ライフサイエンスコーパス: IL-12 p35

1 IL-12 p35 mRNA was constitutive and inducible.

2 PS and MPL to induce interleukin-10 (IL-10), IL-12 p35, IL-12 p40, gamma interferon (IFN-gamma), gluc

3 n the induction of cyclooxygenase 2 (COX-2), IL-12 p35, IL-12 p40, TNF-alpha, IFN-inducible protein (

4 Mitigated induction of COX-2, IL-12 p35, and IL-12 p40 gene expression by CD11b/CD18-d

5 In contrast, for optimal induction of COX-2, IL-12 p35, and IL-12 p40 genes by low concentrations of

6 family of cytokines that is comprised of an IL-12 p35 subunit and an IL-12 p40-related protein subun

7 lation and that IL-23 p19-/-, IL-17R-/-, and IL-12 p35-/- mice also show increased susceptibility to

8 35, a bioactive cytokine comprising EBI3 and IL-12 p35.

9 ) of IL-10 suppression of both IL-12 p40 and IL-12 p35 genes is primarily seen at the transcriptional

10 ed in IRF-1-/- mice, pulmonary IL-12 p40 and IL-12 p35 mRNA were not dysregulated.

11 The accumulation of mRNA for both IL-12 p35 and p40 genes was inhibited by chemokine pretr

12 compound, STA-5326, that down-regulates both IL-12 p35 and IL-12/IL-23 p40 at the transcriptional lev

13 Consistently, IL-12 p35(-/-), IFN-gamma(-/-), and LTbeta(-/-) mice are

14 nity, Th1 development was assessed in either IL-12 p35 knockout (p35-/-) mice, the cells of which are

15 iled to affect steady-state levels of either IL-12 p35 or p40 mRNA, but augmented IL-10 mRNA levels.

16 ession of il12a transcription, which encodes IL-12 p35 chain, by proteins of the Notch family and lys

17 tion, C5a reduced the expression of mRNA for IL-12 p35, p40, IL-23 p19, and IL-27 p28.

18 otection, since mice deficient in IFN-gamma, IL-12 p35, or IL-12 p40 all succumbed to LVS doses that

19 BP-response element (ICSBP-RE), in the human IL-12 p35 promoter through physical association with IRF

20 associated with a proportionate decrease in IL-12 p35 and p40 mRNA accumulation.

21 n-on assays revealed comparable decreases in IL-12 p35 and p40 gene transcription.

22 n of IL-12 p40 was even further increased in IL-12 p35-deficient mice, and in this case, was associat

23 , macrophages exhibited impaired LPS-induced IL-12 p35 mRNA expression.

24 tures increased the induction of MPL-induced IL-12 p35, IL-12 p40, and IFN-gamma mRNA, suggesting tha

25 ation of IL-12 p40 mRNA, but did not inhibit IL-12 p35 and TNF-alpha mRNA.

26 GC-BP selectively inhibits IL-12 p35 gene transcription by binding to its promoter

27 ommon to IL-12 and IL-23) and mice that lack IL-12 p35 (specific for IL-12) were infected and their r

28 The murine IL-12 p35 gene has promoters upstream from each of the f

29 12b(-/-)) or IL-23 p19 (Il23a(-/-)), but not IL-12 p35 (Il12a(-/-)), responded similarly to Tlr7(-/-)

30 ly controlling transcriptional activation of IL-12 p35 gene.

31 mma signaling in the selective activation of IL-12 p35 transcription in synergy with LPS-mediated eve

32 In the brain, expression of IL-12 p35 mRNA was constitutive and did not alter follow

33 LPS was a more potent inducer of IL-12 p35, IL-12 p40, and IFN-gamma mRNA, as well as of

34 ng pathway is essential for the induction of IL-12 p35 transcription by LPS.

35 We demonstrate that the levels of IL-12 p35 protein stimulated by IFN-gamma and lipopolysa

36 ERK1/2 phosphorylation and up-regulation of IL-12 p35 and p40 mRNA expression.

37 a selective impairment in mRNA synthesis of IL-12 p35 but not the p40 gene, and a strong deficiency

38 L-12 p40 steady-state mRNA, but not those of IL-12 p35, IL-1alpha, IL-1beta, or IL-6.

39 in IL-1alpha, IL-1beta, IL-18, TNF-alpha, or IL-12 p35 mRNA expression.

40 lammatory protein 1beta, interleukin-12 p35 (IL-12 p35), IL-23 p19, RANTES, IL-8, IFN-alpha/beta, and

41 LPS, IRF.1-/- mice produced less IL-12 p40, IL-12 p35, and IFN-gamma mRNA in the liver than IRF-1+/+

42 tion caused superinduction of the IL-12 p40, IL-12 p35, and TNF-alpha genes.

43 s revealed that the inhibition of IL-12 p40, IL-12 p35, and TNF-alpha was at the gene transcriptional

44 pretreatment, which selectively up-regulated IL-12 p35 mRNA.

45 Blocking GC-BP by RNA interference restores IL-12 p35 transcription and IL-12 p70 synthesis.

46 e findings, overexpression of TTP suppressed IL-12 p35 and p40 expression at the mRNA and promoter le

47 ance for intact IL-12/23 p40 expression than IL-12 p35 for immunity against Mycobacterium tuberculosi

48 d with nonlesional skin (P = 0.003), but the IL-12 p35 subunit was not increased in lesional skin.

49 ole in the transcriptional activation of the IL-12 p35 gene, but not of the p40 gene, by physically i

50 -gamma directly induces transcription of the IL-12 p35 gene, which encodes the light chain of IL-12,

51 aled that ICSBP is a potent activator of the IL-12 p35 gene.

52 for IL-12 p40 without down-regulation of the IL-12 p35 gene.

53 SBP and IRF-1 synergistically stimulates the IL-12 p35 promoter activity.

54 ting with an inverted IRF element within the IL-12 p35 promoter upon IFN-gamma activation.

55 cytokine, while p19 is distantly related to IL-12 p35.

56 oter and preferentially recruits p65/RelB to IL-12 p35 and p40 promoters, causing a decrease in IL-10

57 but exhibits a unique p19 subunit similar to IL-12 p35.

58 but contains a unique p19 subunit similar to IL-12 p35.

59 40 subunit, and IL-23 p19 overlaps well with IL-12 p35.