%+/-7.7% of GAPDH knockdown, which was significantly higher than tha

168 because disulfide-cross-linked aggregates of GAPDH arise in many disorders and because methionine 46

169 ." Here, free radical-induced aggregation of GAPDH was studied as an in vitro model of nucleocytoplas

170 sing bioluminescence imaging and analysis of GAPDH function and apoptotic markers (caspase-3, caspase

171 effect of high glucose on the association of GAPDH and Siah1.

172 We detected marked augmentation of GAPDH-seven in absentia homolog Siah protein binding in

173 As (siRNAs) followed by Northern blotting of GAPDH, expression of N(pro) had no effect on RNAi silenc

174 ferric, ferrous, and ferrous-CO complexes of GAPDH showed that the heme is bis-ligated with His as th

175 In vitro delivery of GAPDH siRNA by SPACE peptide led to 83.3+/-3.0% knockdow

176 To identify the true instigating event of GAPDH misfolding, we mapped the post-translational modif

177 nes is closely related to high expression of GAPDH in the tumors.

178 fide cross-linking is a prominent feature of GAPDH aggregation, our data show that it is not a primar

179 ecifically with a partially unfolded form of GAPDH and affects the kinetics of folding and unfolding

180 However, extra-glycolytic functions of GAPDH have been described, including regulation of prote

181 ur results revealed that the inactivation of GAPDH by H2O2 induces metabolic levels of glycolysis and

182 Targeted inhibition of GAPDH by using 3-BrPA or shRNA induced apoptosis.

183 Inhibition of GAPDH in highly glycolytic KRAS or BRAF mutant cells lea

184 PDH oligomerization and thus an inhibitor of GAPDH glycolytic activity.

185 psiGAPDH peptide is also an inhibitor of GAPDH oligomerization and thus an inhibitor of GAPDH gly

186 Surprisingly, we found that an inhibitor of GAPDH, 3-bromopyruvic acid (3-BrPa), blocks IFN-gamma, b

187 Percutaneous injection of GAPDH antagonists induces apoptosis and blocks Hep3B tum

188 achieved by using percutaneous injection of GAPDH antagonists-3-bromopyruvate (3-BrPA) or GAPDH-spec

189 Knockdown of GAPDH prevented repression of CYP7A1 by cholate, and blo

190 escued along with a decrease in the level of GAPDH sulfhydration.

191 Nuclear levels of GAPDH increased progressively during gestation in the ma

192 However, the transcriptional levels of GAPDH may be highly up-regulated in some cancers, includ

193 aggregation, and disulfide cross-linking of GAPDH.

194 are inversely linked to the S-nitrosation of GAPDH and (ii) that the NO sensitivity of heme insertion

195 O effects are all linked to S-nitrosation of GAPDH at Cys-152.

196 tocytes, cholate promoted S-nitrosylation of GAPDH and its translocation to the nucleus, accompanied

197 Thus, we found that nitrosylation of GAPDH is not a step toward formation of the more stable

198 S-nitrosylation of GAPDH was assessed using a biotin-switch assay.

199 However, overexpression of GAPDH in these cells prevented the injury-induced RIP3 u

200 es revealed a storage-dependent oxidation of GAPDH at functional Cys152, 156, 247, and His179.

201 ored red blood cells (RBCs) and oxidation of GAPDH at functional residues upon exposure to pro-oxidan

202 Storage-dependent reversible oxidation of GAPDH represents a mechanistic adaptation in stored eryt

203 SMC nucleus, and blocking (or oxidation) of GAPDH active site cysteines suppressed GAPDH/Ape1 intera

204 c acid; Cys to dehydroalanine) oxidations of GAPDH without exogenous supplementation of excess pro-ox

205 The up-regulation pattern of GAPDH positively associated genes in NSCLC is similar to

206 ecently demonstrated that phosphorylation of GAPDH by delta protein kinase C (deltaPKC) inhibits this

207 t with psiGAPDH or direct phosphorylation of GAPDH by deltaPKC decreased GAPDH tetramerization, which

208 APDH and of the resulting phosphorylation of GAPDH by deltaPKC.

209 deltaPKC phosphorylation of GAPDH correlates with increased cell injury following ox

210 increase in the conformational plasticity of GAPDH that likely promotes further oxidation and eventua

211 cell culture is abolished in the presence of GAPDH prefibrillar species.

212 reverses the 2- to 4-fold down-regulation of GAPDH by siRNA in HEK293 and HeLa cells as seen by an ap

213 presented demonstrate that up-regulation of GAPDH positively associated genes is proportional to the

214 Cs by targeting functional thiol residues of GAPDH.

215 1 down-regulation reversed the resistance of GAPDH-overexpressing cells to DNA damage and apoptosis,

216 ascular degeneration, the injured retinas of GAPDH transgenic (Tg) mice and wild-type (WT) littermate

217 r localization, and poly-ADP-ribosylation of GAPDH.

218 To investigate the role of GAPDH in retinal I/R injury-induced neurovascular degene

219 Together, the protective role of GAPDH in retinal neurovascular degeneration after I/R in

220 Thus, the role of GAPDH protofibrils in neuronal proteostasis must be cons

221 Preventing this shift of GAPDH abolishes Sirt1 activation and autophagy, while en

222 -terminal tail of CP12 in the active site of GAPDH stabilizes the binary complex.

223 P-ribosylation, and nuclear translocation of GAPDH.

224 P significantly accelerates the unfolding of GAPDH by selectively stabilizing a transition state that

225 ls of GLUT1 transcripts, and upregulation of GAPDH expression corroborated this finding.

226 as MEK/ERK inhibition alone had no effect on GAPDH localization.

227 d the effect of this interfacial mutation on GAPDH oligomerization by crystallography, small-angle x-

228 any of the 8 responding children since only GAPDH showed amplification.

229 ith respect to the housekeeping genes B2M or GAPDH, mean tumor/normal ratios were 16.1 and 7.5, respe

230 mRNA levels of the housekeeping genes B2M or GAPDH, were over-expressed in 80%, 70% and 40% of the co

231 ith respect to the housekeeping genes B2M or GAPDH.

232 APDH antagonists-3-bromopyruvate (3-BrPA) or GAPDH-specific short hairpin RNA (shRNA).

233 B levels caused by siRNA knockdown of LDH or GAPDH.

234 Irreversibly oxidized GAPDH accumulated in stored erythrocyte membranes and su

235 These data suggest that PA binds to oxidized GAPDH and promotes its cleavage and that the PA and GAPC

236 Phosphorylated GAPDH promotes the accumulation of mitochondria at the p

237 The purified pneumococcal GAPDH protein activated C1 in an in vitro assay unlike t

238 Both recombinant human and pneumococcal GAPDHs interacted avidly with C1q as measured by surface

239 Structural analysis of prefibrillar GAPDH performed by small angle x-ray scattering showed a

240 shRNA; by the drug CGP3466B, which prevents GAPDH nitrosylation; and by mutating cysteine-150 of GAP

241 ich oxidative stress inhibits the protective GAPDH-mediated elimination of damaged mitochondria.

242 Using rational design, we identified pseudo-GAPDH (psiGAPDH) peptide, an inhibitor of deltaPKC-media

243 ccumulated As(V) in the presence of purified GAPDH, D-glceraldehylde 3-phosphate (G3P) and NAD(+) .

244 tramerization, which corresponded to reduced GAPDH glycolytic activity in vitro and ex vivo Taken tog

245 Data analysis demonstrated that up-regulated GAPDH levels are correlated with aberrant gene expressio

246 ing methionine 46 to leucine, which rendered GAPDH highly resistant to free radical-induced aggregati

247 nterface impairs formation of the second RNA-GAPDH complex and leads to changes in the RNA structure.

248 ed for SERPINA3 transcript, and ACTB, RPL19, GAPDH and B2M were used as reference genes.

249 r results, we propose a model for sequential GAPDH binding to RNA via residues located at the dimer a

250 Here we show GAPDH functions as a chaperone, shielding newly released

251 tionally, we find that C3PO hydrolyzes siRNA(GAPDH) at a faster rate than siRNA(Hsp90).

252 s for an approximately 20% increase in siRNA(GAPDH) silencing.

253 -SH or PC12 cells, the introduction of siRNA(GAPDH) [small interfering RNA(glyceraldehyde 3-phosphate

254 bound to C3PO, the hydrolysis rate of siRNA(GAPDH) becomes comparable with siRNA(Hsp90).

255 es and measurements of the reversal of siRNA(GAPDH) to assess the activity of PLCbeta-TRAX complexes

256 C3PO association in cells treated with siRNA(GAPDH) but not siRNA(Hsp90).

257 xpression level due to Trx1 acting as an SNO-GAPDH denitrosylase.

258 NOC-18) and studying changes in cellular SNO-GAPDH levels during and after NO exposure.

259 s Trx1 overexpression greatly diminished SNO-GAPDH buildup and protected heme insertion from NO inhib

260 S) causes buildup of S-nitrosated GAPDH (SNO-GAPDH) in cells, which then inhibits further iNOS matura

261 Trx1 knockdown increased SNO-GAPDH levels in cells, made heme insertion hypersensitiv

262 rtion capacity in association with rapid SNO-GAPDH denitrosation, implying that these processes are l

263 Therefore, Plasmodium-specific GAPDH epitopes may provide novel antigens for the develo

264 Tumor-specific GAPDH inhibition was achieved by using percutaneous inje

265 n) of GAPDH active site cysteines suppressed GAPDH/Ape1 interaction and potentiated apoptosis.

266 rates the therapeutic potential of targeting GAPDH in human HCC.

267 e (GAPDH) on the sporozoite surface and that GAPDH directly interacts with CD68 on the Kupffer cell s

268 We conclude that GAPDH-TNF mRNA binding regulates expression of TNF based

269 RNA immunoprecipitation, we demonstrate that GAPDH-TNF mRNA binding increases when THP-1 monocytes ar

270 We demonstrate that GAPDH-TNF mRNA binding results in posttranscriptional re

271 y into clinical trials by demonstrating that GAPDH expression strongly correlates with c-jun, a proto

272 Here we discovered that GAPDH binds with high affinity to the core ARE from tumo

273 Further, we discovered that GAPDH interacts with the TNF receptor-associated factor

274 In vitro experiments indicate that GAPDH siRNAs conjugated with SPACE-EGF can significantly

275 glycans are present, it seems plausible that GAPDH protofibrils could be assembled in the extracellul

276 They propose that GAPDH catalyzes the formation of 1-arseno-3-phosphoglyce

277 We demonstrate that a mutation at the GAPDH dimer interface impairs formation of the second RN

278 In contrast, the GAPDH Tg mice showed resistance to all of these injury-i

279 tarting copies) and RNA transcripts from the GAPDH housekeeping gene (5.45 ng total mouse embryonic s

280 PCR amplification of the GAPDH gene was demonstrated at a speed of 8.67 s/cycle.

281 we obtained the first all-atom model of the GAPDH protofibril, which was validated by cross-linking

282 hanges are localized along the P axis of the GAPDH tetramer, suggesting that this region is important

283 s article we examined the involvement of the GAPDH/Siah1 interaction in human retinal pericyte (hRP)

284 indings demonstrate that dissociation of the GAPDH/Siah1 pro-apoptotic complex can block high glucose

285 0.3 and a 2:1 prevalent stoichiometry of the GAPDH:PGK complex.

286 with SPACE-EGF can significantly reduce the GAPDH concentration in B16 cells, and c-Myc siRNAs can c

287 We reduced the GAPDH levels in H35 cells with small interfering RNAs.

288 ta protein kinase C (deltaPKC) inhibits this GAPDH-dependent mitochondrial elimination.

289 fic to aerobic glycolysis where flux through GAPDH, the enzyme separating lower and upper glycolysis,

290 bacterial CP12 types are unlikely to bind to GAPDH.

291 ty, and redox sensitivity of heme binding to GAPDH are consistent with it performing heme sensing or

292 ociation between GAPDH and Siah1, and led to GAPDH nuclear translocation.

293 pression is shown as a log ratio relative to GAPDH mRNA (log 2 (-(Ct))).

294 ted GAPDH O-GlcNAcylation disrupts the TRAF2-GAPDH interaction to suppress TRAF2 polyubiquitination a

295 also found that EHEC NleB1 glycosylated two GAPDH arginine residues, Arg(197) and Arg(200), and that

296 Thus, our findings reveal a mechanism where GAPDH sulfhydration appears to be a physiologic determin

297 ompared with its expression (34.3%), whereas GAPDH shRNA inhibited both activity (60.6%) and expressi

298 allow the unequivocal assessment of whether GAPDH aggregation influences disease progression.

299 anonical cyanobacterial CP12 in complex with GAPDH suggests that some of the newly identified cyanoba

300 s in some cancers are highly correlated with GAPDH up-regulation.