ライフサイエンスコーパス: Egr-3

1 and egr-2 mRNA expression but not of that of egr-3.

2 ession is found for family members Egr-2 and Egr-3.

3 known to be induced in the SCN by light, and egr-3, a zinc finger transcription factor not previously

4 Transient expression of Egr-3 alone increased fasL promoter activity in a cyclos

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

6 he expression of other family members Egr-2, Egr-3 and Egr-4.

7 mmunoprecipitation assays reveal that Egr-1, Egr-3, and NFAT1 present in primary human CD4 T cells ar

8 These data support the idea that Egr-2 and Egr-3 are involved in promoting a T cell receptor-induce

9 ere early growth response gene 2 (Egr-2) and Egr-3 as key negative regulators of T cell activation.

10 for the HIV long terminal repeat still binds Egr-3 but can no longer enhance Egr-mediated transactiva

11 oter and demonstrate that activation-induced Egr-3, but not Egr-1, directly upregulates fasL transcri

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

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

14 rly growth receptor (Egr) proteins Egr-2 and Egr-3 have recently been identified as TCR-induced negat

15 ective, overexpressed Egr-2 was as potent as Egr-3 in inducing fasL promoter-dependent reporter const

16 in nonlymphoid cells by forced expression of Egr-3 in the absence of any other stimulus.

17 Overexpression of Egr-2 and Egr-3 induced endogenous ligand upregulation that was in

18 In contrast to known examples, egr-3 induction by light is restricted to the ventral SC

19 Overexpression of Egr-1, but not Egr-3, is capable of augmenting transcription of this re

20 Activation-induced expression of Egr-3, like that of FasL, was inhibited by cyclosporin A

21 gion of the FasL gene, and Egr-1, Egr-2, and Egr-3 mRNA in IEC from mice treated with SEB and from tr

22 for by GILZ-mediated inhibition of Egr-2 and Egr-3, NFAT/AP-1-inducible transcription factors that bi

23 does not affect the induction of Nur-77 and Egr-3 nor the upregulation of CD69.

24 ds Egr family proteins and demonstrated that Egr-3 (PILOT) but not Egr-1 (NGFI-A, Krox-24, Tis-8, and

25 growth, differentiation, and apoptosis; and Egr-3 (PILOT), a transcription factor of no previously k

26 Thus, Egr-2, in addition to Egr-3, regulates FasL expression in activated normal T c

27 s demonstrated the binding of Egr-1, but not Egr-3, to the Arc promoter.

28 se proteins to be Egr-1 and Egr-2 (Krox-20); Egr-3 was not detected.