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CSF3 — IL5

Text-mined interactions from Literome

Akahane et al., Arzneimittelforschung 1990 : The enhanced G-CSF production from NFSA cells may be due at least to interleukin-1 released from muroctasin stimulated macrophages
Lopez et al., J Cell Physiol 1990 (Leukemia, Myelogenous, Chronic, BCR-ABL Positive) : Specificity studies under conditions that prevent receptor internalization showed that the binding of IL-3, GM-CSF, and IL-5 was not inhibited by tumor necrosis factor (TNF)-alpha, IL-1 beta, interferon (IFN)-gamma, or G-CSF
Leizer et al., Blood 1990 : Cytokine regulation of colony stimulating factor production in cultured human synovial fibroblasts : I. Induction of GM-CSF and G-CSF production by interleukin-1 and tumor necrosis factor
Jiang et al., J Int Med Res 2010 (Alzheimer Disease...) : Levels of a7 nAChR protein were significantly increased and levels of interleukin-1ß , tumour necrosis factor-a and nuclear factor-?B ( NF-?B ) protein were significantly decreased in the brain of APP transgenic mice in response to G-CSF
Wang et al., Int J Oncol 1995 : We report that all-trans retinoic acid ( tRA ) synergizes with LPS to enhance the production of granulocyte colony stimulating factor ( G-CSF ) in PMA treated cells, whereas the production of granulocyte-macrophage CSF, interleukin 1-beta (IL-1-beta), and tumor necrosis factor-alpha (TNF-alpha) is minimally affected by tRA
Ogawa et al., Am J Hematol 1996 : IL-2, IL-3, IL-4, IL-5 , and IL-6 were unable to induce G-CSF production
Pajkrt et al., Blood 1997 (Endotoxemia) : In group 1, G-CSF significantly enhanced the release of tumor necrosis factor (TNF), interleukin-6 (IL-6), IL-8, IL-1 receptor antagonist (IL-1ra), and soluble TNF receptors