ライフサイエンスコーパス: Egr-3

コーパス検索結果 (１語後でソート)

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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