التفاصيل البيبلوغرافية
| العنوان: |
Proviral integration site 2 is required for interleukin-6 expression induced by interleukin-1, tumour necrosis factor-α and lipopolysaccharide. |
| المؤلفون: |
Jianfei Yang, Xiang Li, Hanidu, Adedayo, Htut, Tin M., Sellati, Rosemarie, Lian Wang, Huiping Jiang, Jun Li |
| المصدر: |
Immunology; Oct2010, Vol. 131 Issue 2, p174-182, 9p, 6 Graphs |
| مصطلحات موضوعية: |
INTERLEUKIN-6, TUMOR necrosis factors, APOPTOSIS, HELA cells, RNA, RHEUMATOID arthritis |
| مستخلص: |
PIM (proviral integration site) kinases are a distinct class of serine/threonine-specific kinases consisting of PIM1, PIM2 and PIM3. PIM2 is known to function in apoptosis pathways. Expression of PIM2 is highly induced by pro-inflammatory stimuli but the role of PIM2 in the expression of pro-inflammatory cytokines is unclear. In this study, we showed that over-expression of PIM2 in HeLa cells as well as in human umbilical vein endothelial cells enhanced interleukin-1β (IL-1β) -induced and tumour necrosis factor-α-induced IL-6 expression, whereas over-expression of a kinase-dead PIM2 mutant had the opposite effect. Studies with small interfering RNA specific to PIM2 further confirmed that IL-6 expression in HeLa cells requires PIM2. To investigate the function of PIM2 further, we generated PIM2-deficient mice. It was found that IL-6 production was significantly decreased from PIM2-deficient spleen cells after stimulation with lipopolysaccharide. Taken together, we demonstrated an important function of PIM2 in controlling the expression of the pro-inflammatory cytokine IL-6. PIM2 inhibitors may be beneficial for IL-6-mediated diseases such as rheumatoid arthritis. [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: |
Complementary Index |
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