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1                                              LDHA abundance correlated positively with MYC expression
2                                              LDHA also promoted GH3 cell proliferation through induct
3                                              LDHA and LDHB are two main LDH subunits, and both are fr
4                                              LDHA binds to NADH and promotes reactive oxygen species
5                                              LDHA catalyzes pyruvate into lactate instead of leading
6                                              LDHA deficiency crippled cellular redox balance and inhi
7                                              LDHA deficiency cripples cellular redox control and dimi
8                                              LDHA is a pharmacologically tractable EWS-FLI1 transcrip
9                                              LDHA sensing by Al-Py FONPs was found to be highly selec
10 okinase 1 (HK1) and lactate dehydrogenase A (LDHA) - both of which regulate the metabolic switch - an
11 glycolytic flux and lactate dehydrogenase A (LDHA) activity (Warburg effect).
12 tate via the enzyme lactate dehydrogenase A (LDHA) and is a metabolic feature of effector T cells.
13 es the detection of lactate dehydrogenase A (LDHA) by exploiting the AIE property of synthesized naph
14                     Lactate dehydrogenase A (LDHA) catalyzes the conversion of pyruvate to lactate, u
15 lls (HSCs), whereas lactate dehydrogenase A (LDHA) deletion significantly inhibits the function of bo
16 nally regulates the lactate dehydrogenase A (LDHA) gene.
17                     Lactate dehydrogenase A (LDHA) has been reported to be involved in the initiation
18 actate reduction by lactate dehydrogenase A (LDHA) inactivation heightens type I IFN production to pr
19  Here, we show that lactate dehydrogenase A (LDHA) is induced in activated T cells to support aerobic
20 e glycolytic enzyme lactate dehydrogenase A (LDHA) is induced in CD8(+) T effector cells through phos
21 enetic depletion of lactate dehydrogenase A (LDHA) or stiripentol, a lactate dehydrogenase A inhibito
22 trong expression of lactate dehydrogenase A (LDHA) that converts pyruvate to lactate.
23 kinase 2 (HK2), and Lactate Dehydrogenase A (LDHA) were each significantly higher in MYCN-amplified n
24 duced activation of lactate dehydrogenase A (LDHA), an enzyme that catalyses the interconversion of p
25  (UMPS), as well as lactate dehydrogenase A (LDHA), establishing a mechanism by which AHR regulates l
26  upon inhibition of lactate dehydrogenase A (LDHA), our findings hint at a conserved mechanism in whi
27 h as those encoding lactate dehydrogenase A (LDHA), solute transporter MCT1, and hexokinase 1 (HK1) -
28 ransporter MCT1 and lactate dehydrogenase A (LDHA), the enzyme catalyzing label exchange between pyru
29 ctate synthesis via lactate dehydrogenase A (LDHA), traditionally considered to be a 'disallowed' fun
30       Expression of lactate dehydrogenase A (LDHA), which catalyzes (13)C label exchange between pyru
31 ate lactate through lactate dehydrogenase A (LDHA), which is encoded by a target gene of c-Myc and hy
32 g to and activating lactate dehydrogenase A (LDHA), which promoted histones lysine lactylation to ind
33  shown to undertake lactate dehydrogenase A (LDHA)-dependent aerobic glycolysis; however, the specifi
34 es demonstrate that lactate dehydrogenase A (LDHA)-directed extracellular signal-regulated kinase (ER
35 d during hypoxia is lactate dehydrogenase A (LDHA).
36 d overexpression of lactate dehydrogenase A (LDHA).
37 ards glycolysis and lactate dehydrogenase A (LDHA).
38 kinase 1 (PDK1) and lactate dehydrogenase A (LDHA).
39 ic driver of Ewing sarcoma, regulated LDH A (LDHA) expression.
40                                 In addition, LDHA knockdown or LDHA Y10F rescue expression in human c
41 c constriction were treated with oxamate (an LDHA [lactate dehydrogenase A] inhibitor) or sodium lact
42  the strong expression of MCT-4, EMMPRIN and LDHA in perivascular macrophages in MS brains.
43 ts from regulatory regions of PGK1, ENO1 and LDHA genes.
44 pression of a series of downstream genes and LDHA itself.
45  together, these data suggest that HIF1A and LDHA are important targets for hypoxia-driven drug resis
46           Constitutive expression of HK2 and LDHA during differentiation leads to neuronal cell death
47 C, transcriptional activators of the HK2 and LDHA genes, decrease dramatically.
48 onserved canonical E boxes in ENO1, HK2, and LDHA occur in 31- to 111-bp islands with high interspeci
49 roblastoma cells with inhibitors of MCT1 and LDHA, the enzyme responsible for lactate production, res
50 iated with a drop in levels of LDHA mRNA and LDHA and hypoxia-inducible factor-1alpha proteins.
51 red the expression and activity of PDHA1 and LDHA, as both are involved in regulating the direction o
52                      Additionally, PDK1- and LDHA-overexpressing cells exhibited decreased oxygen con
53 RNA encoding the glycolytic enzymes PFKP and LDHA.
54 sion of the glycolytic genes GLUT1, PKM2 and LDHA, and of CDC25A; thus, Cdc25A upregulates itself in
55                       Clinically, POU1F1 and LDHA expression correlate with relapse- and metastasis-f
56 nduction of LDHA required PI3K signaling and LDHA deficiency impaired PI3K-catalyzed PIP3 generation.
57  was highly synergistic with vincristine and LDHA inhibition under cell culture conditions, but this
58 ation pattern on c-Myc target genes, such as LDHA, consequently reprogram glycolytic metabolism for C
59 , thereby activating transcription of BNIP3, LDHA, PDK1, and SLC2A1, which encode proteins that are r
60 ic study, we confirmed that 22 degraded both LDHA and LDHB significantly.
61 such as 63 exhibit low nM inhibition of both LDHA and LDHB, submicromolar inhibition of lactate produ
62 cally, the LDH isoenzyme spectrum imposed by LDHA and LDHB is necessary to optimize glycolysis to mai
63  and LDHB in tumor cells, not only canonical LDHA.
64 in this interval, resulting in the order CEN-LDHA-SAA1-TPH-D11S1310-(D11S1888/KCNC1 )-MYOD1-D11S902D1
65 various heterotetrameric isoforms comprising LDHA and LDHB in tumor cells, not only canonical LDHA.
66                                  Conversely, LDHA knockdown in breast cancer cells that overexpress P
67 rculosis (TB) patients and myeloid deficient LDHA (Ldha(LysM-/-)) mice, we demonstrate that glycolysi
68 leic acid or expression of phospho-deficient LDHA Y10F sensitized the cancer cells to anoikis inducti
69                         22 potently degraded LDHA in a time- and ubiquitin-proteasome system-dependen
70 ression of the enzyme lactate dehydrogenase (LDHA and LDHB combined), and the ratio of lactate transp
71  hexokinase (HK2) and lactate dehydrogenase (LDHA) expression, together with a switch in pyruvate kin
72                             Here, we deleted LDHA in a stage-specific and cell-specific manner.
73                        Accordingly, deleting LDHA suppressed glycolysis, cell proliferation, and diff
74                         Genetically deleting LDHA or LDHB altered the isoenzyme spectrum by removing
75  14 key glycolysis proteins (including ENO1, LDHA, LDHB, ACSS2, ALDOA, and PGK1), compared to CsP alo
76      Inhibition of aerobic glycolysis enzyme LDHA and G6PD had no significant effects on tumor cell s
77 iption factor IRF4 and the glycolytic enzyme LDHA govern the effector differentiation potential of CD
78 oint as well as a ROS promoting function for LDHA and identifies LDHA as a potential therapeutic targ
79 is an achievable and tolerable treatment for LDHA-dependent tumors.
80                                 Furthermore, LDHA phosphorylation at Y10 positively correlated with p
81 icantly associated with expression of GLUT1, LDHA, PDK1, LOX, LOXL2, and L1CAM mRNA in human breast c
82 ne expression of five reference (B2M, H3F3A, LDHA, PPIA and YWHAZ) and five target (CXCL9, CXCL10, CX
83                           On the other hand, LDHA-deleted naive B cells had a severe defect in their
84 ANKRD37, GADD45A) and glycolysis (i.e., HK2, LDHA).
85 and choline metabolism including GLUT1, HK2, LDHA and CHKA.
86 t of its promiscuous activity under hypoxia, LDHA produces L-2 hydroxyglutarate (L-2HG), an epigeneti
87         Insights from a new model identified LDHA as a novel target for group 3 medulloblastoma, pavi
88                      Moreover, we identified LDHA as a novel, specific therapeutic target for this de
89 S promoting function for LDHA and identifies LDHA as a potential therapeutic target for OA treatment.
90 hydrogenase subunit LDHBx can also co-import LDHA, the other LDH subunit, into peroxisomes.
91 )C MRS of pyruvate to monitor alterations in LDHA activity and expression caused by PI3K pathway inhi
92                                     Instead, LDHA maintains high concentrations of acetyl-coenzyme A
93               Combined LDH activity and LDHB/LDHA expression analysis intimated various heterotetrame
94          We observe similar changes in MCT4, LDHA, and LDHB between tumours with primary Gleason patt
95 suggesting that Y10 phosphorylation-mediated LDHA activity promotes cancer cell invasion and anoikis
96 ay crystallography to develop small molecule LDHA inhibitors.
97 ced oxidative phosphorylation in a PI3K/mTOR/LDHA pathway-dependent manner.
98  the aerobic respiration (HIF-1alpha, c-Myc, LDHA, PDK1 and VEGF) was detected by real-time PCR.
99 identified proteins (CRMP1, CRMP2, GDA, NSE, LDHA, LDHB, STIP1, and YBOX) that are highly expressed i
100                     We find that ablation of LDHA in a naive B cell did not profoundly affect its abi
101 lation and transcription of Ifng Ablation of LDHA in T cells protects mice from immunopathology trigg
102                         In turn, ablation of LDHA inhibits PI3K-dependent phosphorylation of Akt and
103 L-2HG as a result of promiscuous activity of LDHA.
104 that three tetrameric isoenzymes composed of LDHA and LDHB (LDH-3/4/5) comprise the LDH spectrum in T
105                         Genetic depletion of LDHA inhibited proliferation of Ewing sarcoma cells and
106 ker for selective and sensitive detection of LDHA by ministering their AIE property.
107        Moreover, robust target engagement of LDHA by lead compounds was demonstrated using the cellul
108 lastoma cells also reduced the expression of LDHA (and lactate), DHODH, and UMPS but did not affect U
109 ansgenic mice showed decreased expression of LDHA and PDK1 when compared with controls.
110                       Elevated expression of LDHA in cancer cells plays a crucial role in cancer prog
111             Notably, increased expression of LDHA served as a vicious positive feedback to reduce tum
112 ramer of LDHB) or LDH-5 (the homotetramer of LDHA), respectively.
113                                 Induction of LDHA required PI3K signaling and LDHA deficiency impaire
114 ple myeloma, and that specific inhibition of LDHA and HIF1A can restore sensitivity to therapeutic ag
115                                Inhibition of LDHA significantly reduced growth of both mouse and huma
116   Accordingly, oxamate-induced inhibition of LDHA suppressed glucose uptake, lactate secretion, invas
117                         Hence, inhibition of LDHA with FX11 is an achievable and tolerable treatment
118    Genetic and pharmacological inhibition of LDHA-mediated tumor-macrophage symbiosis markedly suppre
119 was confirmed by siRNA-mediated knockdown of LDHA and MCT-4, which decreased lactate secretion and ma
120                                 Knockdown of LDHA can restore sensitivity of bortezomib resistance ce
121 and were associated with a drop in levels of LDHA mRNA and LDHA and hypoxia-inducible factor-1alpha p
122 udy, we showed that the expression levels of LDHA mRNA and protein were significantly elevated in inv
123                         In addition, loss of LDHA in T cells severely compromised B cell-dependent im
124                                  A number of LDHA/B small-molecule inhibitors have been developed.
125  breast tumors showed that overexpression of LDHA and the hypoxia marker CAIX was associated with red
126                            Overexpression of LDHA in a PA cell line (GH3) promoted glucose uptake thr
127 ells, suggesting that Y10 phosphorylation of LDHA may represent a promising therapeutic target and a
128            Here, we report that reduction of LDHA by siRNA or its inhibition by a small-molecule inhi
129                Furthermore, how reduction of LDHA expression by interference or antisense RNA inhibit
130           Previous studies with reduction of LDHA expression indicate that LDHA is involved in tumor
131               However, the potential role of LDHA in pituitary adenoma (PA) remains unknown.
132 udies have focused on the ubiquitous role of LDHA in tumor metabolism and growth, our data reveal tha
133 brane influx in vivo, not glycolytic flux or LDHA activity, driving a reinterpretation of this maturi
134 nversion rates, independent of glycolysis or LDHA activity.
135                          Deletion of IRF4 or LDHA in T cells induces transplant acceptance.
136               In addition, LDHA knockdown or LDHA Y10F rescue expression in human cancer cells result
137                       Maintenance of PDK1 or LDHA expression in certain regions of the brain may expl
138 e show that overexpression of either PDK1 or LDHA in a rat CNS cell line (B12) confers resistance to
139 In contrast, cells expressing either PDK1 or LDHA maintained a lower mitochondrial membrane potential
140 s inhibited in the absence of either PKM2 or LDHA, indicating that the cell-state-specific responses
141 ching of their fluorescence by overexpressed LDHA within cancer cells.
142 , MDH2 and CS in one cluster and FBP2, PFKL, LDHA, TPI1 and GAPDH/S in the other cluster, suggest glu
143 ciprocally, infiltrating macrophages produce LDHA-containing extracellular vesicles to promote gliobl
144 e found to be an excellent probe for sensing LDHA through an AIE-based "fluorescence off'' mechanism
145 localization signal (NLS), sequence shuttles LDHA into the nucleus, where it enhances transcription o
146 cing the deposition of the mark by targeting LDHA/B leads to the downregulation of NC genes and the i
147  in multiple myeloma, specifically targeting LDHA, can be beneficial to inhibit tumor growth and over
148 mples of glioblastoma patients confirms that LDHA and its downstream signals are potential biomarkers
149                          We demonstrate that LDHA is phosphorylated at tyrosine 10 by upstream kinase
150                Our findings demonstrate that LDHA phosphorylation and activation provide pro-invasive
151                       Our data indicate that LDHA is involved in promoting the progression of PA, and
152 h reduction of LDHA expression indicate that LDHA is involved in tumor initiation, but its role in tu
153 ctor T cell differentiation and suggest that LDHA may be targeted therapeutically in autoinflammatory
154              These results also suggest that LDHA represents a novel, pharmacologically tractable tar
155 ween a Chk1 inhibitor and chloroquine or the LDHA/LDHB inhibitor GSK 2837808A.
156  specifically attenuated activity with their LDHA-expressed subunits that dominate liver parenchyma.
157 F1 induces a metabolic reprogramming through LDHA regulation in human breast tumor cells, modifying t
158 henotype in inducing drug resistance through LDHA and HIF1A in multiple myeloma, and that specific in
159                                        Thus, LDHA-mediated tumor-macrophage symbiosis provides therap
160 lified neuroblastoma cells are "addicted" to LDHA enzymatic activity, as its depletion completely inh
161       Mechanistically, SEMA3C-319aa binds to LDHA and, via its non-canonical nuclear localization sig
162  FONPs gradually got quenched in response to LDHA due to the conversion of fluorescent pyruvate to no
163  PGK1, PGM1, PGAM1, ENO1, ENO2, GAPDH, TPI1, LDHA, and LDHB) in the glycolytic pathway with concomita
164 l lines while gain-of-function studies using LDHA or HIF1A induced resistance in bortezomib-sensitive
165                                     In vivo, LDHA overexpression promoted tumor growth, and oxamate d
166                             Strikingly, when LDHA was deleted in activated, as opposed to naive, B ce
167 and only in selected tumors, coincident with LDHA expression.
168 RPL4, RPL8, RPL18, RPS9, RPS18, TFRC, YWHAZ, LDHA, SDHA).

 
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