Journal: Cell Death & Disease

Article Title: RIPK3 promotes skin inflammation by enhancing IL-36α signaling and necroptosis in keratinocytes

doi: 10.1038/s41419-025-08096-9

Figure Lengend Snippet: A Correlation between IL-36α and RIPK3 expression in psoriasis patients in the GEO database. GSE13305 : normal (n = 64, green), non-lesional skin (n = 58, blue) and lesional skin (n = 58, red); GSE14905 : normal (n = 21, green), non-lesional skin (n = 28, blue) and lesional skin (n = 33, red). The mRNA expression of Il-36α ( B ); representative western blot ( C ) analysis of IL-36α protein levels and immunofluorescence staining ( D ) of IL-36α levels in the skin. Scale bars, 100 μm. The mRNA expression of IL-36α in primary keratinocytes from RIPK3 f/f and RIPK3 ΔKC mice ( E ) and normal mice ( F ) treated with TSZ for 6 hours. G Representative western blot assay of IL-36α pathway in primary keratinocytes treated with IL-36α for 15 minutes. H The mRNA expression of Ccl20 , Cxcl2 , Cxcl10 and Il-36γ in primary keratinocytes treated with IL-36α for 6 hours. These results are representative of three independent experiments. All dates are shown as means ± SEM. * P < 0.05, *** P < 0.001, compared as indicated, ### P < 0.001, compared with BLANK, were measured by one-way or two-way ANOVA. Significant differences were observed between the RIPK3 f/f and RIPK3 f/f IMQ groups, the RIPK3 f/f and RIPK3 f/f TSZ groups, and the RIPK3 f/f and RIPK3 f/f IL-36α groups.

Article Snippet: Mice received daily intradermal injections into the ear for 5 consecutive days, consisting of either 1 μg of murine IL-36α protein (MedChemExpress) or an equivalent volume of saline, as previously described by Anne Müller et al. [ ].

Techniques: Expressing, Western Blot, Immunofluorescence, Staining

Journal: Cell Death & Disease

Article Title: RIPK3 promotes skin inflammation by enhancing IL-36α signaling and necroptosis in keratinocytes

doi: 10.1038/s41419-025-08096-9

Figure Lengend Snippet: A Representative western blot assay of necroptotic proteins in primary keratinocytes from RIPK3 f/f and RIPK3 ΔKC mice treated with IL-36α for 6 hours. B RT-PCR detection of mRNA expression levels of S100a8 , S100a9 , Il-1α and Il-36α after TSZ induction in primary keratinocytes. C Representative western blot images assay of necroptotic proteins in IL-36α-induced primary keratinocytes. D RT-PCR detection of mRNA expression levels of cytokines such as Cxcl2 , Lcn2 , S100a9 and Il-36α after IL-36α induction in primary keratinocytes. E Representative images of mice treated with saline and IL-36α at day 5 to demonstrate the scaling of the treated area. Ear thickness ( F ) and ear swelling ( G ) in mice treated with saline and IL-36α in each group. n = 5 mice per group. These results are representative of three independent experiments. All dates are shown as means ± SEM. *** P < 0.001, ns indicates no significance, compared as indicated, were measured by two-way ANOVA. Significant differences were observed between the WT and WT TSZ groups, as well as between the WT and WT IL-36α groups.

Article Snippet: Mice received daily intradermal injections into the ear for 5 consecutive days, consisting of either 1 μg of murine IL-36α protein (MedChemExpress) or an equivalent volume of saline, as previously described by Anne Müller et al. [ ].

Techniques: Western Blot, Reverse Transcription Polymerase Chain Reaction, Expressing, Saline

Journal: Cell Death & Disease

Article Title: RIPK3 promotes skin inflammation by enhancing IL-36α signaling and necroptosis in keratinocytes

doi: 10.1038/s41419-025-08096-9

Figure Lengend Snippet: In keratinocytes, RIPK3 orchestrates skin inflammation through a dual pathogenic mechanism. It initiates MLKL-dependent necroptosis, releasing DAMPs like IL-36α. This extracellular IL-36α, in turn, activates the pro-inflammatory NF-κB signaling axis. Beyond merely initiating this cascade, RIPK3 critically functions in an MLKL-independent manner to directly potentiate NF-κB activation, driving robust expression of inflammatory mediators (e.g., CCL20, CXCLs). This interplay constitutes a powerful feed-forward loop that amplifies and sustains cutaneous inflammation.

Article Snippet: Mice received daily intradermal injections into the ear for 5 consecutive days, consisting of either 1 μg of murine IL-36α protein (MedChemExpress) or an equivalent volume of saline, as previously described by Anne Müller et al. [ ].

Techniques: Activation Assay, Expressing

Journal: Disease Markers

Article Title: NFE2L3 Inhibition Induces Cell Cycle Arrest at the G0/G1 Phase in Colorectal Cancer Cells through Downregulating CCND1 and pRb1-ser807/811

doi: 10.1155/2019/2829798

Figure Lengend Snippet: Screening and validation of differential expression genes. (a) Volcano plot of differential expression genes in TCGA COADREAD gene expression dataset. x -axis: log2 fold change; y -axis: -log10 (FDR p value) for each probe; vertical dotted lines: fold change ≥ 2 or ≤2. It showed that 1579 significantly upregulated genes (red color) and 3220 significantly downregulated genes (green color) were selected in this dataset. (b) 11 merged genes were found with the intersection of the top 20 upregulated genes from the COADREAD dataset and 181 upregulated genes from our previous research. (c) NFE2L3 expression levels in 51 normal and 370 tumor samples. NFE2L3 showed significantly higher expression levels in tumor samples than in normal samples ( p < 0.0001). (d) Validation of NFE2L3 expression levels with 48 paired tumor and paratumor samples. The NFE2L3 mRNA expression level was significantly upregulated in tumor samples ( p < 0.0001).

Article Snippet: An NFE2L3 antibody was obtained from Boster Biological Technology.

Techniques: Biomarker Discovery, Quantitative Proteomics, Gene Expression, Expressing

Journal: Disease Markers

Article Title: NFE2L3 Inhibition Induces Cell Cycle Arrest at the G0/G1 Phase in Colorectal Cancer Cells through Downregulating CCND1 and pRb1-ser807/811

doi: 10.1155/2019/2829798

Figure Lengend Snippet: CCND1 mRNA and protein expression levels in colorectal cancer cell lines after NFE2L3 knockdown. (a) The mRNA expression levels of NFE2L3 in HCT116 cells after NFE2L3 knockdown. Inhibition of the NFE2L3 mRNA level was displayed in the si-1 and si-2 groups ( p = 0.0225, p = 0.0184). (b) CCND1 mRNA expression levels in HCT116 cells after NFE2L3 knockdown. Inhibition of CCND1 mRNA expression was detected in the si-1 and si-2 groups ( p = 0.0189, p = 0.0291). (c) Protein expression changes of CCND1 in HCT116 cells when inhibited by NFE2L3 siRNA. Downregulation of CCND1 and pRb1-ser807/811 proteins was observed in the si-1 and si-2 groups. (d) The mRNA expression levels of NFE2L3 in SW480 cells after NFE2L3 knockdown. The NFE2L3 mRNA expression level was significantly inhibited by si-1 and si-2 ( p = 0.0258, p = 0.0232). (e) CCND1 mRNA expression levels in SW480 cells after NFE2L3 knockdown. The CCND1 mRNA level was significantly downregulated in the si-1 group ( p = 0.0374). (f) Protein expression changes of CCND1 in SW480 cells after transfection with NFE2L3 siRNA. CCND1 and pRb1-ser807/811 protein expression levels were downregulated in the si-1 and si-2 groups.

Article Snippet: An NFE2L3 antibody was obtained from Boster Biological Technology.

Techniques: Expressing, Knockdown, Inhibition, Transfection

Journal: Disease Markers

Article Title: NFE2L3 Inhibition Induces Cell Cycle Arrest at the G0/G1 Phase in Colorectal Cancer Cells through Downregulating CCND1 and pRb1-ser807/811

doi: 10.1155/2019/2829798

Figure Lengend Snippet: The expression correlation between CCND1 and NFE2L3 in colorectal tissue samples. (a) CCND1 was upregulated in 380 tumor samples compared to 51 normal samples ( p < 0.0001). (b) Expression level correlation analysis between NFE2L3 and CCND1 in 431 samples (normal and primary tumor samples) of TCGA COADREAD gene expression dataset. A significant positive correlation between NFE2L3 and CCND1 expression was found ( r = 0.5698, p < 0.0001).

Article Snippet: An NFE2L3 antibody was obtained from Boster Biological Technology.

Techniques: Expressing, Gene Expression