IL-32θ downregulates CCL5 expression through its interaction with PKCδ and STAT3

Bak, Yesol; Kang, Jeong Woo; Kim, Man Sub; Park, Yun Sun; Kwon, Taeho; Kim, Soohyun; Jiang, Hong; Yoon, Do‐Young

doi:10.1016/j.cellsig.2014.09.015

Cited by 24 publications

(44 citation statements)

References 80 publications

(105 reference statements)

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“…To determine the molecular mechanisms, the authors used THP-1 cells and show that IL-32u inhibits PKC-d activity and, consequently, the p38 phosphorylation and NF-kB activity that decreases TNF-a production [44]. IL-32u also suppresses the production of CCL5 through interaction with PKC-d and inhibition of STAT3 transcriptional activity [45]. Thus, different isoforms of IL-32 can act as intracellular modulators of inflammation.…”

Section: General Properties Of Il-32mentioning

confidence: 99%

Interleukin 32: a novel player in the control of infectious diseases

Ribeiro‐Dias

Gomes

Silva

et al. 2016

Journal of Leukocyte Biology

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Interleukin 32 (IL-32) is a proinflammatory cytokine, expressed as 9 distinct isoforms. The most active isoform is the predominantly intracellular-functioning IL-32γ. Involvement of IL-32 in infectious diseases is increasingly being appreciated. Production of IL-32 promotes pathways that serve to control bacterial infection, especially those caused by mycobacteria. A similar role for this cytokine is observed in the cellular response to viral infections. In addition to its protective effects against microorganisms, IL-32 is involved in immunopathogenesis of some infectious diseases. In parasitic diseases, it has been demonstrated that this cytokine is induced by Leishmania infection. In this review, we summarize the present data on the role of IL-32 in infectious diseases, highlighting this cytokine as new target for control of infections.

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Section: General Properties Of Il-32mentioning

confidence: 99%

Interleukin 32: a novel player in the control of infectious diseases

Ribeiro‐Dias

Gomes

Silva

et al. 2016

Journal of Leukocyte Biology

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“…Bak et al (2014) reported that IL-32 θ by mediating the phosphorylation of STAT3 on Ser727 downregulates CCL5 expression by interacting with PKC δ and renders this chemokine transcriptionally inactive. This report suggested the role of IL-32 θ as an intracellular modulator of inflammation [ 27 ].…”

Section: Reviewmentioning

confidence: 99%

IL-32: A Novel Pluripotent Inflammatory Interleukin, towards Gastric Inflammation, Gastric Cancer, and Chronic Rhino Sinusitis

Khawar

Abbasi

Sheikh

2016

Mediators of Inflammation

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A vast variety of nonstructural proteins have been studied for their key roles and involvement in a number of biological phenomenona. Interleukin-32 is a novel cytokine whose presence has been confirmed in most of the mammals except rodents. The IL-32 gene was identified on human chromosome 16 p13.3. The gene has eight exons and nine splice variants, namely, IL-32α, IL-32β, IL-32γ, IL-32δ, IL-32ε, IL-32ζ, IL-32η, IL-32θ, and IL-32s. It was found to induce the expression of various inflammatory cytokines including TNF-α, IL-6, and IL-1β as well as macrophage inflammatory protein-2 (MIP-2) and has been reported previously to be involved in the pathogenesis and progression of a number of inflammatory disorders, namely, inflammatory bowel disease (IBD), gastric inflammation and cancer, rheumatoid arthritis, and chronic obstructive pulmonary disease (COPD). In the current review, we have highlighted the involvement of IL-32 in gastric cancer, gastric inflammation, and chronic rhinosinusitis. We have also tried to explore various mechanisms suspected to induce the expression of this extraordinary cytokine as well as various mechanisms of action employed by IL-32 during the mediation and progression of the above said problems.

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“…To determine which domain of IL-32 binds to VHL, the interaction between different IL-32 isoforms and VHL was examined. All isoforms of IL-32 [ 33 ] bound to VHL (Figure 4B ). Since only the exon 7-coded region is common to all isoforms of IL-32, it was the only regions shown to interact with VHL (Figure 4C ).…”

Section: Resultsmentioning

confidence: 99%

Von Hippel-Lindau regulates interleukin-32β stability in ovarian cancer cells

et al. 2017

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Hypoxia-induced interleukin-32β (IL-32β) shifts the metabolic program to the enhanced glycolytic pathway. In the present study, the underlying mechanism by which hypoxia-induced IL-32β stability is regulated was investigated in ovarian cancer cells. IL-32β expression increased under hypoxic conditions in ovarian cancer cells as it did in breast cancer cells. The amount of IL-32β was regulated by post-translational control rather than by transcriptional activation. Under normoxic conditions, IL-32β was continuously eliminated through ubiquitin-dependent degradation by the von-Hippel Lindau (VHL) E3 ligase complex. Oxygen deficiency or reactive oxygen species (ROS) disrupted the interaction between IL-32β and VHL, leading to the accumulation of the cytokine. The fact that IL-32β is regulated by the energy-consuming ubiquitination system implies that it plays an important role in oxidative stress. We found that IL-32β reduced protein kinase Cδ (PKCδ)-induced apoptosis under oxidative stress. This implies that the hypoxia- and ROS-stabilized IL-32β contributes to sustain survival against PKCδ-induced apoptosis.

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IL-32θ downregulates CCL5 expression through its interaction with PKCδ and STAT3

Cited by 24 publications

References 80 publications

Interleukin 32: a novel player in the control of infectious diseases

Interleukin 32: a novel player in the control of infectious diseases

IL-32: A Novel Pluripotent Inflammatory Interleukin, towards Gastric Inflammation, Gastric Cancer, and Chronic Rhino Sinusitis

Von Hippel-Lindau regulates interleukin-32β stability in ovarian cancer cells

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