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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

54 Egr-2 plays essential roles in peripheral nerve myelinat

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

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

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

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

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

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

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

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

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

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

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

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

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

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