Journal: bioRxiv

Article Title: Therapeutic knockdown of MLKL reduces diet-induced obesity and improves insulin signalling in mature adipocytes

doi: 10.64898/2026.04.17.719119

Figure Lengend Snippet: (A) Body weight trajectory comparing no-treatment (NT) and control ASO groups over 22 weeks. (B) Relative Ripk1 mRNA expression in adipose tissue following treatment with control ASO or RIPK1 ASOs (#1 or #2). (C) Relative Mlkl mRNA expression in adipose tissue following treatment with control ASO or MLKL ASOs (#1 or #2). Data are mean ± SEM (n=8 mice/group). Statistical significance was assessed using one-way ANOVA with Dunnett’s multiple-comparison test; *p < 0.05, **p < 0.01, ***p < 0.001.

Article Snippet: For TaqMan-based qPCR, reactions were performed using TaqManTM Fast Universal PCR Master Mix (#4352042, Thermo Fisher Scientific) with Ripk1 (Mm00436354_m1) , Mlkl (Mm01244222_m1) or Hprt (Mm03024075_m1) probes and 5 ng/μL cDNA input.

Techniques: Control, Expressing, Comparison

Journal: bioRxiv

Article Title: Therapeutic knockdown of MLKL reduces diet-induced obesity and improves insulin signalling in mature adipocytes

doi: 10.64898/2026.04.17.719119

Figure Lengend Snippet: Male C57BL/6J mice (n=8/group) were fed a high-fat diet for 12 weeks to establish obesity, followed by weekly administration of control ASO, RIPK1 ASOs (#1 or #2) or MLKL ASO (#1 or #2) as indicated. (A) Hepatic Ripk1 mRNA expression following control or RIPK1 ASOs treatment. (B) Body weight trajectory during RIPK1 ASO therapy. (C) Fat mass, lean mass and body weight following RIPK1 ASOs treatment. (D) Hepatic Mlkl mRNA expression following MLKL ASOs treatment; adipose Ripk1 or Mlkl expression from both models are shown in . (E) Body weight trajectory during MLKL ASO therapy; comparison between PBS no treatment (NT) or control ASO groups is presented in Supplementary Figure 3A. (F) Fat mass, lean mass and body weight following MLKL ASO treatment. (G, H) Glucose Tolerance Test (GTT) following RIPK1 ASOs (G) or MLKL ASOs (H) treatment, with corresponding area under the curve (AUC) shown within the graph. Data are mean ± SEM (n=8 mice/group). For panels A , C , D , F , and G–H (AUC), statistical significance was assessed using one-way ANOVA with Dunnett’s multiple-comparison test; *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. For panels B , E , and G–H (time course), significance was determined using two-way ANOVA with Tukey’s multiple-comparison test. *p < 0.01 and ***p < 0.0001 denote comparisons between control ASO and RIPK1 ASO#1 ( B ) or MLKL ASO#1 ( E ), while # p < 0.05, ### p < 0.001, and #### p < 0.0001 denote comparisons between control ASO and RIPK1 ASO#2 ( B ) or MLKL ASO#2 ( E ).

Article Snippet: For TaqMan-based qPCR, reactions were performed using TaqManTM Fast Universal PCR Master Mix (#4352042, Thermo Fisher Scientific) with Ripk1 (Mm00436354_m1) , Mlkl (Mm01244222_m1) or Hprt (Mm03024075_m1) probes and 5 ng/μL cDNA input.

Techniques: Control, Expressing, Comparison

Journal: Journal of Human Immunity

Article Title: Human ISG15 deficiency unveils impaired healing of ulcerations via type I interferon–mediated fibrosis

doi: 10.70962/jhi.20250011

Figure Lengend Snippet: Cell death markers identified through ST. (A) Left: percentage of spots expressing apoptosis markers ( CASP3 , CASP8 , BAX , BAK1 , and CYCS ) out of total biopsy. Middle and right: percentage of spots expressing either two or five apoptosis markers in total biopsy, epidermis only, or dermis only (respectively). (B) Left: percentage of spots expressing necroptosis markers ( RIPK1 and MLKL ) out of total biopsy. Middle and right: percentage of spots expressing either RIPK1 or MLKL in total biopsy, epidermis only, or dermis only (respectively). (C) Percentage of spots expressing at least one apoptotic marker ( CASP3 , CASP8 , BAX , BAK1 , or CYCS ) that also express or not at least one of the ISGs ( IFIT1 , USP18 , MX1 , IFI27 , IFI44L , or OAS1 ). (D) Percentage of spots out of total biopsy, epidermis only, and dermis only that express ZBP1 . P values were calculated with a two-tailed t test. *P < 0.05; **P < 0.01.

Article Snippet: Relevant samples were pretreated with 10 mM of the RIPK1 inhibitor, necrostatin-1 (S8037; Selleck Chemicals) for 30 min before an 48-h stimulation with 1,000 IU ml −1 IFN-α2b (Merck IntronA).

Techniques: Expressing, Marker, Two Tailed Test