Oligomerized CARD16 promotes caspase‐1 assembly and IL‐1β processing

Karasawa, Tadayoshi; Kawashima, Akira; Usui, Fumitake; Kimura, Hiroaki; Shirasuna, Koumei; Inoue, Yoshiyuki; Komada, Takanori; Kobayashi, Michie; Mizushina, Yoshiko; Sagara, Junji; Takahashi, Masafumi

doi:10.1016/j.fob.2015.04.011

Cited by 53 publications

(50 citation statements)

References 25 publications

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“…All protein levels were tested by Western blot analysis. and CARD16 [35] have been demonstrated as tumourrelevant genes (tumour-promoter or tumour-suppressor) in some cancers. By performing qRT-PCR, CYR61, IGFBP3 and WNT16B were negatively regulated, while NT5E, GDF15 and CARD16 were positively regulated through H2A.X Y39ph .…”

Section: Discussionmentioning

confidence: 99%

KRas-ERK signalling promotes the onset and maintenance of uveal melanoma through regulating JMJD6-mediated H2A.X phosphorylation at tyrosine 39

Peng

Zou

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Since DNA damage is a first incident occurred during a tumour attack, it is rational that histone H2A.X phosphorylation on tyrosine 39 (H2A.X Y39ph) may act as a tumour-relevant factor. This study was aimed to test the authenticity of the hypothesis. Uveal melanoma MP65 cells were transfected for expression of KRas mutated. H2A.X phosphorylation and ERK1/2 was measured, and transwell experiment was performed to examine the consequents of H2A.X Y39ph on MP65 cells developing and migration. Regulatory relationship between H2A.X Y39ph and ERK1/2 downstream genes were measured. Moreover, whether JMJD6 and MDM2 are involved in H2A.X phosphorylation was studied. Mutation of Ras activated ERK1/ 2 signalling and inhibited H2A.X phosphorylation at Y39. Silence of H2A.X Y39ph contributed to the regulation of MP65 cells growth, migration and transcription of ERK1/2 downstream genes, including CYR61, IGFBP3, WNT16B, NT5E, GDF15 and CARD16. The repressed H2A.X phosphorylation through Ras-ERK1/2 signalling might be through MDM2-mediated JMJD6 degradation. Our study suggested that Ras-ERK1/2 signalling inhibited H2A.X phosphorylation at Y39, which led to the uncontrolled developing and migration of uveal melanoma cells. In addition, H2A.X phosphorylation was mediated possibly through JMJD6 which could be degraded by MDM2.

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Section: Discussionmentioning

confidence: 99%

KRas-ERK signalling promotes the onset and maintenance of uveal melanoma through regulating JMJD6-mediated H2A.X phosphorylation at tyrosine 39

Peng

Zou

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…The NLRP3 inflammasome, a complex composed of NLRP3, ASC, and caspase‐1, is one of the best investigated inflammasomes and has been demonstrated to promote the production of proinflammatory cytokines . Upon stimulated by several substances, including LPS, the specific activation of NLRP3 and the assembly of the inflammasome complex can be achieved to recruit and activate caspase‐1 . Once active, caspase‐1 can further promote the synthesis and secretion of many downstream inflammatory cytokines, such as IL‐1β and IL‐18 .…”

Section: Discussionmentioning

confidence: 99%

“…15 Upon stimulated by several substances, including LPS, the specific activation of NLRP3 and the assembly of the inflammasome complex can be achieved to recruit and activate caspase-1. 14,29 Once active, caspase-1 can further promote the synthesis and secretion of many downstream inflammatory cytokines, such as IL-1β and IL-18. 30,31 In addition, the activation of caspase-l has also been shown to induce pyroptosis, which is a proinflammatory form of programmed cell death.…”

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confidence: 99%

Ginsenoside Rg1 attenuates cardiomyocyte apoptosis and inflammation via the TLR4/NF‐kB/NLRP3 pathway

Luo

Yan

Sun

et al. 2019

J of Cellular Biochemistry

152

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Sepsis‐induced myocardial dysfunction (SIMD) causes high mortality in seriously ill patients. Ginsenoside Rg1 has been proven to have effective anti‐inflammatory and antiapoptotic properties. However, the specific role of Rg1 in SIMD and the molecular mechanism remain unclear. Hence, we aimed to investigate the latent effects of ginsenoside Rg1 against SIMD and explore its underlying mechanisms. Male C57BL/6J mice and neonatal rat cardiomyocytes (NRCMs) were used as in vivo and in vitro models, respectively. Western blot analysis was used to detect the level of protein expression, and reverse transcription polymerase chain reaction was conducted to determine the messenger RNA expression of inflammatory factors. The terminal deoxynucleotidyl transferase‐mediated nick end labeling assay and flow cytometry were used to determine the apoptosis rate. Echocardiography was performed to assess cardiac function. The results showed that Rg1 improved cardiac function and attenuated lipopolysaccharide (LPS)‐induced apoptosis and inflammation in mice. In addition, in NRCMs, Rg1 downregulated the expression of LPS‐induced inflammatory cytokines and reversed the increased expression of Toll‐like receptor 4 (TLR4), nuclear factor‐κB (NF‐κB), and NOD‐like receptor 3 (NLRP3). In addition, treatment with TLR4 small interfering RNA (siRNA), a p‐NF‐κB inhibitor, or NLRP3 siRNA suppressed LPS‐induced apoptosis and inflammation. In conclusion, Rg1 can attenuate LPS‐induced inflammation and apoptosis both in NRCMs and septic mice and restore impaired cardiac function. Moreover, Rg1 may exert its effect via blocking the TLR4/NF‐κB/NLRP3 pathway.

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“…Western blot analysis was performed as described previously. 20 Samples were separated by SDS-PAGE and transferred to polyvinylidene fluoride membranes. After blocking with Tris-buffered saline containing 2% casein, the membranes were incubated with the primary antibodies against β-actin (clone AC-15; Sigma), IL-1β (clone 2805; R&D Systems), and NLRP3 (clone Cryo-2; Enzo Life Sciences).…”

Section: Western Blot Analysismentioning

confidence: 99%

“…BSA PA (200) PA (200) + OA (20) SA (200) SA (200) + OA (100) BSA PA (200) + OA (40) SA (200) + OA (40) SA (200) + OA (20) SA (200) + OA (200) PA (200) + OA (100) PA (200) + OA (200) * * Figure 4. Saturated fatty acids cause intracellular crystal formation.…”

Section: Sfa Crystals Provoke Il-1β-mediated Inflammatory Responses Imentioning

confidence: 99%

Saturated Fatty Acids Undergo Intracellular Crystallization and Activate the NLRP3 Inflammasome in Macrophages

Karasawa

Kawashima

Usui-Kawanishi

et al. 2018

ATVB

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120

101

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Oligomerized CARD16 promotes caspase‐1 assembly and IL‐1β processing

Cited by 53 publications

References 25 publications

KRas-ERK signalling promotes the onset and maintenance of uveal melanoma through regulating JMJD6-mediated H2A.X phosphorylation at tyrosine 39

KRas-ERK signalling promotes the onset and maintenance of uveal melanoma through regulating JMJD6-mediated H2A.X phosphorylation at tyrosine 39

Ginsenoside Rg1 attenuates cardiomyocyte apoptosis and inflammation via the TLR4/NF‐kB/NLRP3 pathway

Saturated Fatty Acids Undergo Intracellular Crystallization and Activate the NLRP3 Inflammasome in Macrophages

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