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PeproTech recombinant myostatin
A) Schematic of the multi-hit MASLD model in iPSC-derived hepatocytes and respective injury trajectories. B) Representative fluorescence microscopic images of HLCs cumulatively exposed to Oleic Acid and Palmitic Acid (OA/PA), <t>Resistin</t> and Myostatin (Res/Myo) and peripheral blood mono-nuclear cells (PBMCs) indicated as respective injury hit models and stained with LipidSpot and Mitotracker Red. C) Quantification of steatotic area normalized to respective Mitotracker area in percent. Dots represent independent wells. Tukey-Post Hoc analysis to test for significance. D) Quantification of Mitotracker signal intensity, normalized to untreated cells. Dots represent independent wells. Wilcoxon test to test for significance. E) Number of differentially expressed genes from bulk RNAsequencing in different injury conditions compared to untreated cells F) Pooled injury curve fits including the scaled injury parameters steatosis, mitochondrial membrane potential alterations and number of DEGs from RNA sequencing. Injury scores were normalized to PNPLA3-wt conditions for which no hits represented 0% and all hits represent 100%.
Recombinant Myostatin, supplied by PeproTech, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/recombinant myostatin/product/PeproTech
Average 90 stars, based on 1 article reviews
recombinant myostatin - by Bioz Stars, 2026-02
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Images

1) Product Images from "Dissecting compounded hepatocyte injury in a model of MASLD progression from human induced pluripotent stem cells"

Article Title: Dissecting compounded hepatocyte injury in a model of MASLD progression from human induced pluripotent stem cells

Journal: bioRxiv

doi: 10.1101/2024.10.10.617610

A) Schematic of the multi-hit MASLD model in iPSC-derived hepatocytes and respective injury trajectories. B) Representative fluorescence microscopic images of HLCs cumulatively exposed to Oleic Acid and Palmitic Acid (OA/PA), Resistin and Myostatin (Res/Myo) and peripheral blood mono-nuclear cells (PBMCs) indicated as respective injury hit models and stained with LipidSpot and Mitotracker Red. C) Quantification of steatotic area normalized to respective Mitotracker area in percent. Dots represent independent wells. Tukey-Post Hoc analysis to test for significance. D) Quantification of Mitotracker signal intensity, normalized to untreated cells. Dots represent independent wells. Wilcoxon test to test for significance. E) Number of differentially expressed genes from bulk RNAsequencing in different injury conditions compared to untreated cells F) Pooled injury curve fits including the scaled injury parameters steatosis, mitochondrial membrane potential alterations and number of DEGs from RNA sequencing. Injury scores were normalized to PNPLA3-wt conditions for which no hits represented 0% and all hits represent 100%.
Figure Legend Snippet: A) Schematic of the multi-hit MASLD model in iPSC-derived hepatocytes and respective injury trajectories. B) Representative fluorescence microscopic images of HLCs cumulatively exposed to Oleic Acid and Palmitic Acid (OA/PA), Resistin and Myostatin (Res/Myo) and peripheral blood mono-nuclear cells (PBMCs) indicated as respective injury hit models and stained with LipidSpot and Mitotracker Red. C) Quantification of steatotic area normalized to respective Mitotracker area in percent. Dots represent independent wells. Tukey-Post Hoc analysis to test for significance. D) Quantification of Mitotracker signal intensity, normalized to untreated cells. Dots represent independent wells. Wilcoxon test to test for significance. E) Number of differentially expressed genes from bulk RNAsequencing in different injury conditions compared to untreated cells F) Pooled injury curve fits including the scaled injury parameters steatosis, mitochondrial membrane potential alterations and number of DEGs from RNA sequencing. Injury scores were normalized to PNPLA3-wt conditions for which no hits represented 0% and all hits represent 100%.

Techniques Used: Derivative Assay, Fluorescence, Staining, Membrane, RNA Sequencing



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A) Schematic of the multi-hit MASLD model in iPSC-derived hepatocytes and respective injury trajectories. B) Representative fluorescence microscopic images of HLCs cumulatively exposed to Oleic Acid and Palmitic Acid (OA/PA), <t>Resistin</t> and Myostatin (Res/Myo) and peripheral blood mono-nuclear cells (PBMCs) indicated as respective injury hit models and stained with LipidSpot and Mitotracker Red. C) Quantification of steatotic area normalized to respective Mitotracker area in percent. Dots represent independent wells. Tukey-Post Hoc analysis to test for significance. D) Quantification of Mitotracker signal intensity, normalized to untreated cells. Dots represent independent wells. Wilcoxon test to test for significance. E) Number of differentially expressed genes from bulk RNAsequencing in different injury conditions compared to untreated cells F) Pooled injury curve fits including the scaled injury parameters steatosis, mitochondrial membrane potential alterations and number of DEGs from RNA sequencing. Injury scores were normalized to PNPLA3-wt conditions for which no hits represented 0% and all hits represent 100%.
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A) Schematic of the multi-hit MASLD model in iPSC-derived hepatocytes and respective injury trajectories. B) Representative fluorescence microscopic images of HLCs cumulatively exposed to Oleic Acid and Palmitic Acid (OA/PA), <t>Resistin</t> and Myostatin (Res/Myo) and peripheral blood mono-nuclear cells (PBMCs) indicated as respective injury hit models and stained with LipidSpot and Mitotracker Red. C) Quantification of steatotic area normalized to respective Mitotracker area in percent. Dots represent independent wells. Tukey-Post Hoc analysis to test for significance. D) Quantification of Mitotracker signal intensity, normalized to untreated cells. Dots represent independent wells. Wilcoxon test to test for significance. E) Number of differentially expressed genes from bulk RNAsequencing in different injury conditions compared to untreated cells F) Pooled injury curve fits including the scaled injury parameters steatosis, mitochondrial membrane potential alterations and number of DEGs from RNA sequencing. Injury scores were normalized to PNPLA3-wt conditions for which no hits represented 0% and all hits represent 100%.
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A) Schematic of the multi-hit MASLD model in iPSC-derived hepatocytes and respective injury trajectories. B) Representative fluorescence microscopic images of HLCs cumulatively exposed to Oleic Acid and Palmitic Acid (OA/PA), <t>Resistin</t> and Myostatin (Res/Myo) and peripheral blood mono-nuclear cells (PBMCs) indicated as respective injury hit models and stained with LipidSpot and Mitotracker Red. C) Quantification of steatotic area normalized to respective Mitotracker area in percent. Dots represent independent wells. Tukey-Post Hoc analysis to test for significance. D) Quantification of Mitotracker signal intensity, normalized to untreated cells. Dots represent independent wells. Wilcoxon test to test for significance. E) Number of differentially expressed genes from bulk RNAsequencing in different injury conditions compared to untreated cells F) Pooled injury curve fits including the scaled injury parameters steatosis, mitochondrial membrane potential alterations and number of DEGs from RNA sequencing. Injury scores were normalized to PNPLA3-wt conditions for which no hits represented 0% and all hits represent 100%.
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A) Schematic of the multi-hit MASLD model in iPSC-derived hepatocytes and respective injury trajectories. B) Representative fluorescence microscopic images of HLCs cumulatively exposed to Oleic Acid and Palmitic Acid (OA/PA), <t>Resistin</t> and Myostatin (Res/Myo) and peripheral blood mono-nuclear cells (PBMCs) indicated as respective injury hit models and stained with LipidSpot and Mitotracker Red. C) Quantification of steatotic area normalized to respective Mitotracker area in percent. Dots represent independent wells. Tukey-Post Hoc analysis to test for significance. D) Quantification of Mitotracker signal intensity, normalized to untreated cells. Dots represent independent wells. Wilcoxon test to test for significance. E) Number of differentially expressed genes from bulk RNAsequencing in different injury conditions compared to untreated cells F) Pooled injury curve fits including the scaled injury parameters steatosis, mitochondrial membrane potential alterations and number of DEGs from RNA sequencing. Injury scores were normalized to PNPLA3-wt conditions for which no hits represented 0% and all hits represent 100%.
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Image Search Results


A) Schematic of the multi-hit MASLD model in iPSC-derived hepatocytes and respective injury trajectories. B) Representative fluorescence microscopic images of HLCs cumulatively exposed to Oleic Acid and Palmitic Acid (OA/PA), Resistin and Myostatin (Res/Myo) and peripheral blood mono-nuclear cells (PBMCs) indicated as respective injury hit models and stained with LipidSpot and Mitotracker Red. C) Quantification of steatotic area normalized to respective Mitotracker area in percent. Dots represent independent wells. Tukey-Post Hoc analysis to test for significance. D) Quantification of Mitotracker signal intensity, normalized to untreated cells. Dots represent independent wells. Wilcoxon test to test for significance. E) Number of differentially expressed genes from bulk RNAsequencing in different injury conditions compared to untreated cells F) Pooled injury curve fits including the scaled injury parameters steatosis, mitochondrial membrane potential alterations and number of DEGs from RNA sequencing. Injury scores were normalized to PNPLA3-wt conditions for which no hits represented 0% and all hits represent 100%.

Journal: bioRxiv

Article Title: Dissecting compounded hepatocyte injury in a model of MASLD progression from human induced pluripotent stem cells

doi: 10.1101/2024.10.10.617610

Figure Lengend Snippet: A) Schematic of the multi-hit MASLD model in iPSC-derived hepatocytes and respective injury trajectories. B) Representative fluorescence microscopic images of HLCs cumulatively exposed to Oleic Acid and Palmitic Acid (OA/PA), Resistin and Myostatin (Res/Myo) and peripheral blood mono-nuclear cells (PBMCs) indicated as respective injury hit models and stained with LipidSpot and Mitotracker Red. C) Quantification of steatotic area normalized to respective Mitotracker area in percent. Dots represent independent wells. Tukey-Post Hoc analysis to test for significance. D) Quantification of Mitotracker signal intensity, normalized to untreated cells. Dots represent independent wells. Wilcoxon test to test for significance. E) Number of differentially expressed genes from bulk RNAsequencing in different injury conditions compared to untreated cells F) Pooled injury curve fits including the scaled injury parameters steatosis, mitochondrial membrane potential alterations and number of DEGs from RNA sequencing. Injury scores were normalized to PNPLA3-wt conditions for which no hits represented 0% and all hits represent 100%.

Article Snippet: To account for inter-organ signaling in our model, we tested recombinant resistin and myostatin (both Peprotech), both using 100 ng/ml concentration.

Techniques: Derivative Assay, Fluorescence, Staining, Membrane, RNA Sequencing