ライフサイエンスコーパス: PRDX6

1 onformational and thermodynamic stability of Prdx6.

2 e influence of pH on the oligomeric state of Prdx6.

3 eroxidase and phospholipase A2 activities of Prdx6.

4 nd the glial expression of Prdx1, Prdx4, and Prdx6.

5 t the effect requires the PLA(2) activity of Prdx6.

6 Peroxiredoxin 6 (Prdx6), a bifunctional enzyme with glutathione peroxidas

7 Peroxiredoxin 6 (Prdx6), a bifunctional protein with phospholipase A2 (ai

8 We identified peroxiredoxin 6 (Prdx6), a host factor that contributes to pulmonary surf

9 ound that uterine levels of peroxiredoxin-6 (PRDX6), a unique antioxidant, are significantly lower in

10 Peroxiredoxin 6 (Prdx6), a unique non-seleno peroxidase, is a bifunctiona

11 PRDX6 activation generates reactive oxygen species via N

12 (GSTP1), a key antioxidant enzyme needed for PRDX6 activation, demonstrated synergistic effects both

13 ur data point to the potential usefulness of Prdx6 activators or inhibitors for controlling different

14 lack the phospholipase A2 activity (PLA2) of Prdx6; addition of either lysophosphatidylcholine (LPC)

15 Peroxiredoxin 6 (PRDX6) (also called antioxidant protein 2, or AOP2) is a

16 Four proteins, TNNT1, MDH1, PRDX6 and ENO3 were qualified and verified for tendernes

17 Moreover, combined inhibition of PRDX6 and glutathione S-transferase Pi 1 (GSTP1), a key

18 Notably, both PRDX6 and GSTP1 are highly expressed in the developing m

19 sults provide insights into the potential of PRDX6 and GSTP1 as therapeutic targets for differentiati

20 e association between elevated expression of PRDX6 and human MYCN-amplified neuroblastoma subtype.

21 ld-type cells resulted in phosphorylation of Prdx6 and its subsequent translocation from the cytosol

22 se beads, a pull-down assay using His-tagged Prdx6 and Ni(2) -chelating beads, co-immunoprecipitation

23 Recombinant human Prdx6 and SP-A isolated from human alveolar proteinosis

24 ings implicate miR-371-3p as a suppressor of PRDX6 and suggest that co-targeting of peroxiredoxin 6 o

25 se 2 and 3 (GPx2 and GPx3), peroxiredoxin 6 (Prdx6), and sulfyhydryl oxidase Q6 (Qscn6).

26 1-cysteine peroxiredoxin (1-Cys Prx, Prx VI, Prdx6, and AOP2).

27 Prdx1, Prdx2, and to a lesser extent Prdx4, Prdx6, and Trx1 are localized mainly in the nucleus of n

28 ated levels of ROS and reduced expression of PRDX6, and underwent apoptosis.

29 ioredoxins, and glutaredoxins between normal Prdx6-/- and Prdx6+/+ mice and those injected with paraq

30 e (Prdx6+/+) macrophages, and of paraquat on Prdx6-/- and Prdx6+/+ mice.

31 rogen peroxide, and t-butyl hydroperoxide on Prdx6-/- and wild-type (Prdx6+/+) macrophages, and of pa

32 We identified Prdx6 as an important player in different phases of skin

33 This study identifies peroxiredoxin 6 (PRDX6) as a crucial modulator of glutathione peroxidase

34 Here, we identify peroxiredoxin 6 (PRDX6) as a promising therapeutic target in NB.

35 f Prdx6 that triggers the oligomerization of Prdx6 at low pH.

36 e showed calcium-independent SP-A binding to Prdx6 at pH 4.0 and partial Ca(2+) dependence of binding

37 Interaction of SP-A and Prdx6 at pH 7.4 was shown by Prdx6-mediated inhibition o

38 Pla cleaves Prdx6 at three distinct sites, and these cleavages disru

39 ow that the transduction of Peroxiredoxin 6 (PRDX6) attenuates TNF-alpha- and glutamate-induced RGC d

40 nd biochemical analyses, we demonstrate that PRDX6 binds to GPX4 via a C47 disulfide bond, facilitati

41 Selective inhibition of PRDX6 blocks Galphai depalmitoylation, prevents the enha

42 tute for Ser for the enzymatic activities of Prdx6 but not for its targeting to LB.

43 x6 null cells with wild-type and C47S mutant Prdx6, but not with mutants of the PLA(2) active site (S

44 ism for regulation of the PLA(2) activity of Prdx6 by SP-A.

45 MJ33 inhibited the PRDX6 Ca(2+)-iPLA2 activity and reduced these parameters

46 In conclusion, the inhibition of the PRDX6 Ca(2+)-iPLA2 activity promotes an oxidative stress

47 Mechanistically, we demonstrate that PRDX6 can readily react with selenide and interact with

48 da and fusion with the oolemma were lower in Prdx6 (-/-) capacitated spermatozoa than WT capacitated

49 rf2 activator, Sulforaphane (SFN), augmented Prdx6, catalase and GSTpi expression in dose-dependent f

50 llectively, our results suggest that loss of Prdx6 caused by dysregulation of ARE/Nrf2 can be attenua

51 effect on cells or lungs from Prdx6-null or Prdx6-D140A-knock-in mice that lack the phospholipase A2

52 with either wild-type or Deltapla Y. pestis, Prdx6-deficient mice exhibit no differences in bacterial

53 also inactivates dopamine D2 receptors in a PRDX6-dependent manner.

54 Collectively, our findings delineate a PRDX6-dependent mechanism in ferroptosis defense, offeri

55 n by U50,488 and dynorphin B also stimulated PRDX6-dependent ROS production but with an inverted U-sh

56 PRDX6, endowed with phospholipase A2 activity, catalyzes

57 Furthermore, high PRDX6 expression correlates with shorter progression-fre

58 PRDX6 expression is associated with poor prognosis in ca

59 mportantly, knockdown of Prdx6 revealed that Prdx6 expression was prerequisite for SFN-mediated cytop

60 load during aging was linked to a decline in Prdx6 expression.

61 32 has been identified as the active site in Prdx6 for aiPLA2 activity, and this activity was abolish

62 Results provide a rationale for use of PRDX6 for blocking ROS-mediated pathophysiology in glauc

63 r instance, under acidic condition (pH 4.0), Prdx6 forms higher oligomers with concommittant gain in

64 urements and analytical SEC revealed that Wt Prdx6 forms oligomers at low pH but not the mutant prote

65 Thus, while Pla is able to disrupt Prdx6 function in vitro and reduce Prdx6 levels in vivo,

66 mouse model carrying an S32T mutation in the Prdx6 gene but were absent from isolated LB.

67 Thus, PRDX6 has a critical role in the protection of the mouse

68 Prdx6 has been localized to both cytosol and lamellar bo

69 reduce Prdx6 levels in vivo, the cleavage of Prdx6 has little detectable impact on the progression or

70 ith a decrease in the levels of catalase and PRDX6 in exosomes derived from HIV-1-infected cells.

71 uamous cell carcinomas, indicating a role of Prdx6 in human skin carcinogenesis.

72 Finally, we found strong expression of PRDX6 in keratinocytes of normal human skin and in the t

73 kin tumorigenesis, whereas overexpression of Prdx6 in keratinocytes of transgenic mice had the opposi

74 Loss of Prdx6 in mice enhanced the susceptibility to skin tumori

75 ning of rat retina disclosed the presence of PRDX6 in RGCs, and Western and real-time PCR analysis re

76 ese results confirm an important role for LB Prdx6 in the degradation and remodeling of lung surfacta

77 estis reduces the abundance of extracellular Prdx6 in the lungs compared to that after infection with

78 urrent study, we aimed to define the role of PRDX6 in the pathophysiology of type 2 diabetes (T2D) us

79 tapla Y. pestis, suggesting that Pla cleaves Prdx6 in the pulmonary compartment.

80 Sec metabolism mediated by peroxiredoxin 6 (PRDX6), independent of SCLY.

81 and lower in WT spermatozoa treated with the PRDX6 inhibitor.

82 In conclusion, we demonstrated that PRDX6 is a key mediator of overt hyperglycemia in T2D gl

83 Our study provides in vivo evidence that PRDX6 is a unique non-redundant antioxidant that functio

84 We now demonstrate that Prdx6 is required for agonist-induced NOX2 activation in

85 Peroxiredoxin 6 (Prdx6) is a "moonlighting" protein with both GSH peroxid

86 Peroxiredoxin 6 (PRDX6) is a key regulator of cellular redox balance, wit

87 The antioxidant enzyme peroxiredoxin 6 (Prdx6) is a key regulator of the cellular redox balance,

88 Peroxiredoxin 6 (Prdx6) is essential for activation of NADPH oxidase type

89 wing opioid administration, peroxiredoxin 6 (PRDX6) is recruited to the opioid receptor complex by c-

90 )activity of phosphorylated peroxiredoxin 6 (Prdx6) is required for activation of NADPH oxidase (NOX2

91 thophysiology of type 2 diabetes (T2D) using PRDX6 knockout (-/-) mice.

92 dx6 transgenic mice and the higher levels in Prdx6-knockout mice than in control animals.

93 We propose that Prdx6 LB targeting facilitates its role in the metabolis

94 ffect in tumor prevention, overexpression of Prdx6 led to an acceleration of malignant progression of

95 d that Fkbp52(-/-) mice with reduced uterine PRDX6 levels are susceptible to paraquat-induced oxidati

96 o disrupt Prdx6 function in vitro and reduce Prdx6 levels in vivo, the cleavage of Prdx6 has little d

97 erine OS in Fkbp52(-/-) females with reduced PRDX6 levels induces implantation failure even in the pr

98 at Fkbp52 deficiency associated with reduced PRDX6 levels promotes H(2)O(2)-induced cell death, which

99 inishes the threshold against OS by reducing PRDX6 levels.

100 tyl hydroperoxide on Prdx6-/- and wild-type (Prdx6+/+) macrophages, and of paraquat on Prdx6-/- and P

101 Prdx6-/- macrophages had higher hydrogen peroxide levels

102 Prdx6 (-/-) male mice are subfertile, and the deficiency

103 pamine receptors stimulates peroxiredoxin 6 (PRDX6)-mediated production of reactive oxygen species (R

104 ion of SP-A and Prdx6 at pH 7.4 was shown by Prdx6-mediated inhibition of SP-A binding to agarose bea

105 We demonstrated that PRDX6(-/-) mice developed a phenotype similar to early-s

106 Impaired insulin signaling was present in PRDX6(-/-) mice, leading to reduction of muscle glucose

107 nd glutaredoxins between normal Prdx6-/- and Prdx6+/+ mice and those injected with paraquat.

108 macrophages, and of paraquat on Prdx6-/- and Prdx6+/+ mice.

109 n peroxide levels, and lower survival rates; Prdx6-/- mice had significantly lower survival rates, mo

110 nctions, we generated Prdx6-targeted mutant (Prdx6-/-) mice, confirmed the gene disruption by Souther

111 Prdx6 mRNA was also expressed in every tissue examined.

112 ed in perfused lungs and isolated PMVEC from Prdx6 null mice.

113 after Ang II treatment in wild-type but not Prdx6 null PMVEC.

114 had much less effect on cells or lungs from Prdx6-null or Prdx6-D140A-knock-in mice that lack the ph

115 We elucidate the impact of the lack of PRDX6 or inhibition of its calcium-independent phospholi

116 sphorylated p67(phox) did not bind to either Prdx6 or phosphoPrdx6.

117 We identify PRDX6 (peroxiredoxin 6) as a key target of miR-371-3p in

118 strongly to phosphoPrdx6 but bound poorly to Prdx6; phosphorylated p67(phox) did not bind to either P

119 us, agonist-induced MAPK activation leads to Prdx6 phosphorylation and translocation to the cell memb

120 MJ33, an inhibitor of Prdx6 PLA(2) activity, blocked agonist-induced PLA(2) ac

121 y PMVECs required Prdx6-PLA2 We propose that Prdx6-PLA2 modulates NOX2 activation by generation of LP

122 Thus, Prdx6-PLA2 modulates NOX2 activation through generation

123 The generation of LPC by PMVECs required Prdx6-PLA2 We propose that Prdx6-PLA2 modulates NOX2 act

124 The PRDX6 played dual roles in EC barrier function through g

125 Among the six isoforms (PRDX1-PRDX6), PRDX3 is the only protein exclusively localized

126 reduction in Nrf2/ARE binding (-357/-349) of Prdx6 promoter.

127 A supply of PRDX6 protected RGCs from glutamate and TNF-alpha induce

128 l-time PCR analysis revealed an abundance of PRDX6 protein and mRNA.

129 Prdx6 protein expression and aiPLA2 activity were normal

130 ohistochemistry, we have determined that the PRDX6 protein was widely expressed in every tissue exami

131 These findings establish JNK-dependent PRDX6 recruitment and oxidation-induced Galphai depalmit

132 Rather, endogenous and overexpressed Prdx6 reduced oxidative stress as reflected by the lower

133 Pharmacological inhibition of PRDX6 reduces MYCN levels, induces apoptosis, and promot

134 Importantly, knockdown of Prdx6 revealed that Prdx6 expression was prerequisite fo

135 Target genes include HuR for miR-139-3p and Prdx6, Runx1, and Suz12 for miR-199a-3p.

136 , and lung LB was increased significantly in Prdx6-S32T mutant lungs, whereas degradation of internal

137 This study shows that FKBP52-PRDX6 signaling protects pregnancy from overt OS.

138 ilization and blastocyst rates were lower in Prdx6 (-/-) spermatozoa than in C57BL/6J wild-type (WT)

139 The widespread expression of Prdx6 suggested that its functions were quite important.

140 e addition of NAC or by forced expression of PRDX6, suggesting that Fkbp52 deficiency diminishes the

141 To determine these functions, we generated Prdx6-targeted mutant (Prdx6-/-) mice, confirmed the gen

142 nion (O2(* horizontal line )) were higher in Prdx6 (-/-) than in WT spermatozoa (p </= 0.05).

143 ach other to induce conformational change of Prdx6 that triggers the oligomerization of Prdx6 at low

144 e that SP-A regulates the PLA(2) activity of Prdx6 through direct protein-protein interaction.

145 sections demonstrated the inability of S32T Prdx6 to bind to the chaperone protein, 14-3-3, that is

146 y was unaffected by mutation of serine 32 in Prdx6 to threonine (S32T).

147 eceptor activation recruits peroxiredoxin 6 (PRDX6) to the receptor-Galphai complex by c-Jun N-termin

148 phospholipids in the protumorigenic skin of Prdx6 transgenic mice and the higher levels in Prdx6-kno

149 recipitation of p67(phox) and phosphorylated Prdx6 was demonstrated with lysates of mouse pulmonary m

150 eraction of p67(phox) with nonphosphorylated Prdx6 was relatively weak.

151 Indeed, Prdx1, Prdx4, and Prdx6, which are expressed in glial cells in the adult C

152 rough NRF2-dependent regulation of Mgst3 and Prdx6, which encode two glutathione-dependent peroxidase

153 dicate a direct interaction between SP-A and Prdx6, which provides a mechanism for regulation of the

154 The tumor-preventive effect of Prdx6, which was observed in a human papilloma virus 8-i

155 Combining the inhibition of PRDX6 with ferroptosis inducers increases lipid peroxida

156 We investigated the interaction of Prdx6 with p67(phox) and its effect on NOX2 activity.