ライフサイエンスコーパス: Egr-2

1 re unchanged in Th17 cells in the absence of Egr-2.

2 Furthermore, alpha-GalCer-induced egr-2/3 in hepatic NKT cells upregulated their TRAIL in

3 small interfering RNA-mediated depletion of Egr-2 5 days after anergy induction does not appear to a

4 , we show that early growth response gene 2 (Egr-2), a zinc-finger transcription factor, is expressed

5 was significantly increased, suggesting that Egr-2 activates the expression of genes involved in the

6 Although the early growth response-2 (Egr-2, alias Krox20) protein shows structural and functi

7 essed c-Fos and Egr-1, as has been shown for Egr-2, all of which are the immediate early genes (IEGs)

8 hat the early growth response genes 2 and 3 (EGR 2 and EGR3), transcription factors that negatively r

9 no effect on the FasL promoter, it binds to Egr-2 and -3 and synergizes with them to superinduce exp

10 REB) activation and nuclear translocation of EGR-2 and c-fos proteins.

11 These data support the idea that Egr-2 and Egr-3 are involved in promoting a T cell recep

12 The early growth receptor (Egr) proteins Egr-2 and Egr-3 have recently been identified as TCR-ind

13 Overexpression of Egr-2 and Egr-3 induced endogenous ligand upregulation t

14 s positive selection, inhibits expression of Egr-2 and Egr-3, but not Egr-1.

15 accounted for by GILZ-mediated inhibition of Egr-2 and Egr-3, NFAT/AP-1-inducible transcription facto

16 rn of expression is found for family members Egr-2 and Egr-3.

17 clerosis patients have reduced expression of Egr-2 and increased expression of IL-17 following stimul

18 d mutual repression circuits of Gfi1 against Egr-2 and of TCF-1 against PU.1 as proposed elsewhere, b

19 ero (P0) gene, early growth response gene 2 (EGR-2) and connexin-32 gene, which are expressed in Schw

20 dentified here early growth response gene 2 (Egr-2) and Egr-3 as key negative regulators of T cell ac

21 iate early gene transcription factors EGR-1, EGR-2, and c-fos, with roles in learning and memory, and

22 promoter region of the FasL gene, and Egr-1, Egr-2, and Egr-3 mRNA in IEC from mice treated with SEB

23 from prostate tissues was probed with EGR-1, EGR-2, and EGR-alpha cDNA for Northern blots and digoxig

24 in diminished expression of c-Fos, Egr-1 and Egr-2, and partially rescued the neutrophil development

25 inhibited the expression of c-Fos, Egr-1 and Egr-2, and rescued neutrophil development in cells expre

26 stimulation with anti-CD28 failed to enhance Egr-2 binding and Zbtb16 expression.

27 e splicing regulation was also observed with egr-2, but not with c-myc.

28 eling and wound healing were up-regulated by Egr-2, but the Egr-2-regulated gene expression profile o

29 In the absence of Egr-2, CD4 T cells produce high levels of Th17 cytokines

30 In the absence of Egr-2, CD44(high), but not CD44(low) T cells, are hyperr

31 ent kinase inhibitor p21cip1 was impaired in Egr-2-deficient T cells, whereas the expression of IFN-g

32 IL-27 suppressed osteoclastogenesis in an Egr-2-dependent manner that up-regulates Id2, the repres

33 brotic TGF-beta responses were attenuated in Egr-2-depleted fibroblasts.

34 The EGR family comprises of EGR 1, EGR 2, EGR 3 and EGR 4 which are involved in the transac

35 ering the expression of other family members Egr-2, Egr-3 and Egr-4.

36 Gene array screening revealed high Egr-2 expression distinctly persists in anergized but no

37 ed mothers, showing higher c-fos, egr-1, and egr-2 expression in response to the hallucinogenic drug

38 o enhance IL-2 and Egr-1 expression, whereas Egr-2 expression is greatly increased.

39 These data indicate that sustained Egr-2 expression is necessary to induce a full anergic s

40 bited osteoblast apoptosis through increased Egr-2 expression, which induces anti-apoptotic factors l

41 reased serum IL-27 levels along with reduced Egr-2 expression.

42 Egr-1 and Egr-2 function redundantly to activate macrophage genes

43 Silencing Egr-2 gene expression by small interfering RNA treatment

44 Thus, Egr-2, in addition to Egr-3, regulates FasL expression i

45 Egr-2 interacts with Batf in CD4 T cells and suppresses

46 hese results provide the first evidence that Egr-2 is a functionally distinct transcription factor th

47 These results demonstrate that Egr-2 is an intrinsic regulator of effector T cells and

48 Collectively, our results demonstrate that Egr-2 is an intrinsic regulator that controls Th17 diffe

49 IL-17 expression and Th17 differentiation by Egr-2 is due to inhibition of Batf, a transcription fact

50 expression in activated normal T cells, and Egr-2 is likely to play a direct role in aberrant fasL u

51 ysis revealed these proteins to be Egr-1 and Egr-2 (Krox-20); Egr-3 was not detected.

52 ification of the early growth response gene (Egr-2; Krox-20), a zinc-finger transcription factor, as

53 -mediated downregulation of c-Fos, Egr-1 and Egr-2 may contribute to the role of Gfi1 in granulopoies

54 Targeting Egr-2 might represent a novel therapeutic strategy to co

55 tial suppression of basal striatal egr-1 and egr-2 mRNA expression but not of that of egr-3.

56 iated suppression of basal fra-1, egr-1, and egr-2 mRNA levels suggests that their basal expression i

57 alyses demonstrated increased EGR-1, but not EGR-2 or EGR-alpha expression, in malignant prostate tis

58 Together, these findings suggest that Egr-2 plays an important nonredundant role in the pathog

59 Thus, Egr-2 plays an important role to intrinsically control T

60 Egr-2 plays essential roles in peripheral nerve myelinat

61 rogation of anergy causes rapid depletion of Egr-2 protein.

62 healing were up-regulated by Egr-2, but the Egr-2-regulated gene expression profile overlapped only

63 ; thus, these genes, which include Egr-1 and Egr-2, represent candidate mediators of positive selecti

64 T cells lacking Egr-2 show increased propensity for Th17, but not Th1 or

65 inhibits the expression of c-Fos, Egr-1 and Egr-2 through direct transcriptional repression and indi

66 Supplementation of IL-27 activates Egr-2 to induce IL-10 producing Tr1 cells.

67 owth response protein (Egr)-2 and binding of Egr-2 to the promoter of Zbtb16, which encodes PLZF, and

68 Egr-1, Egr-2, Vitamin D Receptor, MafB/c: Fos and PU.1:interfer

69 pressed Egr-1 was ineffective, overexpressed Egr-2 was as potent as Egr-3 in inducing fasL promoter-d

70 As with egr-3, expression of egr-2 was blocked by cyclosporin A.

71 Moreover, elevated Egr-2 was noted in biopsy specimens of skin and lung fro

72 Overexpression of Egr-2 was sufficient to stimulate collagen gene expressi

73 contains binding sites for Sp1, AP1TFII and EGR-2, was important for EMMPRIN transcription in both T

74 Levels of Egr-2 were elevated in lesional tissue from mice with bl

75 rker expression of M2-like markers CD206 and EGR-2 were present on macrophages.

76 We have now discovered that Egr-2, which is induced by TGF-beta and IL-6, negatively