ライフサイエンスコーパス: LDH-A

1 LDH-A gene expression is believed to be upregulated by b

2 LDH-A overexpression is required for c-Myc-mediated tran

3 egulating molecules lactate dehydrogenase A (LDH-A) and heat shock factor 1 (HSF1).

4 Lactate dehydrogenase A (LDH-A) catalyzes the interconversion of lactate and pyru

5 The lactate dehydrogenase A (LDH-A) gene, whose product participates in normal anaero

6 factor 1 (HSF1) and lactate dehydrogenase A (LDH-A) in ErbB2-positive cancer cells, resulting in tumo

7 ed stabilization of lactate dehydrogenase A (LDH-A) mRNA and identified four cytoplasmic proteins of

8 plex binding to the lactate dehydrogenase A (LDH-A) promoter was characterized.

9 Lactate dehydrogenase A (LDH-A) regulates the last step of glycolysis that genera

10 es, such as rcl and lactate dehydrogenase A (LDH-A), is critical for understanding the mechanisms of

11 ologous homologs of lactate dehydrogenase-A (LDH-A) (EC 1.1.1.27; NAD+:lactate oxidoreductase) of six

12 acrophage-expressed lactate dehydrogenase-A (LDH-A) to tumor formation in a K-Ras murine model of lun

13 am islets including lactate dehydrogenase-A (LDH-A), lactate (monocarboxylate) transporters, glucose-

14 Lactate dehydrogenase-A (LDH-A), responsible for conversion of pyruvate to lactat

15 ctate by the enzyme lactate dehydrogenase-A (LDH-A), suggesting a possible vulnerability at this targ

16 omplexes was absolutely necessary to achieve LDH-A mRNA stabilization.

17 However, how oncogenic signals activate LDH-A to regulate cancer cell metabolism remains unclear

18 Moreover, increased glycolysis via HSF1 and LDH-A contributes to trastuzumab resistance.

19 In this study, we report that Rcl and LDH-A act synergistically to induce anchorage-independen

20 These findings confirm Rcl and LDH-A as critical components of the cell transformation

21 Cells expressing both Rcl and LDH-A form tumors after s.c. injection into nude mice, a

22 The inability of Rcl and LDH-A to fully recapitulate c-Myc activity, however, ind

23 because lowering its level through antisense LDH-A expression reduces soft agar clonogenicity of c-My

24 mply a cause and effect relationship between LDH-A mRNA stabilization and CSR-phosphoprotein binding

25 ells (MDSCs) in the spleens of mice carrying LDH-A-depleted tumors.

26 In rat C6 glioma cells, LDH-A mRNA is stabilized by activation and synergistic i

27 er cells with stable knockdown of endogenous LDH-A and rescue expression of a catalytic hypomorph LDH

28 ggest that tyrosine phosphorylation enhances LDH-A enzyme activity to promote the Warburg effect and

29 Phosphorylation at Y10 and Y83 enhances LDH-A activity by enhancing the formation of active, tet

30 d cAMP-stabilizing region (CSR) required for LDH-A mRNA stability regulation by the protein kinase A

31 NK cells from LDH-A-depleted tumors had improved cytolytic function.

32 The lactate dehydrogenase-A gene (LDH-A), whose product participates in normal anaerobic g

33 d rescue expression of a catalytic hypomorph LDH-A mutant, Y10F, demonstrate increased respiration th

34 irpin RNA-mediated knockdown of hypothalamic LDH-A, an astrocytic component of the ANLS, also blunted

35 ss I: B23 (NPM1), CAD, CDK4, cyclin D2, ID2, LDH-A, MNT, PTMa, ODC, NM23B, nucleolin, prohibitin, SHM

36 he existence of a cAMP-stabilizing region in LDH-A 3'-UTR.

37 These observations suggest that an increased LDH-A level is required for the growth of a transformed

38 RNA and subsequent increase of intracellular LDH-A mRNA levels.

39 ical determinant for the (Sp)-cAMPS-mediated LDH-A mRNA stabilizing activity.

40 Correspondingly, adenoviral vector-mediated LDH-A overexpression reduced insulin secretion stimulate

41 Lentiviral vector-mediated LDH-A short hairpin RNA knockdown Pan02 pancreatic cance

42 chemical optimization, resulted in nanomolar LDH-A inhibitors that demonstrated stoichiometric bindin

43 tantly, PGC-1alpha reduces the expression of LDH A and one of its regulators, the transcription facto

44 active, tetrameric LDH-A and the binding of LDH-A substrate NADH, respectively.

45 We used a full-length cDNA clone of LDH-A of S. lucasana to test, by site-directed mutagenes

46 h RSW extracts, and the kinetics of decay of LDH-A mRNA was determined.

47 Myeloid-specific deletion of LDH-A promoted accumulation of macrophages with a CD86(h

48 Ectopic expression of LDH-A alone in Rat1a fibroblasts was sufficient to induc

49 regulation of HSF1 reduced the expression of LDH-A and subsequently decreased cancer cell glycolysis

50 Although antisense expression of LDH-A did not affect the growth of c-Myc-transformed fib

51 Our results suggest that expressions of LDH-A and lactate by macrophage in the tumor microenviro

52 tudies have linked c-Myc to the induction of LDH-A, whose expression increases lactate production and

53 The inhibition of LDH-A by small molecules is therefore of interest for po

54 we used FX11, a small-molecule inhibitor of LDH-A, to investigate this possible vulnerability in a p

55 cribe the identification and optimization of LDH-A inhibitors by fragment-based drug discovery.

56 Moreover, Y10 phosphorylation of LDH-A is common in diverse human cancer cells, which cor

57 responsible for the relatively rapid rate of LDH-A mRNA turnover in the cytoplasm.

58 The sequence of LDH-A from S. lucasana differs from that of S. idiastes

59 occurs through PKA-mediated stabilization of LDH-A mRNA and subsequent increase of intracellular LDH-

60 regulates the PKA-mediated stabilization of LDH-A mRNA.

61 ly through the HSF1-mediated upregulation of LDH-A.

62 on on the 3'-untranslated region (3'-UTR) of LDH-A mRNA.

63 and PKC results in a potentiating effect on LDH-A mRNA stabilization.

64 l techniques, that the muscle form (M-LDH or LDH-A) and the heart form (H-LDH or LDH-B) of lactate de

65 tion into nude mice, although neither Rcl or LDH-A overexpression alone induces tumorigenesis.

66 ansfected Rat1a fibroblasts that overexpress LDH-A alone or those transformed by c-Myc overproduce la

67 yrosine kinase FGFR1 directly phosphorylates LDH-A.

68 PKA and PKC act synergistically and prolong LDH-A mRNA half-life more than 21-fold.

69 supporting the concept of targeting stromal LDH-A as an effective strategy to blunt tumoral immune e

70 sion of the lactate dehydrogenase A subunit (LDH-A) gene can be controlled by transcriptional as well

71 nhancing the formation of active, tetrameric LDH-A and the binding of LDH-A substrate NADH, respectiv

72 pendent growth in Ratla fibroblasts and that LDH-A is required for cell transformation by c-Myc.

73 t not with serum withdrawal, suggesting that LDH-A mediates the unique apoptotic effect of c-Myc when

74 In both the LDH-A promoter and the erythropoietin 3' enhancer, forma

75 cAMP-stabilizing region (CSR) located in the LDH-A 3'-untranslated region which, in combination with

76 ansactivation) of the VEGF promoter than the LDH-A promoter.

77 R) of beta-globin had been replaced with the LDH-A 3'-UTR.

78 t at least three sequence domains within the LDH-A 3'-UTR consisting of nucleotides 1286-1351, 1453-1

79 o identify low affinity fragments binding to LDH-A.

80 that demonstrated stoichiometric binding to LDH-A.

81 HSF1 bound to LDH-A promoter and the downregulation of HSF1 reduced th

82 cer as a biomarker to predict sensitivity to LDH-A inhibition, with regard to both real-time noninvas