ライフサイエンスコーパス: Warburg

1 Warburg effect is a hallmark of cancer manifested by con

2 Warburg effect linked to cognitive-executive deficits in

3 Warburg Micro syndrome (WARBM1) is a severe autosomal re

4 Warburg Micro syndrome and Martsolf syndrome are heterog

5 acitor, an electron-transfer resistor, and a Warburg impedance around each electrode, was introduced

6 lic ATP/ADP, activation of glycolysis, and a Warburg metabolic phenotype in proliferating cells.

7 The spectra contain a Warburg feature from which the concentration and diffusi

8 metabolism in MDA-MB-231 cells, which have a Warburg metabolic phenotype; these experiments indicated

9 e injury, which activates AMPK and induces a Warburg-like glycolysis in satellite cells.

10 AMPKalpha1(-/-) MuSCs showed a Warburg-like switch of their metabolism to higher glycol

11 This metabolic reprogramming toward a Warburg phenotype occurred as a result of contact with p

12 ls by longwave UVA radiation, possibly via a Warburg-like effect, promotes melanoma invasiveness.

13 Hence, cancer cells allocate Warburg metabolism to their corrupted CAFs, exploiting t

14 Although Warburg effect is considered a peculiarity critical for

15 entifies MPI as a novel regulator of p53 and Warburg metabolism.

16 ulin-VDAC interaction by erastin antagonizes Warburg metabolism and restores oxidative mitochondrial

17 ndicated that CO transiently induces an anti-Warburg effect by rapidly fueling cancer cell bioenerget

18 metabolic requirement, a phenomenon known as Warburg effect.

19 e beyond oxidative needs, a paradox noted by Warburg almost a century ago.

20 As noted by Warburg, many cancer cells depend on the consumption of

21 aerobic glycolysis was initially proposed by Warburg to be due to mitochondrial impairment, recent st

22 ain a growth advantage through the so-called Warburg effect by shifting glucose metabolism from oxida

23 abolism to aerobic glycolysis, the so-called Warburg effect.

24 arity to the glycolytic phenotype in cancer (Warburg effect).

25 Loss-of-function mutations in TBC1D20 cause Warburg Micro syndrome 4 (WARBM4), which is an autosomal

26 ostate tumors that did not exhibit a classic Warburg phenotype were equally sensitive.

27 may be an approach for altering the classic Warburg effect characteristic of aberrant metabolism in

28 The classic Warburg effect described in macrophages infected by Myco

29 CEFs (Ski-CEFs) do not display the classical Warburg effect.

30 Despite being known for decades (Warburg effect), the molecular mechanisms regulating thi

31 uman neurological and developmental disorder Warburg Micro syndrome.

32 y an important mechanism by which Wnt-driven Warburg metabolism directs the use of glucose for cancer

33 duced HIF transcriptional activity and drove Warburg metabolic reprogramming, coupling AMPK-dependent

34 finite-length diffusion (OFLD) or the finite Warburg circuit, but with the boundary conditions modifi

35 finite-length diffusion (OFLD) or the finite Warburg circuit, but with the boundary conditions modifi

36 e topology function is similar to the finite Warburg impedance in certain limits.

37 te kinase M2 (PKM2), a glycolytic enzyme for Warburg effect, is strongly upregulated in BC.

38 Having originated from Warburg's seminal observation of aerobic glycolysis in t

39 aerobic production of lactate from glucose (Warburg effect), extensive glutamine utilization and imp

40 ryos transiently exhibit aerobic glycolysis (Warburg effect), a metabolic adaptation also observed in

41 ng in Akt activation and aerobic glycolysis (Warburg effect), associated with ulceration.

42 both animal models and patients, glycolysis (Warburg effect) is also an early manifestation of CRPC t

43 metabolic genes associated with glycolysis (Warburg effect), fatty acid metabolism (lipogenesis, oxi

44 It is thought that cancer cells engage in Warburg metabolism to meet intrinsic biosynthetic requir

45 HIF1alpha, but not HIF2alpha, induced Warburg-like metabolism characterized by increased glyco

46 llectively, these findings indicate that key Warburg effect enzymes play a central role in mediating

47 ) as a metabolic enzyme required to maintain Warburg metabolism in zebrafish embryos and in both prim

48 mor growth by suppressing the HIF-1-mediated Warburg effect and angiogenesis.

49 e for the pyruvate kinase M2 (PKM2)-mediated Warburg effect, namely aerobic glycolysis, in the regula

50 ts another hallmark of tumorigenesis, namely Warburg metabolism.

51 nce of a synaptic activity-mediated neuronal Warburg effect that may promote mitochondrial homeostasi

52 the other subpopulations, these hypoxic "non-Warburg" cells had highest oxygen consumption rates and

53 These respiring ("non-Warburg") cells were previously thought not to play a ke

54 The clinical features of Warburg Micro syndrome patients with RAB3GAP1 or RAB3GAP

55 of the loss of cavin-3 include induction of Warburg metabolism (aerobic glycolysis), accelerated cel

56 ation analysis revealed a uniform pattern of Warburg effect mutations influencing prognosis across al

57 t in vitro proof of concept that reversal of Warburg effect might be a novel therapy for GBM.

58 Otto Warburg discovered that cancer cells exhibit a high rate

59 Otto Warburg's theory on the origins of cancer postulates tha

60 In 1956, Otto Warburg proposed that the origin of cancer cells was clo

61 Decades ago, Otto Warburg observed that cancers ferment glucose in the pre

62 Although Otto Warburg first described aerobic glycolysis in cancer cel

63 Although Otto Warburg observed aerobic glycolysis nearly 90 years ago,

64 n 80 years ago, the renowned biochemist Otto Warburg described how cancer cells avidly consume glucos

65 ucose flux, a phenomenon first noted by Otto Warburg approximately 80 years ago and currently exploit

66 aerobic glycolysis, was first noted by Otto Warburg more than 75 yr ago.

67 itions, has been shown first in 1926 by Otto Warburg.

68 Despite Otto Warburg's 1931 Nobel Prize for his work affirming the ro

69 t glycolysis even in the presence of oxygen (Warburg effect) and use of glutamine for increased biosy

70 3 and induction of the glycolytic phenotype (Warburg effect).

71 ll of origin, thereby inhibiting a potential Warburg effect.

72 -dependent HIF activation and the subsequent Warburg metabolic transformation.

73 n part, been attributable to the notion that Warburg's description of a relation between a shift to g

74 pers by Chang et al. and Ho et al. show that Warburg metabolism enables tumor cells to restrict gluco

75 uncoupling, it is tempting to speculate that Warburg's observations may indeed be the result of the p

76 We demonstrated that "Warburg effect" is not modulated in the initial stage of

77 The Warburg effect adapts cells to tumor environments and is

78 The Warburg effect contributes to cancer progression and is

79 The Warburg effect defines a pro-oncogenic metabolism switch

80 The Warburg effect describes an increase in aerobic glycolys

81 The Warburg effect is a chronic increase in glycolytic index

82 The Warburg effect is a tumorigenic metabolic adaptation pro

83 The Warburg effect, a common metabolic alteration of most tu

84 Described decades ago, the Warburg effect of aerobic glycolysis is a key metabolic

85 suppressor in PCa that prevents EMT and the Warburg effect, and indicates that ABHD5 is a potential

86 insights into the regulation of VEGF and the Warburg effect, which describes the propensity for cance

87 ion, activation of the PI3K pathway, and the Warburg effect.

88 tures of tumor cells: glutaminolysis and the Warburg effect.

89 intellectual disability, apoptosis, and the Warburg effect.

90 factor-1alpha's downstream processes and the Warburg effect; induction of autophagy; augmentation of

91 asis, immune escape, tumor angiogenesis, the Warburg effect and oncogene addiction and has been valid

92 This phenomenon is known as the Warburg effect and is considered as one of the most fund

93 Known as the Warburg effect in the context of cancer growth, this phe

94 etabolic phenotype of cancer is known as the Warburg effect or aerobic glycolysis that consists of in

95 umption and lactate production, known as the Warburg effect, are almost universal hallmarks of solid

96 Drastic metabolic alterations, such as the Warburg effect, are found in most if not all types of ma

97 oxygen-rich environment, referred to as the Warburg effect, has been noted as a nearly universal bio

98 etabolism of most solid tumors, known as the Warburg effect, is associated with resistance to apoptos

99 Reversing this phenomenon, known as the Warburg effect, may offer a generalized anticancer strat

100 Historically known as the Warburg effect, this altered metabolic phenotype has lon

101 eference of aerobic glycolysis, known as the Warburg effect, which facilitates cell proliferation.

102 he degree of aerobic glycolysis-known as the Warburg effect-is thus predicted to represent an adaptat

103 ase in aerobic glycolysis, also known as the Warburg effect.

104 onditions, a hallmark of cancer known as the Warburg effect.

105 f mitochondrial function and is known as the Warburg effect.

106 energy production, a phenomenon known as the Warburg effect.

107 tic state of aerobic glycolysis known as the Warburg effect.

108 n to generate ATP, a phenomenon known as the Warburg effect.

109 in cancer cells, commonly referred to as the Warburg effect.

110 ential use of glucose, which is known as the Warburg effect.

111 oA in the presence of oxygen is known as the Warburg effect.

112 ation in the cell, a phenomenon known as the Warburg effect.

113 lysis for ATP production, referred to as the Warburg effect.

114 is abundant, a phenomenon referred to as the Warburg effect.

115 erobic glycolysis, a phenomenon known as the Warburg effect.

116 increase in aerobic glycolysis known as the Warburg effect.

117 eir energy supply, a phenomenon known as the Warburg effect.

118 toward aerobic glycolysis, also known as the Warburg effect.

119 on to aerobic glycolysis, referred to as the Warburg effect.

120 presented by a glycolytic shift known as the Warburg effect.

121 gulate non-cell-cycle functions, such as the Warburg effect.

122 s the glycolytic adaptation described as the Warburg Effect.

123 utrients for biomass production known as the Warburg effect.

124 as an increased glycolytic rate known as the Warburg effect.

125 lysis-driven metabolic program, known as the Warburg effect; however, few have been identified.

126 to the altered metabolic state known as the Warburg effect; one metabolic pathway, highly dependent

127 te despite abundant oxygen availability (the Warburg effect).

128 Because the Warburg effect and hypoxia are frequently seen in human

129 udy of tumor metabolism above and beyond the Warburg effect.

130 tralization of the acidosis generated by the Warburg glycolytic shift.

131 rease in glycolytic index, quantified by the Warburg index.

132 melanoma cells that are not described by the Warburg phenomenon.

133 ilability of oxygen, a phenomenon called the Warburg effect, is important for cancer cell growth.

134 imiting glycolytic enzyme known to cause the Warburg effect.

135 ated aerobic glycolysis in cancer cells (the Warburg effect) may be attributed to respiration injury

136 ism and is up-regulated in cancer cells (the Warburg Effect).

137 Therefore, similar to cancer cells, the Warburg effect is necessary for maintaining KSHV latentl

138 This metabolic change, the Warburg effect, was one of the first alterations in canc

139 tp53 GOF and a mechanism for controlling the Warburg effect.

140 tion in aerobic glycolysis counteracting the Warburg effect of cancer cells.

141 3 decreased proliferation and diminished the Warburg-like phenotype in SIRT3-deficient cell lines, an

142 GT1A_i2 proteins in HT115 cells enforced the Warburg effect, with a higher glycolytic rate at the exp

143 ic metabolism in an aerobic environment, the Warburg effect, but the explanation for this preference

144 regulating energy metabolism, especially the Warburg effect, and antioxidant defense, and thus the fu

145 In this Essay, we re-examine the Warburg effect and establish a framework for understandi

146 All melanoma cells exhibited the Warburg phenomenon; they used more glucose and produced

147 tions and therefore do not fully explain the Warburg effect.

148 her innate or acquired, helps to explain the Warburg phenomenon.

149 conserved mammalian UCPs may facilitate the Warburg effect in the absence of permanent respiratory i

150 h HIF-1alpha and N-Myc are essential for the Warburg effect (aerobic glycolysis) in neuroblastomas by

151 tion provides a possible explanation for the Warburg effect and offers new clues as to how p53 might

152 a lack of a quantitative explanation for the Warburg effect in cancer.

153 rkin deficiency is a novel mechanism for the Warburg effect in tumors.

154 ory axis is an important determinant for the Warburg effect in tumour cells and provide a mechanistic

155 IF1, revealing a potential mechanism for the Warburg effect, an elevation in aerobic glycolytic metab

156 ruvate kinase M2 (PKM2) is essential for the Warburg effect.

157 increased glycolysis for ATP generation (the Warburg effect) due in part to mitochondrial respiration

158 ignant cells exhibit aerobic glycolysis (the Warburg effect) and become dependent on de novo lipogene

159 Aerobic glycolysis (the Warburg effect) is a metabolic hallmark of activated T c

160 e data indicate that aerobic glycolysis (the Warburg effect) is not an intrinsic component of the tra

161 r cells rely more on aerobic glycolysis (the Warburg effect) than mitochondrial oxidative phosphoryla

162 ost tumour cells use aerobic glycolysis (the Warburg effect) to support anabolic growth and evade apo

163 s glucose uptake and aerobic glycolysis; the Warburg effect.

164 It remains a matter of debate as to how the Warburg effect is regulated during tumor progression.

165 Here we explore how the Warburg effect might be linked to inflammation and infla

166 It is unclear how the Warburg effect that exemplifies enhanced glycolysis in t

167 ossible to directly and indirectly image the Warburg effect with hyperpolarized (13)C-pyruvate and (1

168 umarate and succinate may play a role in the Warburg effect providing that appropriate relative conce

169 Notwithstanding the renewed interest in the Warburg effect, cancer cells also depend on continued mi

170 2, a fetal anabolic enzyme implicated in the Warburg effect, was activated by insulin in vivo and in

171 the lactate produced by cancer cells in the Warburg effect.

172 Larger increases in the Warburg elements and cell impedance are also found with

173 c alterations in cancer cells, including the Warburg effect that describes an increased glycolysis in

174 rofound metabolic alterations, including the Warburg effect wherein cancer cells oxidize a decreased

175 similar metabolic alterations, including the Warburg effect.

176 ing oxygen consumption, thereby inducing the Warburg effect.

177 er cells, SR9243 significantly inhibited the Warburg effect and lipogenesis by reducing glycolytic an

178 ion due, in part, to respiration injury (the Warburg effect).

179 provide a novel mechanistic insight into the Warburg effect and explain how metabolic alteration in c

180 This is the Warburg effect, which provides substrates for cell growt

181 ngly, the molecular mechanisms that link the Warburg effect with the suppression of apoptosis are not

182 A new parameter measuring the Warburg effect (the ratio of lactate production flux to

183 thod has proven highly useful to monitor the Warburg effect in cancer, through MR detection of increa

184 ealing how CD44 could be a gatekeeper of the Warburg effect (aerobic glycolysis) in cancer cells and

185 We propose that KSHV induction of the Warburg effect adapts infected cells to tumor microenvir

186 ese results support an interpretation of the Warburg effect and glutamine addiction as features of a

187 duced kinase 1 (PINK1) is a regulator of the Warburg effect and negative regulator of glioblastoma gr

188 This results in the reversal of the Warburg effect and the inhibition of breast cancer cell

189 wild-type p53 prevents manifestation of the Warburg effect by controlling Pdk2.

190 remutation, we evaluated the presence of the Warburg effect in peripheral blood mononuclear cells (PB

191 M1 (adult) isoform leads to reversal of the Warburg effect, as judged by reduced lactate production

192 Imaging of the Warburg effect, which is the principal but not the sole

193 ess, enabling non-invasive monitoring of the Warburg effect.

194 it a glycolytic phenotype reminiscent of the Warburg effect.

195 that p53 status is a key determinant of the Warburg effect.

196 der aerobic conditions characteristic of the Warburg effect.

197 oxia can explain some characteristics of the Warburg effect.

198 vide new insights into the regulation of the Warburg effect.

199 ropensity of AKT to modulate elements of the Warburg effect.

200 se M2 isoform (PKM2), a key regulator of the Warburg effect.

201 n and supporting a localized reversal of the Warburg shift toward aerobic glycolysis.

202 DER exerted no effect on the Warburg pattern of gene expression or on other aspects o

203 tween two models of carcinogenesis, one (the Warburg hypothesis) based on increased energy production

204 Aerobic glycolysis or the Warburg Effect (WE) is characterized by the increased me

205 Aerobic glycolysis or the Warburg effect links the high rate of glucose fermentati

206 y a preference for aerobic glycolysis or the Warburg effect, and the cells resist matrix detachment-i

207 ed role of PKM2 in aerobic glycolysis or the Warburg effect, its non-metabolic functions remain elusi

208 e of ATP to fuel cellular proliferation (the Warburg effect).

209 nhances LDH-A enzyme activity to promote the Warburg effect and tumor growth by regulating the NADH/N

210 osphorylation activates PDHK1 to promote the Warburg effect and tumor growth.

211 ert to regulate PDC activity and promote the Warburg effect.

212 ert to regulate PDC activity and promote the Warburg effect.

213 h cancer-specific splicing that promotes the Warburg effect and breast cancer progression.

214 itochondrial membrane potential-promotes the Warburg effect in leukemia cells, and may contribute to

215 mediated PKM2 dephosphorylation promotes the Warburg effect, cell proliferation and brain tumorigenes

216 is an anticancer agent that can reverse the Warburg effect by inhibiting a key enzyme in cancer cell

217 ion, agents that scavenge ROS or reverse the Warburg effect prevent the transformation and malignant

218 mented that methylene blue (MB) reverses the Warburg effect evidenced by the increasing of oxygen con

219 estoration of Parkin expression reverses the Warburg effect in cells.

220 rylation, restores PDC activity, reverts the Warburg metabolic phenotype, decreases normoxic HIF-1alp

221 t mechanistically connects aberrant ROS, the Warburg effect, and carcinogenesis.

222 ecreased HIF-1alpha expression, shifting the Warburg phenotype to OXPHOS and inhibiting glioblastoma

223 43B osteosarcoma (OS) cell lines showing the Warburg effect in comparison with actively respiring Sao

224 that tumour-associated mutp53 stimulates the Warburg effect in cultured cells and mutp53 knockin mice

225 Mutp53 stimulates the Warburg effect through promoting GLUT1 translocation to

226 gely abolishes mutp53 GOF in stimulating the Warburg effect.

227 se findings imply that efforts to target the Warburg effect for cancer prevention are mechanistically

228 ize the potential benefit from targeting the Warburg effect.

229 lls benefit from this phenomenon, termed the Warburg effect, have renewed discussions about its exact

230 ose metabolism in cancer cells is termed the Warburg effect, which describes the propensity of most c

231 tochondria (OXPHOS), a phenomenon termed the Warburg effect, which is a general feature of oncogenesi

232 aerobic glycolysis, a phenomenon termed the Warburg effect.

233 aerobic glycolysis, a phenomenon termed "the Warburg effect." Aerobic glycolysis is an inefficient wa

234 Here I show that the Warburg effect can be explained as a form of cooperation

235 This study reveals a mechanism that the Warburg effect is regulated by CHIP through its function

236 izing higher-grade tumors, we found that the Warburg effect is relatively more prominent at the expen

237 These results suggest that the Warburg effect, more specifically, diminished glucose ox

238 that regulate the PI3K pathway, and thus the Warburg effect, are elusive.

239 ies document a therapeutical approach to the Warburg effect and demonstrate that oxidative stress and

240 s miR-199a maturation to link hypoxia to the Warburg effect and suggest a promising therapeutic strat

241 tivation of either Akt or c-Myc leads to the Warburg effect as indicated by increased cellular glucos

242 the glycolytic pathway and contribute to the Warburg effect in cancer cells.

243 ase (PKM2), a key enzyme contributing to the Warburg effect in cancer, is significantly induced in DM

244 mitochondrial function, contributing to the Warburg effect in cancer.

245 How ACAT1 is "hijacked" to contribute to the Warburg effect in human cancer remains unclear.

246 by DERL3 epigenetic loss contributes to the Warburg effect in the studied cells and pinpoints a subs

247 We suggest that, similar to the Warburg effect observed in tumor cells, starving yeast a

248 report that loss of PINK1 contributes to the Warburg effect through ROS-dependent stabilization of hy

249 Due to the Warburg effect, cancerous colonocytes rely on glucose as

250 This bioenergetic shift is similar to the Warburg effect, the metabolic signature of cancer cells.

251 lar composition of PDC and contribute to the Warburg effect.

252 s a new molecular player contributing to the Warburg effect.

253 iferating cancer cells and contribute to the Warburg effect.

254 es mitochondrial respiration, leading to the Warburg effect.

255 ten develop an acidic environment due to the Warburg effect.

256 mmHg, ATP levels rapidly decrease due to the Warburg effect.

257 rosine phosphorylation and gives rise to the Warburg effect.

258 Furthermore, contrary to the Warburg hypothesis, AML relies on oxidative phosphorylat

259 se complex (PDC) activity contributes to the Warburg metabolic and malignant phenotype in human head

260 sition to aerobic glycolysis, similar to the Warburg metabolism displayed by cancer cells.

261 tabolism in HepG2 cells, contributing to the Warburg phenomenon.

262 tion of cancerous colonocytes undergoing the Warburg effect.

263 estigate molecular mechanisms underlying the Warburg effect, we first compared oxygen consumption amo

264 lonocytes and cancerous colonocytes when the Warburg effect was prevented from occurring, whereas it

265 the pathways classically associated with the Warburg effect.

266 terns of expression were consistent with the Warburg effect.

267 The "Warburg effect" describes a peculiar metabolic feature o

268 Today this phenomenon is known as the "Warburg effect" and recognized as a hallmark of cancer.

269 er normoxic conditions, commonly called the "Warburg effect." Aerobic glycolysis often directly corre

270 gulation of glycolysis in cancer cells (the "Warburg effect") is common and has implications for prog

271 abolism, notably of aerobic glycolysis (the "Warburg effect"), the potential involvement of hypoxia-i

272 profound effect on aerobic glycolysis (the 'Warburg effect').

273 , development of multi-drug resistance, the 'Warburg effect', angiogenesis and cell growth (i.e. dist

274 metabolism (a cancer phenomenon termed the 'Warburg effect').

275 that mutations in TBC1D20 may contribute to Warburg micro syndrome (WARBM); WARBM constitutes a spec

276 under normoxic conditions, with parallels to Warburg reprogramming.

277 mediator linking noncanonical Shh pathway to Warburg-like glycolysis in satellite cells, which is req

278 state hyperplasia revealed that CAFs undergo Warburg metabolism and mitochondrial oxidative stress.

279 ose by 20%, thereby illustrating an in vitro Warburg-like effect on cell metabolism.

280 Walker-Warburg Syndrome (WWS) and muscle-eye-brain disease (MEB

281 Walker-Warburg syndrome (WWS) is a severe congenital disease th

282 Walker-Warburg syndrome (WWS) is clinically defined as congenit

283 ), Muscle-Eye-Brain disease (MEB) and Walker-Warburg syndrome (WWS), which are associated with brain

284 , muscle-eye-brain disease (MEB), and Walker-Warburg syndrome are congenital muscular dystrophies (CM

285 ama CMD, muscle-eye-brain disease and Walker-Warburg syndrome, each associated with eye abnormalities

286 nditions muscle-eye-brain disease and Walker-Warburg syndrome.

287 ns in the POMT1 gene can lead to both Walker-Warburg syndrome (WWS) and limb girdle muscular dystroph

288 the congenital muscular dystrophies, Walker-Warburg syndrome, to mild forms of adult-onset limb-gird

289 ify genetic mutations responsible for Walker-Warburg syndrome (WWS), a genetically heterogeneous auto

290 rain and eye anomalies and range from Walker-Warburg syndrome to Fukuyama congenital muscular dystrop

291 clinical manifestations ranging from Walker-Warburg syndrome, the most severe form of dystroglycanop

292 tal muscular dystrophies that include Walker-Warburg syndrome, muscle-eye-brain disease, and Fukuyama

293 to a variety of phenotypes including Walker-Warburg syndrome (WWS), limb girdle muscular dystrophy (

294 nital muscular dystrophies, including Walker-Warburg syndrome, muscle-eye-brain disease, Fukuyama con

295 PD), are a relatively common cause of Walker-Warburg syndrome.

296 es range from severe congenital onset Walker-Warburg syndrome (WWS) with severe structural brain and

297 ominantly muscle phenotypes to severe Walker-Warburg syndrome and muscle-eye-brain disease with strik

298 can, which not only causes the severe Walker-Warburg syndrome but is also a common cause of the milde

299 tal muscular dystrophy 1C (MDC1C), to Walker-Warburg Syndrome and Muscle-Eye-Brain disease.

300 rom limb girdle muscular dystrophy to Walker-Warburg syndrome.