anti β mhc  (Proteintech)

Journal: Journal of Sport and Health Science

Article Title: Influence of diet-induced obesity and voluntary exercise training on cardiac lipids and mitochondrial function in mice

doi: 10.1016/j.jshs.2025.101095

Figure Lengend Snippet: Impact of high fat feeding and voluntary exercise on left ventricle morphology in male mice. (A) Representative images of Picrosirius red staining for measurement of interstitial and perivascular fibrosis with 20× magnification. (B) Representative images for Hematoxylin and Eosin for measurement of cardiomyocyte width and area with 40× magnification. (C) Representative images of Oil red O staining for measurement of interstitial lipid deposition with 40× magnification. Quantitative analysis of percent area of (D) interstitial and (E) perivascular fibrosis expressed as fold change from sedentary chow group. Quantitative analysis of (F) cardiomyocyte width and (G) cardiomyocyte area. (H) Quantitative analysis of percent area of lipid deposition expressed as fold change from sedentary chow group left ventricle mRNA expression of fatty acid transporters (I) FABP3, (J) CD36, and hypertrophy markers (K) β-MHC and (L) ANP in male VET or sedentary mice fed an HFD or chow diet. Values were calculated relative to 18S housekeeper. Analysis was performed using two-way analysis of variance with Tukey’s post hoc test for multiple comparisons. Data are expressed as mean ± standard error of the mean. (D–H) n : 8–12 per group. (I–L) n : 8–9 per group. * p < 0.05, **** p < 0.0001. ANP = atrial natriuretic peptide; β-MHC = beta myosin heavy chain; CD36 = platelet glycoprotein 4; FABP3 = fatty acid-binding protein 3; HFD = high fat diet; Myh7 = moysin heavy chain 7; VET = voluntary exercise training.

Article Snippet: The following TaqMan assay gene transcripts were used: fatty acid-binding protein 3 (FABP3, Mm02342495_m1), platelet glycoprotein 4 (CD36, Mm00432403_m1), beta myosin heavy chain (β-MHC, Mm00600555_m1), atrial natriuretic peptide (ANP, Mm01255747_g1), OPA1 (Mm01349707_g1), DRP1 (Mm01342903_m1), robosomal18S (18S, Mm03928990_g1).

Techniques: Staining, Expressing, Binding Assay

Journal: bioRxiv

Article Title: c-MAF transduces motor neuron firing to sustain fast-glycolytic myofibers and neuromuscular junctions

doi: 10.64898/2026.02.05.703983

Figure Lengend Snippet: a , Immunofluorescence of distal hindlimb cryosections showing MYH isoform distribution and Laminin (white, fiber boundaries). Top rows: MYH1 (cyan, type IIx), MYH2 (green, type IIa), MYH7 (red, type I). Bottom rows: MYH4 (cyan, type IIb), MYH2 (green), MYH7 (red). Columns show: Control HSA-Cre + (leftmost), myofiber constitutive HSA-Cre;c-Maf flox/flox , myofiber inducible HSA-CreERT2;c-Maf flox/flox at 7 days, 15 days, and 30 days post-tamoxifen, Region A deleted (f Myh super enhancer deletion, EnhA -/- ), and ALS 90 days old. Major muscles labeled in control: TA (tibialis anterior), Tibia, EDL (extensor digitorum longus), FHL-TP (flexor hallucis longus-tibialis posterior), Sol (soleus), Plant (plantaris), Gas (gastrocnemius). c-Maf loss shows fiber type transition in peroneal group muscles (FHL-TP, central TA) with preserved EDL. ALS models displayed similar regional fiber type switch. b , RT-qPCR of fast-glycolytic genes in inducible c-Maf mutant 7 and 15 dpi of Tamoxifen. Bottom: Myh4 and Myh1 showing temporal changes. c-Maf loss reduces Myh4 expression while delayed Myh1 increase. Top shows Pvalb (parvalbumin), Atp2a1 (SERCA1), and Mybpc2 (fast MyBP-C) downregulation. White bars: control (CTL); pink bars: 7 dpi; red bars: 15 dpi. *p < 0.05 by one-way ANOVA with individual data points. c , RT-qPCR at 4 weeks post-tamoxifen comparing circadian timepoints ZT03 and ZT15. Left: Myh4 expression is reduced only at ZT03 (red bars) versus controls (white bars). Right: Myh1 upregulation in KO at ZT03. *p < 0.05, **p < 0.01 showing sustained fiber type shift. d , RT-qPCR on 90 days old ALS G93A mice comparing circadian timepoints ZT03 and ZT15. Top c-Maf expression sharply down regulated (grey bars) versus control (white bars). Middle left: Myh4 expression is constitutively reduced versus controls. Middle right: Myh1 is upregulated specifically at ZT03. Bottom left Myh4 expression only in 90 days old ALS mice is upregulated at ZT15. Bottom right same with Myh1. e, RNA-FISH on isolated TA fibers at ZT03 and ZT15, 4 weeks post-tamoxifen, targeting pre-mRNA of Myh4 (red), Myh1 (yellow), Myh2 (green). DAPI (blue) marks myonuclei. Yellow box shows high-magnification view of transcription foci shown in panel f . g, c-Maf mutant myofibers show increased myonuclei expressing non-dominant Myh isoforms, more pronounced at ZT03 than ZT15, indicating spatio-temporal discoordination of the fMyh locus. Violin plots, white color control, red c-Maf mutant. The % of heterogeneity is the % of f Myh allele that differs from the dominant f Myh allele per myofiber as estimated by Rnascope experiments. *p < 0.05, ***p < 0.001 ****p < 0.0001 by one-way ANOVA.

Article Snippet: For cryosections, antibodies included MYH2 (1:100, SC-71 clone, DSHB), MYH4 (1:200, BF-F3 clone, DSHB), MYH1 (1:100, 6H1 clone, DSHB), MYH7 (1:40, BA-F8, DSHB), Laminin (1:750, L9393, Sigma), FOXO3A (1:400, 75D8, Cell Signaling), and c-MAF (1:100, HPA028289, Sigma-Aldrich).

Techniques: Immunofluorescence, Control, Muscles, Labeling, Quantitative RT-PCR, Mutagenesis, Expressing, Isolation, RNAscope

Journal: bioRxiv

Article Title: c-MAF transduces motor neuron firing to sustain fast-glycolytic myofibers and neuromuscular junctions

doi: 10.64898/2026.02.05.703983

Figure Lengend Snippet: a , Immunofluorescence of distal hindlimb cryosections comparing muscle-specific large Maf family mutant models ( HSA-Cre;c-Maf flox/flox , HSA-Cre;Mafb flox/flox and Mafa null mice). Four panels showing transverse sections from: wild-type (WT), c-Maf single mutant, Mafa single mutant, and Mafb single mutant mice. Myosin heavy chain (MYH) isoforms visualized by immunostaining: MYH7 (blue, slow oxidative), MYH2 (red, fast oxidative), MYH1 (white, fast oxidative-glycolytic), MYH4 (green, fast glycolytic), and Laminin (magenta, basal lamina marking fiber boundaries). White arrows indicating flexor hallucis longus (FHL) and tibialis posterior (TP) muscles showing region-specific fiber type transition in c-Maf mutant. b , RT-qPCR quantification of genes specifically dysregulated in c-Maf mutant compared to Mafb and Mafa mutants. Seven bar graphs show relative mRNA expression for: Klk1b26 , Prkaa2 , Fbxo32 , Foxo3 , Fkbp5 , Fbxo31 , and Eif4e . X-axis categories: CTL (control), total Mafa mutant, muscle specific Mafb mutant, muscle specific c-Maf mutant . Statistical comparisons by one-way ANOVA with post-hoc testing. Asterisks indicate significance: *p < 0.05, **p < 0.01, ***p < 0.001.

Article Snippet: For cryosections, antibodies included MYH2 (1:100, SC-71 clone, DSHB), MYH4 (1:200, BF-F3 clone, DSHB), MYH1 (1:100, 6H1 clone, DSHB), MYH7 (1:40, BA-F8, DSHB), Laminin (1:750, L9393, Sigma), FOXO3A (1:400, 75D8, Cell Signaling), and c-MAF (1:100, HPA028289, Sigma-Aldrich).

Techniques: Immunofluorescence, Mutagenesis, Immunostaining, Muscles, Quantitative RT-PCR, Expressing, Control