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UCSC Genome Browser Gene Interaction Graph
Gene interactions and pathways from curated databases and text-mining

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CSF2 — IKBKB

Pathways - manually collected, often from reviews:

  • OpenBEL Selventa BEL large corpus: CSF2 → IKBKB (increases, CSF2 Activity) Newton et al., J Pharmacol Exp Ther 2007*
    Evidence: In these studies, IBN and dominantnegative IKK2, but not dominant-negative IKK1 or an empty (null) virus, prevented the induction of NF-B DNA binding and the induction of NF-B-dependent transcription in A549 cells (Catley et al., 2005). This previous study documented a parallel inhibitory effect on the expression of ICAM-1, GMCSF, and IL-8. In the current investigation, we have reexamined the supernatants from this earlier study and now extend our observations to include IL-6 (Fig. 1)
  • NCI Pathway Database GMCSF-mediated signaling events: IKK beta (IKBKB) → GMCSF/GMR alpha/CSF2RB (dimer) complex (CSF2RB-CSF2-CSF2RA) (modification, collaborate)
    Ebner et al., Blood 2003
    Evidence: physical interaction
  • NCI Pathway Database GMCSF-mediated signaling events: IKK beta (IKBKB) → GMCSF/GMR alpha/CSF2RB (dimer)/IKK beta complex (CSF2RB-IKBKB-CSF2-CSF2RA) (modification, collaborate)
    Ebner et al., Blood 2003
    Evidence: physical interaction
  • NCI Pathway Database GMCSF-mediated signaling events: GMCSF/GMR alpha/CSF2RB (dimer) complex (CSF2RB-CSF2-CSF2RA) → GMCSF/GMR alpha/CSF2RB (dimer)/IKK beta complex (CSF2RB-IKBKB-CSF2-CSF2RA) (modification, collaborate)
    Ebner et al., Blood 2003
    Evidence: physical interaction

Text-mined interactions from Literome

Catley et al., Br J Pharmacol 2005 (Asthma) : Similarly, IKK beta ( KA ) and I kappa B alpha delta N overexpression also inhibited IL-1beta- and TNF alpha dependent increases in ICAM-1, IL-8 and GM-CSF in addition to IL-1beta mediated increases in cyclooxygenase-2 expression, whereas IKK alpha ( KM ) overexpression had little effect on these outputs
Brummer et al., Med Mycol 2005 (Inflammation) : We postulated that DEX inhibition of NF-kappaB was opposed by induction of IkappaB kinases (IKK) by GM-CSF + conidia stimulation, degradation of IkappaB, and release of nuclear factor kappa B (NF-kappaB)
Catley et al., Mol Pharmacol 2006 (Pulmonary Disease, Chronic Obstructive) : As observed above, ICAM-1, IL-6, IL-8, GM-CSF , RANTES, MCP-1, GROalpha, NAP-2, and ENA-78 expression was reduced by the IKK inhibitors
Grund et al., Mol Pharmacol 2008 (Endometriosis...) : Interestingly, MEK, p38, and IKK inhibitors block TNF-alpha induced IL-8, IL-6, and GM-CSF secretion and 12z invasion, whereas the PI3K inhibitors do not