Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:P10145 (
IL-8
)
23,849
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Expression of interleukin-1 receptor type II (IL1R2), a decoy receptor for pro-inflammatory interleukin 1 (IL-1), is enhanced by chronic exposure of the human uroepithelial cell line HUC-1 to arsenite. To explore the function of IL1R2, we ectopically expressed IL1R2 in HUC-1 cells. IL1R2 overexpression results in changes in cell morphology, actin rearrangement, and promoted cell migration. Ectopic expression of IL1R2 specifically blocked exogenous IL-1beta signaling but increased expression of the precursor form of IL-1alpha (pIL-1alpha) and its downstream targets, including interleukin 6 (IL-6),
interleukin 8
(
IL-8
), and type I collagen alpha1 (COL1A1). However, depleting gene expression using small RNA interference specific to either pIL-1alpha or COL1A1, but not IL-6 or
IL-8
, significantly attenuated the migration of IL1R2-overexpressing cells. Furthermore, IL1R2 overexpression was associated with enhanced expression of
Smad-interacting protein 1
(
SIP-1
) and reduced expression of E-cadherin. Because
SIP-1
is a repressor of COL1A1-induced E-cadherin expression, the present results suggest that IL1R2 overexpression is likely through activation of the pIL-1alpha pathway to enhance cell migration.
...
PMID:Ectopic expression of interleukin-1 receptor type II enhances cell migration through activation of the pre-interleukin 1alpha pathway. 1902 58
