ライフサイエンスコーパス: IL-3R

1 hinella-induced basophil responses were IL-3-IL-3R independent but critically dependent on TSLP-TSLPR

2 could elicit basophil responses in both IL-3-IL-3R-sufficient and -deficient environments, and genome

3 mice, we report in this study that the IL-3/IL-3R system is absolutely required to recruit circulati

4 on activates transcription factor CREB after IL-3R engagement.

5 he entire cytoplasmic domain of IL-3R alpha [IL-3R alpha(CD)] or carrying a substitution of trp for l

6 d to residues 306 through 379 of GM-R alpha [IL-3R alpha/GM-R alpha-DS] also failed to bind 125I-IL-3

7 subunit of the GM-CSF receptor (GM-R alpha) [IL-3R alpha/GM-R alpha] or the first 118 aa of GM-R alph

8 a 104 through 378 of IL-3R alpha [GM-R alpha/IL-3R alpha] failed to bind 125I-IL-3 in the presence of

9 n was potent because it inhibited FDC-P1, an IL-3R-expressing murine myelomonocytic tumor line (IC50

10 Preincubation of HUVECs with an IL-3R-blocking Ab (CD123) before the addition of IL-3 in

11 ile up-regulating alpha-chain mRNAs for both IL-3R and GM-CSFR as well as the beta-chain mRNA.

12 he CD11c+ DC subset (48-fold) and the CD11c- IL-3R+ DC precursors (13-fold).

13 e G-CSF domain can alter the ratio of G-CSFR:IL-3R agonist activities, demonstrating that it is a use

14 l line (Ba/F3), which endogenously expresses IL-3R.

15 (+) lymphoid progenitor population expresses IL-3R and proliferates in response to IL-3 and that IL-3

16 Cell lines not expressing IL-3R were not inhibited by the fusion protein.

17 , whereas enhanced accumulation of mRNAs for IL-3R alpha and the beta-chain results from reduced mRNA

18 anisms that are distinct from those used for IL-3R alpha and GM-CSFR alpha.

19 d basophil rolling and adhesion, implicating IL-3R activation on endothelial cells.

20 f GM-R alpha joined to aa 104 through 378 of IL-3R alpha [GM-R alpha/IL-3R alpha] failed to bind 125I

21 omposed of the first 104 amino acids (aa) of IL-3R alpha joined to aa 118 through 400 of the alpha su

22 king almost the entire cytoplasmic domain of IL-3R alpha [IL-3R alpha(CD)] or carrying a substitution

23 ar domain of EpoR fused to the endodomain of IL-3R beta-chain (E/beta), while the other contained the

24 ha, respectively, fused to the endodomain of IL-3R beta-chain.

25 human chondrocytes show strong expression of IL-3R at gene and protein levels.

26 might be heterogenous in their expression of IL-3R.

27 To identify regions of IL-3R alpha critical for ligand binding and receptor fun

28 ceptor composed of the first 281 residues of IL-3R alpha fused to residues 306 through 379 of GM-R al

29 exhibited significant surface expression of IL-3Rs and GM-CSFRs, as well as ERK1/2 phosphorylation i

30 subunit of the human interleukin-3 receptor (IL-3R alpha) is a 70-kD glycoprotein member of the hemat

31 F (cpG-CSF) sequences with an IL-3 receptor (IL-3R) agonist moiety attached at locations that corresp

32 nd downregulation of interleukin-3 receptor (IL-3R) beta-chain expression, and accelerated G-CSF-stim

33 lasm, in contrast to the mitogenic receptors IL-3R, IL-5R, GM-CSFR, which assemble as alphabeta heter

34 ukemias can express interleukin-3 receptors (IL-3R).

35 anulocyte-macrophage CSF (GM-CSF) receptors (IL-3R and GM-CSFR).

36 econdary transfer experiments indicated that IL-3R is not uniformly expressed on all primitive progen

37 We have recently shown that IL-3R occupancy activates a phosphatidylcholine-specific

38 atment of myeloid leukemias that express the IL-3R.

39 Approximately 38% of BMCPs expressed the IL-3R alpha-chain.

40 to be more potent than the coaddition of the IL-3R agonist and G-CSF in stimulating the production of

41 are distinguishable by the expression of the IL-3R alpha chain, the receptor of an early-acting hemat

42 3 cross-linking is due to stimulation of the IL-3R and induction of PDC maturation.

43 tions were found in which the linkage to the IL-3R agonist domain either restored (e.g., attachment a

44 of the beta subunit but, in contrast to the IL-3R alpha/GM-R alpha hybrid, demonstrated weak surface

45 The MPOs retained the ability to bind to the IL-3R with affinities similar to that of the parental MP

46 MPO in which the IL-3R agonist domain is attached to the cpG-CSF(L1)[133/

47 MPOs with the IL-3R agonist domain linked to cpG-CSFs in the first (re

48 3 with nearly the same affinity as wild-type IL-3R alpha.