ライフサイエンスコーパス: M-CSF receptor

1 yte differentiation, as well as mRNA for the M-CSF receptor.

2 immediate early genes, and induction of the M-CSF receptor.

3 is mutation inhibited the degradation of the M-CSF receptor.

4 ge differentiation and activation, including M-CSF receptor.

5 of G- and GM-CSF receptors and no detectable M-CSF receptors.

6 asts genetically engineered to express human M-CSF receptors (3T3-FMS cells) and human monocytes.

7 NIH 3T3 fibroblasts expressing mutant human M-CSF receptors (3T3-FMS(Y809F)) that fail to activate R

8 om the macrophage colony-stimulating factor (M-CSF) receptor, a highly related receptor tyrosine kina

9 ll line RAW264; 2) SHIP2 associated with the M-CSF receptor after M-CSF stimulation; and 3) SHIP2 ass

10 ng from impaired signaling downstream of the M-CSF receptor and alpha(v)beta3 integrin.

11 duced expression of c-fms, which encodes the M-CSF receptor and is obligatory for macrophage differen

12 bolism, which in turn promoted expression of M-CSF receptor and transcription factors PU.1 and IRF8,

13 in Ba/F3 cells expressing both the G-CSF and M-CSF receptors and in lineage-negative murine marrow ce

14 Although the GM-CSF and M-CSF receptors are unrelated, both couple to Ras-depend

15 her c-Jun could promote the induction of the M-CSF receptor by collaborating with PU.1.

16 er partner CBF beta synergistically activate M-CSF receptor by more then 60 fold.

17 The CSF-1/M-CSF receptor c-fms and RAFTK appeared to associate in

18 wn-regulating cell surface expression of the M-CSF receptor c-Fms by a matrix metalloprotease- and MA

19 ion of Tyr-721, the PI3K binding site in the M-CSF receptor c-Fms, fails to suppress cytoskeletal rem

20 or the macrophage colony-stimulating factor (M-CSF) receptor c-Fms.

21 ed by the kinetic appearance of mRNA for the M-CSF receptor, c-fms, at day 3 following culture initia

22 treated them with a mAb directed against the M-CSF receptor, c-Fms.

23 so exhibited a higher level of expression of M-CSF receptor compared with normal controls.

24 M-CSF-activated AMPK is via M-CSF receptor-dependent reactive oxygen species product

25 -CSF monoclonal or polyclonal Abs or soluble M-CSF receptors, dramatically inhibited HIV-1 replicatio

26 These M-CSF receptor events correlated with activation of the

27 ndependent coactivator of PU.1, resulting in M-CSF receptor expression and development of the monocyt

28 The upregulation of M-CSF receptor expression by AML1-ETO may contribute to

29 ls exhibited a significantly higher level of M-CSF receptor expression than U937 cells.

30 Endogenous M-CSF receptor expression was examined in Kasumi-1 cells

31 genous macrophage colony-stimulating factor (M-CSF) receptor, Fms, we have analyzed the role of a new

32 ted by macrophage colony-stimulating factor (M-CSF), receptor for activation of NF-kappa B ligand (RA

33 EBPalpha, and CBF, regulate the NE, MPO, and M-CSF Receptor genes.

34 1, we have restored expression of the G- and M-CSF receptors in PU.1-deficient cells using retroviral

35 First, myeloid-specific expression of the M-CSF receptor is regulated transcriptionally by three f

36 of the macrophage colony-stimulating factor (M-CSF) receptor is regulated by three transcription fact

37 age RNA: Emr1 (F4/80), Itgam (CD11b), Csf1r (M-CSF Receptor), Itgal (CD11a), Tnf, and Nos2 Additional

38 hat SHIP-1 was involved in the regulation of M-CSF receptor (M-CSF-R)-induced Akt activation.

39 at the level of receptor expression and that M-CSF receptor (M-CSFR) may be used as an early marker o

40 sed by macrophage colony-stimulating factor (M-CSF) receptor mutations.

41 ch up-regulates the expression of functional M-CSF receptors on monocytes.

42 g from macrophage colony-stimulating factor (M-CSF) receptors or Fc receptors to the actin cytoskelet

43 human macrophage colony-stimulating factor (M-CSF) receptor presents an excellent model with which w

44 12-O-tetradecanoylphorbol-13-acetate-induced M-CSF receptor promoter activity during monocytic differ

45 ces the ability of PU.1 to transactivate the M-CSF receptor promoter as well as a minimal thymidine k

46 c-Jun does not directly bind to the M-CSF receptor promoter but associates via its basic dom

47 c differentiation, but the monocyte-specific M-CSF receptor promoter has no AP-1 consensus binding si

48 shown that AML1 and C/EBPalpha activate the M-CSF receptor promoter in a synergistic manner.

49 DNA binding to and transactivation of the M-CSF receptor promoter, a direct PU.1 target gene, were

50 ors interacting with critical regions of the M-CSF receptor promoter, including PU.1 and AML1.PU.1 is

51 L1 work synergistically to transactivate the M-CSF receptor promoter, thus exhibiting a different act

52 t, the macrophage colony-stimulating factor (M-CSF) receptor promoter.

53 Gab2, Gab3 is tyrosine phosphorylated after M-CSF receptor stimulation and associates transiently wi

54 al hematopoietic growth factor receptor, the M-CSF receptor, suggesting a mechanism of how the AML1 f

55 as the macrophage colony-stimulating factor (M-CSF) receptor, the granulocyte colony-stimulating fact

56 se the expression and internalization of the M-CSF receptor, thus overriding the IL-6/M-CSF pathway.

57 M-CSF treatment induced M-CSF receptor tyrosine phosphorylation and recruitment

58 ecific macrophage colony-stimulating factor (M-CSF) receptor, which is critical for monocytic cell su