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1 g HCEKs could be restored by the addition of c-kit ligand.
2 ls, such as those triggered by alpha-MSH and c-Kit ligand.
3 members of this family include M-CSF and the c-kit ligand.
4 /Fas-L-dependent signals that are blocked by c-kit ligand.
5 an be regulated in vitro by IL-3, IL-10, and c-kit ligand.
6 us different doses of stem cell factor (SCF; c-kit ligand) after chemotherapy or G-CSF alone after ch
7 lymphopoiesis is preceded by the actions of c-Kit ligand (also called stem cell factor; SCF) and fet
8 Culture of CD34(+) HPCs in the presence of c-Kit ligand and Axl-Fc resulted in a significant decrea
9 IL-3 to the combination of steel factor (SF, c-kit ligand) and IL-11 abrogated the B-lymphoid potenti
10 lls, during pre-expansion by thrombopoietin, c-kit ligand, and FLT-3 ligand, on recombinant fibronect
12 now report that glucocorticoids inhibit the c-kit ligand- and IL-3-induced proliferation of mBMMC, t
13 reated with either GM-CSF, GM-CSF plus IL-4, c-kit ligand (c-kitL), or G-CSF, class II+ CD11c+ cells
14 cells developed with interleukin (IL) 10 and c-kit ligand contain mMCP-9 transcript, whereas those de
17 cytokines (interleukin-2 [IL-2], IL-3, IL-7, c-kit ligand), FLT-3 ligand (FL), and stroma-derived fac
19 recursors when cultured for 12 to 14 days in c-kit ligand, granulocyte-macrophage colony-stimulating
20 s produced by nonosteoblastic stromal cells (c-Kit ligand, IL-6, and IL-3) shifted the cultures towar
22 , IDO, fms-related tyrosine kinase 3 ligand, c-kit ligand, inducible NO synthase, arginase-1, TNF-alp
27 PO and interleukin-3 (IL-3), or with TPO and c-kit ligand (KL) in the presence of a murine stromal ce
28 with interleukin (IL)-3 can be stimulated by c-kit ligand (KL) in the presence of IL-10 and IL-1beta
29 stimulation of Mo7 hematopoietic cells with c-Kit ligand (KL) induces phosphatidylinositol (PI) 3-ki
32 in the presence of interleukin (IL)-3, IL-6, c-kit ligand (KL), and leukemia inhibitory factor (LIF).
33 the expression patterns of Flt3 ligand (FL), c-Kit ligand (KL), and macrophage colony-stimulating fac
34 d limited clonal growth, but synergized with c-kit ligand (KL), flt3 ligand (FL), or IL-3 to potently
35 with interleukin-7 (IL-7), flt3 ligand (FL), c-kit ligand (KL), IL-3, IL-2, and AFT024, a murine feta
37 l system in which lack of transmembrane type c-kit ligand (KL2) expression on the somatic Sertoli cel
40 nd that seven markers at 12p22 within KITLG (c-KIT ligand) reached genome-wide significance (P < 5.0
41 rough analysis of the stem cell factor (SCF)/c-kit ligand receptor pair, we describe an additional di
46 ockout (-/-) mice after stimulation with the c-Kit ligand, stem cell factor (SCF), an important regul
47 ported that repetitive administration of the c-kit ligand, stem cell factor (SCF), can increase mast
49 munohistochemistry, expression levels of the c-kit ligand, stem cell factor, in skin and epidermis ar
50 s with VRP alone and in combination with the c-kit ligand/stem cell factor increased cell growth.
52 se to vascular endothelial growth factor and c-kit ligand these precursors give rise to colonies cont
53 EKs) transduced with FIH-1 were treated with c-kit ligand to establish further a FIH-1/c-kit interact
54 of specific cytokines in response to IgE or c-Kit ligand was markedly reduced in MEKK2(-/-) ESMC rel
55 edium with thrombopoietin, flk-2 ligand, and c-kit ligand, with or without IL-3 and found that CAFCs
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