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 and PRK are coregulated by the redox state of a co

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

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

5 GAPDH catalyzes the reduction step of the CB cycle with

6 GAPDH colocalizes with alpha-synuclein in amyloid aggreg

7 GAPDH down-regulation potentiated H2O2-induced DNA damag

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

9 GAPDH is thus a pivotal and central regulator of autopha

10 GAPDH levels were reduced in atherosclerotic plaque SMCs

11 GAPDH nitrosylation was assessed in normal and cholestat

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

13 GAPDH up-regulated Ape1 via a transcription factor homeo

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

15 GAPDH, Actin, and EF1alpha were among the most stable HK

16 GAPDH, by engaging/disengaging glycolysis and through fl

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

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

19 nd examined whether expressing WT GAPDH or a GAPDH variant defective in heme binding recovers heme de

20 DH by suppressing Src signaling or through a GAPDH Tyr41 mutation impairs its response to DNA damage.

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

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

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

24 DH influences substrate accessibility of all GAPDH active sites in the binary and ternary inhibited c

25 reference genes (beta-ACT, ArgK, EF1-alpha, GAPDH, RPL12, RPS23, alpha-TUB, 18S and 28S) in A. eugen

26 ACTB and GAPDH, the most frequent calibrators in real-time RT-qPC

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

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

29 y direct targeting of c-Myc, Akt, IGF1R, and GAPDH expression.

30 tein interaction studies showed that LDH and GAPDH can form a leaky channeling complex only at the li

31 between the NAD(H) binding sites on LDH and GAPDH tetramers can merge in the LDH-GAPDH complex.

32 showed that LDH activity with free NADH and GAPDH-NADH complex always take place in parallel.

33 PDI, ATP synthase subunit alpha, PRDX1, and GAPDH are associated with anti-proliferation, induction

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

35 d and identified as elongation factor Tu and GAPDH.

36 and RPS23), all temperatures (alpha-TUB and GAPDH), starvation (RPL12 and alpha-TUB), and dsRNA expo

37 Arabidopsis GAPDH activity was reversibly inhibited by nitrosylation

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

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

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

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

42 Because GAPDH can be secreted outside the cell where glycosamino

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

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

45 We also studied interaction between GAPDH and sGCbeta in cells and their complex formation a

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

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

48 show how CP12 modulates the activity of both GAPDH and PRK.

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

50 This causes GAPDH to redistribute into the nucleus.

51 ng in live cells, assessed how lowering cell GAPDH expression impacts heme delivery, and examined whe

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

53 very to apo-sGCbeta correlates with cellular GAPDH expression levels and depends on the ability of GA

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

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

56 Conversely, GAPDH overexpression decreased DNA damage and protected

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

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

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

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

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

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

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

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

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

66 nd glyceraldehyde 3-phosphate dehydrogenase (GAPDH) are essential CB-cycle enzymes that control subst

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

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

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

70 Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is a key enzyme involved in energy metabolism.

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

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

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

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

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

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

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

78 D-glyceraldehyde-3-phosphate dehydrogenase (GAPDH) to L-lactate Dehydrogenase (LDH) using enzymes fr

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

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

81 ), glyceraldehyde-3 phosphate dehydrogenase (GAPDH), 40 S ribosomal protein S9 (RpS9) and ubiquitin-c

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

83 of glyceraldehyde-3-phosphate dehydrogenase (GAPDH), a critical node in the glycolysis pathway.

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

85 ts glyceraldehyde-3-phosphate dehydrogenase (GAPDH), a rate-controlling glycolytic enzyme, during the

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

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

88 ), glyceraldehyde-3-phosphate dehydrogenase (GAPDH), hypoxanthine-guanine phosphoribosyltransferase 1

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

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

91 te glyceraldehyde 3-phosphate dehydrogenase (GAPDH).

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

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

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

95 e, glyceraldehyde-3-phosphate dehydrogenase (GAPDH).

96 m; glyceraldehyde 3-phosphate dehydrogenase (GAPDH; a glycolysis enzyme); ATP levels; and cytoplasmic

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

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

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

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

101 f these candidates, including ACT, EF1alpha, GAPDH, HSP60, HSP70, alphaTUB, UBC, RPS18, ATPase and GS

102 Indeed, iodoacetate (IA), an effective GAPDH inhibitor, caused about 70% drop in MDA-MB-231 cel

103 ALDOA, ALDOC, PGK1, PGM1, PGAM1, ENO1, ENO2, GAPDH, TPI1, LDHA, and LDHB) in the glycolytic pathway w

104 sequestration/inactivation of the EMP enzyme GAPDH.

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

106 hnRNPA1 and PABP1 and the glycolysis enzyme GAPDH.

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

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

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

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

111 genes is really quite huge (e.g. 44 fold for GAPDH in one data set), suggesting that the cure (of usi

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

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

114 genase-catalyzed regeneration of NAD(+) from GAPDH-generated NADH because an increased NADH:NAD(+) ra

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

116 Furthermore, GAPDH knockdown dramatically decreases BER efficiency an

117 Furthermore, GAPDH overexpression reduced HIF1alpha expression and im

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

119 DNA (cDNA) on the GMR for the reference gene GAPDH.

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

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

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

123 How GAPDH binds to these AREs is still unknown.

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

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

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

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

128 olytic signaling pathway proteins, including GAPDH and G6PD.

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

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

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

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

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

134 ause an increased NADH:NAD(+) ratio inhibits GAPDH.

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

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

137 hether heme delivery to apo-sGCbeta involves GAPDH.

138 of nrITS, GAPDH and TUB2 for CASC, and ITS, GAPDH, CAL, ACT, TUB2, APN2, ApMat and GS genes for CGSC

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

140 NAD(H)-channeling within the LDH-GAPDH complex can be an extension of NAD(H)-channeling w

141 LDH and GAPDH tetramers can merge in the LDH-GAPDH complex.

142 e overlap between the off-rates for the LDH-(GAPDH-NADH) complex and the GAPDH-NADH complex.

143 In the case of a transient LDH-(GAPDH-NADH) complex, the relative contribution from the

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

145 In resting macrophages, GAPDH binds to and suppresses translation of several inf

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

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

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

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

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

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

156 ompounds that decrease glutathione normalize GAPDH-Rheb complexes and mTOR activity in S47 cells.

157 multi-locus phylogenetic analyses of nrITS, GAPDH and TUB2 for CASC, and ITS, GAPDH, CAL, ACT, TUB2,

158 Nuclear GAPDH is recruited to DNA lesions and associates with DN

159 Nuclear GAPDH promotes Pol beta polymerase activity and increase

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

161 Instead, cell death requires nuclear GAPDH accumulation.

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

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

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

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

166 ression levels and depends on the ability of GAPDH to bind intracellular heme, that apo-sGCbeta assoc

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

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

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

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

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

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

173 e is low, supported by reduced expression of GAPDH encoding the catalysing enzyme for this step.

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

175 mechanistic insight into the new function of GAPDH in DNA repair and suggest a potential therapeutic

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

177 Blocking the nuclear import of GAPDH by suppressing Src signaling or through a GAPDH Ty

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

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

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

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

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

183 Importantly, the knockdown of GAPDH in colon cancer SW480 cells and xenograft models e

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

185 improperly cropped, leading to four lanes of GAPDH endogenous loading controls for five lanes of PD-L

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

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

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

189 aggregation, and disulfide cross-linking of GAPDH.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

204 This phosphorylation of GAPDH is essential for its nuclear translocation and DNA

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

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

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

208 Cs by targeting functional thiol residues of GAPDH.

209 1 down-regulation reversed the resistance of GAPDH-overexpressing cells to DNA damage and apoptosis,

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

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

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

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

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

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

216 ls; this is due to an altered redox state of GAPDH in S47 cells that inhibits its ability to bind and

217 ial homologs, we solve crystal structures of GAPDH with different cofactors and CP12 bound, and the t

218 P-ribosylation, and nuclear translocation of GAPDH.

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

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

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

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

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

224 ith respect to the housekeeping genes B2M or GAPDH.

225 Irreversibly oxidized GAPDH accumulated in stored erythrocyte membranes and su

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

227 d under DNA damage stress and phosphorylates GAPDH at Tyr41.

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

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

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

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

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

233 en heme binds sGCbeta, and that the purified GAPDH-heme complex binds to apo-sGCbeta and transfers it

234 nly written as 'GAPHD'; it should have read 'GAPDH'.

235 Recently, GAPDH has been suggested to have extraglycolytic functio

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

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

238 st time malonylation as a signal, regulating GAPDH mRNA binding to promote inflammation.

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

240 2d, the Western blot panels representing GAPDH endogenous loading controls were improperly croppe

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

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

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

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

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

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

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

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

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

250 Upon LPS stimulation, GAPDH undergoes malonylation on lysine 213, leading to i

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

252 KH-1E hairless mice significantly suppressed GAPDH expression with no clinical evidence of toxicity.

253 A synthetic GAPDH single-stranded DNA (ssDNA) standard was used to c

254 vely for 15 and 18-cycle amplified synthetic GAPDH PCR products.

255 12), sex (RPS23 and RPL12), low temperature (GAPDH and alpha-TUB), high temperature (alpha-TUB and RP

256 nt cofactors and CP12 bound, and the ternary GAPDH-CP12-PRK complex by electron cryo-microscopy, we r

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

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

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

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

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

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

263 Given that GAPDH displays properties of a heme chaperone for induci

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

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

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

267 ering, and MS-based analyses, we report that GAPDH and NAMPT form a stable complex that is essential

268 Our results revealed that GAPDH and EF2 are the most uniformly expressed genes acr

269 ree NADH concentration is negligible and the GAPDH-NADH complex is dominant.

270 tes for the LDH-(GAPDH-NADH) complex and the GAPDH-NADH complex.

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

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

273 repair, but the underlying mechanism for the GAPDH response to DNA damage remains unclear.

274 rangement leading to CD4 expression from the GAPDH promoter.

275 wo DNA double-strand breaks, one each in the GAPDH and CD4 genes, that caused a deletion rearrangemen

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

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

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

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

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

281 0.3 and a 2:1 prevalent stoichiometry of the GAPDH:PGK complex.

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

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

284 Studying the GAPDH-CD4 deletion rearrangement in multiple cell lines,

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

286 We observed that this GAPDH-CD4 deletion rearrangement activates CD4+ cells th

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

288 bacterial CP12 types are unlikely to bind to GAPDH.

289 We find that CP12 binding to GAPDH influences substrate accessibility of all GAPDH ac

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

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

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

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

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

295 s of these results, we propose a model where GAPDH obtains mitochondrial heme and then forms a comple

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

297 lular heme, that apo-sGCbeta associates with GAPDH in cells and dissociates when heme binds sGCbeta,

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

299 ults indicate that by forming a complex with GAPDH, NAMPT can translocate to the nucleus and thereby

300 tribution, and family composition (e.g. with GAPDH and ribosomal proteins being the largest families)

301 delivery, and examined whether expressing WT GAPDH or a GAPDH variant defective in heme binding recov