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1                                              Warburg effect is a hallmark of cancer manifested by con
2                                              Warburg effect linked to cognitive-executive deficits in
3                                              Warburg effect or aerobic glycolysis provides selective
4                                              Warburg Micro syndrome and Martsolf syndrome are heterog
5 lic ATP/ADP, activation of glycolysis, and a Warburg metabolic phenotype in proliferating cells.
6  of increased aerobic glycolysis, known as a Warburg effect, including cytosolic PKM2 (pyruvate kinas
7 e role of UQCRH in cells that have entered a Warburg-like state through other mechanisms.
8 metabolism in MDA-MB-231 cells, which have a Warburg metabolic phenotype; these experiments indicated
9         Previously, our attempts to induce a Warburg-like state pharmaceutically via CPI-613 and PS48
10 e injury, which activates AMPK and induces a Warburg-like glycolysis in satellite cells.
11 y and modulates cell metabolism, promoting a Warburg-like metabolic phenotype.
12               AMPKalpha1(-/-) MuSCs showed a Warburg-like switch of their metabolism to higher glycol
13 ell types acquire a proteome that supports a Warburg phenotype with enhanced cell migration and proli
14        This metabolic reprogramming toward a Warburg phenotype occurred as a result of contact with p
15 ls by longwave UVA radiation, possibly via a Warburg-like effect, promotes melanoma invasiveness.
16 n particular, reovirus infection accentuated Warburg-like metabolic perturbations in cell lines relat
17 and lactate dehydrogenase A (LDHA) activity (Warburg effect).
18                 Hence, cancer cells allocate Warburg metabolism to their corrupted CAFs, exploiting t
19                                     Although Warburg effect is considered a peculiarity critical for
20 ehyde-3-phosphate dehydrogenase activity and Warburg metabolism.
21 (ct)), double-layer capacitance (C(dl)), and Warburg impedance (W).
22 entifies MPI as a novel regulator of p53 and Warburg metabolism.
23 ulin-VDAC interaction by erastin antagonizes Warburg metabolism and restores oxidative mitochondrial
24 ndicated that CO transiently induces an anti-Warburg effect by rapidly fueling cancer cell bioenerget
25 s while decreasing glycolysis, i.e. an 'anti-Warburg' effect.
26 metabolic requirement, a phenomenon known as Warburg effect.
27 were related to energy production as well as Warburg effect pathways, which may shed light on how ene
28 Aerobic glycolysis, originally identified by Warburg as a hallmark of cancer, has recently been impli
29 e beyond oxidative needs, a paradox noted by Warburg almost a century ago.
30                                  As noted by Warburg, many cancer cells depend on the consumption of
31 ain a growth advantage through the so-called Warburg effect by shifting glucose metabolism from oxida
32 arity to the glycolytic phenotype in cancer (Warburg effect).
33  Loss-of-function mutations in TBC1D20 cause Warburg Micro syndrome 4 (WARBM4), which is an autosomal
34 ostate tumors that did not exhibit a classic Warburg phenotype were equally sensitive.
35                                  The classic Warburg effect described in macrophages infected by Myco
36 ons in chRCC tumors, including the classical Warburg effect, the downregulation of gluconeogenesis an
37 CEFs (Ski-CEFs) do not display the classical Warburg effect.
38             Despite being known for decades (Warburg effect), the molecular mechanisms regulating thi
39 reasing HDO signal could be used to diagnose Warburg (cancer) metabolism.
40 uman neurological and developmental disorder Warburg Micro syndrome.
41 y an important mechanism by which Wnt-driven Warburg metabolism directs the use of glucose for cancer
42 duced HIF transcriptional activity and drove Warburg metabolic reprogramming, coupling AMPK-dependent
43 olism to a highly glycolytic phenotype, i.e. Warburg effect, is a common phenotype of cancer and acti
44          Its relationship to the established Warburg impedance model is validated theoretically and e
45 te kinase M2 (PKM2), a glycolytic enzyme for Warburg effect, is strongly upregulated in BC.
46  aerobic production of lactate from glucose (Warburg effect), extensive glutamine utilization and imp
47 ryos transiently exhibit aerobic glycolysis (Warburg effect), a metabolic adaptation also observed in
48 ated androgen signaling, aerobic glycolysis (Warburg effect), and aberrant activation of transcriptio
49 ng in Akt activation and aerobic glycolysis (Warburg effect), associated with ulceration.
50 both animal models and patients, glycolysis (Warburg effect) is also an early manifestation of CRPC t
51  metabolic genes associated with glycolysis (Warburg effect), fatty acid metabolism (lipogenesis, oxi
52    It is thought that cancer cells engage in Warburg metabolism to meet intrinsic biosynthetic requir
53 n altered metabolism, including an increased Warburg effect and glutamine dependence, making the glut
54        HIF1alpha, but not HIF2alpha, induced Warburg-like metabolism characterized by increased glyco
55 llectively, these findings indicate that key Warburg effect enzymes play a central role in mediating
56 ) as a metabolic enzyme required to maintain Warburg metabolism in zebrafish embryos and in both prim
57 mor growth by suppressing the HIF-1-mediated Warburg effect and angiogenesis.
58 e for the pyruvate kinase M2 (PKM2)-mediated Warburg effect, namely aerobic glycolysis, in the regula
59 ts another hallmark of tumorigenesis, namely Warburg metabolism.
60 nce of a synaptic activity-mediated neuronal Warburg effect that may promote mitochondrial homeostasi
61 the other subpopulations, these hypoxic "non-Warburg" cells had highest oxygen consumption rates and
62                        These respiring ("non-Warburg") cells were previously thought not to play a ke
63                              The adoption of Warburg metabolism is critical for the activation of mac
64                     The clinical features of Warburg Micro syndrome patients with RAB3GAP1 or RAB3GAP
65 ctivated T cells, which display hallmarks of Warburg metabolism, physiologically activated CD8(+) T c
66 r role in T-cell activation and induction of Warburg effect.
67  of the loss of cavin-3 include induction of Warburg metabolism (aerobic glycolysis), accelerated cel
68 bed energy metabolism hindering induction of Warburg phenotype.
69 ed glycolysis and visibly reduced markers of Warburg effect in ADPGK knock-out cells, finally leading
70 ation analysis revealed a uniform pattern of Warburg effect mutations influencing prognosis across al
71   However, targeting oncogenic regulators of Warburg effect has always been challenging owing to the
72 t in vitro proof of concept that reversal of Warburg effect might be a novel therapy for GBM.
73                                         Otto Warburg discovered that cancer cells exhibit a high rate
74                                         Otto Warburg's theory on the origins of cancer postulates tha
75                            Decades ago, Otto Warburg observed that cancers ferment glucose in the pre
76                                Although Otto Warburg first described aerobic glycolysis in cancer cel
77                                Although Otto Warburg observed aerobic glycolysis nearly 90 years ago,
78 ature of solid tumours were reported by Otto Warburg almost a century ago.
79 itions, has been shown first in 1926 by Otto Warburg.
80  One of the major features of cancer is Otto Warburg's observation that many tumors have increased ex
81 t glycolysis even in the presence of oxygen (Warburg effect) and use of glutamine for increased biosy
82 ll of origin, thereby inhibiting a potential Warburg effect.
83                            APOBEC3G promotes Warburg-like metabolic remodeling in HuT78 T cells under
84 wever, this treatment demonstrated a Reverse Warburg effect phenotype observed in cancer-associated s
85 amming in concert with disruption of several Warburg effect-related super-enhancers.
86                                        Since Warburg's observation that most cancers exhibit elevated
87                                        Since Warburg's observation, the importance of extracellular a
88 -dependent HIF activation and the subsequent Warburg metabolic transformation.
89 pers by Chang et al. and Ho et al. show that Warburg metabolism enables tumor cells to restrict gluco
90                        We demonstrated that "Warburg effect" is not modulated in the initial stage of
91                                          The Warburg effect contributes to cancer progression and is
92                                          The Warburg effect defines a pro-oncogenic metabolism switch
93                                          The Warburg effect describes an increase in aerobic glycolys
94                                          The Warburg effect is a chronic increase in glycolytic index
95                                          The Warburg effect is a tumor-related phenomenon that could
96                                          The Warburg effect is a tumorigenic metabolic adaptation pro
97                                          The Warburg effect is one of the metabolic hallmarks of canc
98                                          The Warburg effect, a common metabolic alteration of most tu
99                                          The Warburg effect, which originally described increased pro
100 n in the presence of abundant oxygen(4) (the Warburg effect).
101  suppressor in PCa that prevents EMT and the Warburg effect, and indicates that ABHD5 is a potential
102 ion, activation of the PI3K pathway, and the Warburg effect.
103 tures of tumor cells: glutaminolysis and the Warburg effect.
104  intellectual disability, apoptosis, and the Warburg effect.
105 factor-1alpha's downstream processes and the Warburg effect; induction of autophagy; augmentation of
106  and its focus expanded from glucose and the Warburg's effects on other nutrients, such as glutamine.
107 asis, immune escape, tumor angiogenesis, the Warburg effect and oncogene addiction and has been valid
108          A metabolic phenomenon known as the Warburg effect has been characterized in certain cancero
109                                 Known as the Warburg effect in the context of cancer growth, this phe
110 etabolic phenotype of cancer is known as the Warburg effect or aerobic glycolysis that consists of in
111   Drastic metabolic alterations, such as the Warburg effect, are found in most if not all types of ma
112      Reversing this phenomenon, known as the Warburg effect, may offer a generalized anticancer strat
113 eference of aerobic glycolysis, known as the Warburg effect, which facilitates cell proliferation.
114 he degree of aerobic glycolysis-known as the Warburg effect-is thus predicted to represent an adaptat
115 eir energy supply, a phenomenon known as the Warburg effect.
116 toward aerobic glycolysis, also known as the Warburg effect.
117 on to aerobic glycolysis, referred to as the Warburg effect.
118 presented by a glycolytic shift known as the Warburg effect.
119 gulate non-cell-cycle functions, such as the Warburg effect.
120 s the glycolytic adaptation described as the Warburg Effect.
121 utrients for biomass production known as the Warburg effect.
122 as an increased glycolytic rate known as the Warburg effect.
123 ase in aerobic glycolysis, also known as the Warburg effect.
124 onditions, a hallmark of cancer known as the Warburg effect.
125 f mitochondrial function and is known as the Warburg effect.
126 energy production, a phenomenon known as the Warburg effect.
127 tic state of aerobic glycolysis known as the Warburg effect.
128 n to generate ATP, a phenomenon known as the Warburg effect.
129 in cancer cells, commonly referred to as the Warburg effect.
130 ential use of glucose, which is known as the Warburg effect.
131 oA in the presence of oxygen is known as the Warburg effect.
132 ation in the cell, a phenomenon known as the Warburg effect.
133 is abundant, a phenomenon referred to as the Warburg effect.
134 e quiescent state, a phenomenon known as the Warburg effect.
135 lysis for ATP production, referred to as the Warburg effect.
136 lysis-driven metabolic program, known as the Warburg effect; however, few have been identified.
137  to the altered metabolic state known as the Warburg effect; one metabolic pathway, highly dependent
138 eased oxygen consumption, and attenuated the Warburg effect at the cellular level.
139 udy of tumor metabolism above and beyond the Warburg effect.
140 tralization of the acidosis generated by the Warburg glycolytic shift.
141 rease in glycolytic index, quantified by the Warburg index.
142 melanoma cells that are not described by the Warburg phenomenon.
143 ilability of oxygen, a phenomenon called the Warburg effect, is important for cancer cell growth.
144 imiting glycolytic enzyme known to cause the Warburg effect.
145 ated aerobic glycolysis in cancer cells (the Warburg effect) may be attributed to respiration injury
146 ism and is up-regulated in cancer cells (the Warburg Effect).
147  the ERK and JNK pathways in controlling the Warburg effect in cancer and discuss their implication i
148 tp53 GOF and a mechanism for controlling the Warburg effect.
149 tion in aerobic glycolysis counteracting the Warburg effect of cancer cells.
150 3 decreased proliferation and diminished the Warburg-like phenotype in SIRT3-deficient cell lines, an
151 GT1A_i2 proteins in HT115 cells enforced the Warburg effect, with a higher glycolytic rate at the exp
152                  MicroRNA-31-5p enhances the Warburg effect via targeting FIH.
153 ic metabolism in an aerobic environment, the Warburg effect, but the explanation for this preference
154 regulating energy metabolism, especially the Warburg effect, and antioxidant defense, and thus the fu
155             All melanoma cells exhibited the Warburg phenomenon; they used more glucose and produced
156                   Tumor cells exhibiting the Warburg effect rely on aerobic glycolysis for ATP produc
157 olic status of cancer cells experiencing the Warburg effect(2,3).
158 tions and therefore do not fully explain the Warburg effect.
159 her innate or acquired, helps to explain the Warburg phenomenon.
160 a lack of a quantitative explanation for the Warburg effect in cancer.
161 rkin deficiency is a novel mechanism for the Warburg effect in tumors.
162 ory axis is an important determinant for the Warburg effect in tumour cells and provide a mechanistic
163 IF1, revealing a potential mechanism for the Warburg effect, an elevation in aerobic glycolytic metab
164 ruvate kinase M2 (PKM2) is essential for the Warburg effect.
165 ignant cells exhibit aerobic glycolysis (the Warburg effect) and become dependent on de novo lipogene
166                      Aerobic glycolysis (the Warburg effect) is a metabolic hallmark of activated T c
167 r cells rely more on aerobic glycolysis (the Warburg effect) than mitochondrial oxidative phosphoryla
168 ost tumour cells use aerobic glycolysis (the Warburg effect) to support anabolic growth and evade apo
169 Most tumor cells use aerobic glycolysis (the Warburg effect) to support anabolic growth and promote t
170  It remains a matter of debate as to how the Warburg effect is regulated during tumor progression.
171                      Here we explore how the Warburg effect might be linked to inflammation and infla
172                        It is unclear how the Warburg effect that exemplifies enhanced glycolysis in t
173 ossible to directly and indirectly image the Warburg effect with hyperpolarized (13)C-pyruvate and (1
174 ion and underlying mechanism of UQCRH in the Warburg effect metabolism of ccRCC have not been charact
175 2, a fetal anabolic enzyme implicated in the Warburg effect, was activated by insulin in vivo and in
176  the lactate produced by cancer cells in the Warburg effect.
177                      Larger increases in the Warburg elements and cell impedance are also found with
178 c alterations in cancer cells, including the Warburg effect that describes an increased glycolysis in
179 rofound metabolic alterations, including the Warburg effect wherein cancer cells oxidize a decreased
180 similar metabolic alterations, including the Warburg effect.
181 ing oxygen consumption, thereby inducing the Warburg effect.
182 ignaling pathway may be a way to inhibit the Warburg Effect to disrupt tumor growth.
183 er cells, SR9243 significantly inhibited the Warburg effect and lipogenesis by reducing glycolytic an
184 ngly, the molecular mechanisms that link the Warburg effect with the suppression of apoptosis are not
185                A new parameter measuring the Warburg effect (the ratio of lactate production flux to
186 thod has proven highly useful to monitor the Warburg effect in cancer, through MR detection of increa
187 ealing how CD44 could be a gatekeeper of the Warburg effect (aerobic glycolysis) in cancer cells and
188        We propose that KSHV induction of the Warburg effect adapts infected cells to tumor microenvir
189 ese results support an interpretation of the Warburg effect and glutamine addiction as features of a
190 duced kinase 1 (PINK1) is a regulator of the Warburg effect and negative regulator of glioblastoma gr
191          This results in the reversal of the Warburg effect and the inhibition of breast cancer cell
192  wild-type p53 prevents manifestation of the Warburg effect by controlling Pdk2.
193 cose to lactate conversion indicative of the Warburg effect can be imaged without hyper-polarization
194 ve recently emerged as key regulators of the Warburg effect during tumorigenesis and normal cellular
195 remutation, we evaluated the presence of the Warburg effect in peripheral blood mononuclear cells (PB
196  However, evidence for the occurrence of the Warburg effect in physiological processes has also been
197 tory axis is an important determinant of the Warburg effect in tumor cells, and provide a mechanistic
198                         The discovery of the Warburg effect, the preference of cancer cells to genera
199                               Imaging of the Warburg effect, which is the principal but not the sole
200 vide new insights into the regulation of the Warburg effect.
201 ropensity of AKT to modulate elements of the Warburg effect.
202 se M2 isoform (PKM2), a key regulator of the Warburg effect.
203 ess, enabling non-invasive monitoring of the Warburg effect.
204 it a glycolytic phenotype reminiscent of the Warburg effect.
205  that p53 status is a key determinant of the Warburg effect.
206 se M2 isoform (PKM2), a key regulator of the Warburg effect.
207 ma enabled quantitative visualization of the Warburg effect.
208 der aerobic conditions characteristic of the Warburg effect.
209 n and supporting a localized reversal of the Warburg shift toward aerobic glycolysis.
210 extracting the component that depends on the Warburg impedance from the total impedance.
211                    Aerobic glycolysis or the Warburg effect (WE) is characterized by increased glucos
212                    Aerobic glycolysis or the Warburg Effect (WE) is characterized by the increased me
213                    Aerobic glycolysis or the Warburg effect links the high rate of glucose fermentati
214 olism of enhanced aerobic glycolysis (or the Warburg effect) is known as a hallmark of cancer.
215 gramming, known as aerobic glycolysis or the Warburg effect, allows tumor cells to sustain their fast
216 y a preference for aerobic glycolysis or the Warburg effect, and the cells resist matrix detachment-i
217 ed role of PKM2 in aerobic glycolysis or the Warburg effect, its non-metabolic functions remain elusi
218 inflammatory sites undergoing hypoxia or the Warburg effect.
219 even in the presence of abundant oxygen (the Warburg effect).
220 e of ATP to fuel cellular proliferation (the Warburg effect).
221 nhances LDH-A enzyme activity to promote the Warburg effect and tumor growth by regulating the NADH/N
222 osphorylation activates PDHK1 to promote the Warburg effect and tumor growth.
223 ert to regulate PDC activity and promote the Warburg effect.
224 ert to regulate PDC activity and promote the Warburg effect.
225 h cancer-specific splicing that promotes the Warburg effect and breast cancer progression.
226 is study reveals that miR-31-5p promotes the Warburg effect via direct targeting of FIH.
227 mediated PKM2 dephosphorylation promotes the Warburg effect, cell proliferation and brain tumorigenes
228 cogenic signaling pathways that regulate the Warburg effect in cancer cells has therefore become an a
229 decline of mitochondria thus reinforcing the Warburg effect.
230 ion, agents that scavenge ROS or reverse the Warburg effect prevent the transformation and malignant
231 mented that methylene blue (MB) reverses the Warburg effect evidenced by the increasing of oxygen con
232 estoration of Parkin expression reverses the Warburg effect in cells.
233 discovery has led researchers to revisit the Warburg hypothesis, first postulated in the 1950s, of ab
234 t mechanistically connects aberrant ROS, the Warburg effect, and carcinogenesis.
235 ecreased HIF-1alpha expression, shifting the Warburg phenotype to OXPHOS and inhibiting glioblastoma
236 43B osteosarcoma (OS) cell lines showing the Warburg effect in comparison with actively respiring Sao
237 that tumour-associated mutp53 stimulates the Warburg effect in cultured cells and mutp53 knockin mice
238                        Mutp53 stimulates the Warburg effect through promoting GLUT1 translocation to
239 gely abolishes mutp53 GOF in stimulating the Warburg effect.
240  Finally, miR-644a expression suppresses the Warburg effect by direct targeting of c-Myc, Akt, IGF1R,
241 ize the potential benefit from targeting the Warburg effect.
242 tochondria (OXPHOS), a phenomenon termed the Warburg effect, which is a general feature of oncogenesi
243  aerobic glycolysis, a phenomenon termed the Warburg effect.
244                         Here I show that the Warburg effect can be explained as a form of cooperation
245 ese findings support the hypothesis that the Warburg effect is a precisely regulated developmental me
246      This study reveals a mechanism that the Warburg effect is regulated by CHIP through its function
247 izing higher-grade tumors, we found that the Warburg effect is relatively more prominent at the expen
248               These results suggest that the Warburg effect, more specifically, diminished glucose ox
249 that regulate the PI3K pathway, and thus the Warburg effect, are elusive.
250 s miR-199a maturation to link hypoxia to the Warburg effect and suggest a promising therapeutic strat
251 the glycolytic pathway and contribute to the Warburg effect in cancer cells.
252 ase (PKM2), a key enzyme contributing to the Warburg effect in cancer, is significantly induced in DM
253  mitochondrial function, contributing to the Warburg effect in cancer.
254 erized by a glycolytic switch similar to the Warburg effect in cancer.
255 How ACAT1 is "hijacked" to contribute to the Warburg effect in human cancer remains unclear.
256  by DERL3 epigenetic loss contributes to the Warburg effect in the studied cells and pinpoints a subs
257 report that loss of PINK1 contributes to the Warburg effect through ROS-dependent stabilization of hy
258                                   Due to the Warburg effect, cancerous colonocytes rely on glucose as
259    This bioenergetic shift is similar to the Warburg effect, the metabolic signature of cancer cells.
260 rosine phosphorylation and gives rise to the Warburg effect.
261 er-enhancers in several genes related to the Warburg effect.
262 lar composition of PDC and contribute to the Warburg effect.
263 s a new molecular player contributing to the Warburg effect.
264 iferating cancer cells and contribute to the Warburg effect.
265 es mitochondrial respiration, leading to the Warburg effect.
266                 Furthermore, contrary to the Warburg hypothesis, AML relies on oxidative phosphorylat
267 sition to aerobic glycolysis, similar to the Warburg metabolism displayed by cancer cells.
268 tabolism in HepG2 cells, contributing to the Warburg phenomenon.
269 tion of cancerous colonocytes undergoing the Warburg effect.
270 estigate molecular mechanisms underlying the Warburg effect, we first compared oxygen consumption amo
271 lonocytes and cancerous colonocytes when the Warburg effect was prevented from occurring, whereas it
272 the pathways classically associated with the Warburg effect.
273 ite matter (P < .001) in accordance with the Warburg theorem.
274 ycolysis was observed in accordance with the Warburg theorem.
275                                         The "Warburg effect" describes a peculiar metabolic feature o
276       Today this phenomenon is known as the "Warburg effect" and recognized as a hallmark of cancer.
277 er normoxic conditions, commonly called the "Warburg effect." Aerobic glycolysis often directly corre
278 gulation of glycolysis in cancer cells (the "Warburg effect") is common and has implications for prog
279 abolism, notably of aerobic glycolysis (the "Warburg effect"), the potential involvement of hypoxia-i
280 nas is dominated by aerobic glycolysis (the "Warburg Effect"), which allows only a small fraction of
281  profound effect on aerobic glycolysis (the 'Warburg effect').
282  metabolism (a cancer phenomenon termed the 'Warburg effect').
283                               In contrast to Warburg's original hypothesis, accumulating evidence dem
284  that mutations in TBC1D20 may contribute to Warburg micro syndrome (WARBM); WARBM constitutes a spec
285 under normoxic conditions, with parallels to Warburg reprogramming.
286 mediator linking noncanonical Shh pathway to Warburg-like glycolysis in satellite cells, which is req
287 induced cancer cells, displaying the typical Warburg effect, to death or survival upon progressive gl
288 state hyperplasia revealed that CAFs undergo Warburg metabolism and mitochondrial oxidative stress.
289                                       Walker-Warburg syndrome (WWS) is clinically defined as congenit
290 nditions muscle-eye-brain disease and Walker-Warburg syndrome.
291  the congenital muscular dystrophies, Walker-Warburg syndrome, to mild forms of adult-onset limb-gird
292 ify genetic mutations responsible for Walker-Warburg syndrome (WWS), a genetically heterogeneous auto
293 rain and eye anomalies and range from Walker-Warburg syndrome to Fukuyama congenital muscular dystrop
294  clinical manifestations ranging from Walker-Warburg syndrome, the most severe form of dystroglycanop
295 nital muscular dystrophies, including Walker-Warburg syndrome, muscle-eye-brain disease, Fukuyama con
296 PD), are a relatively common cause of Walker-Warburg syndrome.
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.

 
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