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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