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rhoa flox flox  (Cyagen Biosciences)


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    Cyagen Biosciences rhoa flox flox
    A Changes of <t>RhoA</t> mRNA expression in injured spinal cord obtained from different GEO databases. B Temporal changes of RhoA protein level in spinal cord following SCI ( n = 5). C Major cell type classification in the GSE196928 dataset. D Distribution map of RhoA expression. E RhoA expression levels across different cell types. F Immunostaining shows the RhoA expression in microglia (IBA-1 + ) at different stages after SCI ( n = 3). Data are presented as mean ± SD. Statistical significance: ∗ p < 0.05, ∗∗ p < 0.005, ∗∗∗ p < 0.001 (vs. sham group).
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    Images

    1) Product Images from "Loss of RhoA in microglia disables glycolytic adaptation and impairs spinal cord injury recovery through Arhgap25/HIF-1α pathway"

    Article Title: Loss of RhoA in microglia disables glycolytic adaptation and impairs spinal cord injury recovery through Arhgap25/HIF-1α pathway

    Journal: Cell Death & Disease

    doi: 10.1038/s41419-025-07947-9

    A Changes of RhoA mRNA expression in injured spinal cord obtained from different GEO databases. B Temporal changes of RhoA protein level in spinal cord following SCI ( n = 5). C Major cell type classification in the GSE196928 dataset. D Distribution map of RhoA expression. E RhoA expression levels across different cell types. F Immunostaining shows the RhoA expression in microglia (IBA-1 + ) at different stages after SCI ( n = 3). Data are presented as mean ± SD. Statistical significance: ∗ p < 0.05, ∗∗ p < 0.005, ∗∗∗ p < 0.001 (vs. sham group).
    Figure Legend Snippet: A Changes of RhoA mRNA expression in injured spinal cord obtained from different GEO databases. B Temporal changes of RhoA protein level in spinal cord following SCI ( n = 5). C Major cell type classification in the GSE196928 dataset. D Distribution map of RhoA expression. E RhoA expression levels across different cell types. F Immunostaining shows the RhoA expression in microglia (IBA-1 + ) at different stages after SCI ( n = 3). Data are presented as mean ± SD. Statistical significance: ∗ p < 0.05, ∗∗ p < 0.005, ∗∗∗ p < 0.001 (vs. sham group).

    Techniques Used: Expressing, Immunostaining

    A t-SNE and unsupervised clustering of all cells based on biomarkers. B GSEA analysis highlighting differences in microglial subsets compared to other cell types. C High-resolution reclustering of microglia into ten distinct clusters. D Expression of key markers identified in the reclustered microglia. E Pseudotime trajectory analysis of microglial cells. F Visualization of ten microglial subclusters, each represented by a distinct color. Microglial subsets with significant differences in oxidative phosphorylation pathways ( G subcluster 0, 2, 3, 4, 7) and glycolysis pathways ( H subcluster 2, 3, 4, 7) identified through GSEA analysis. I CellChat analysis showing interactions between glycolysis-differentiated microglia (subcluster 2, 3, 4, 7) and other cell types. J PCA of bulk mRNA transcriptomics in primary microglial cells. K Heatmap illustrating the results of mRNA sequencing analysis. GSEA analysis of glycolysis-related ( L ) and oxidative phosphorylation-related ( M ) differences between flox and cKO groups. N PCA of metabolomic profiling data. O , P Comparative analysis of glycolysis and TCA cycle metabolic changes between cKO and flox groups. RhoA deletion decreases ATP production ( Q ), accompanied by reduced ECAR ( R ), OCR ( S ), and glucose consumption in the culture medium ( T ). Data are presented as mean ± SD; each dot represents an individual mouse. Statistical significance: *** p < 0.001.
    Figure Legend Snippet: A t-SNE and unsupervised clustering of all cells based on biomarkers. B GSEA analysis highlighting differences in microglial subsets compared to other cell types. C High-resolution reclustering of microglia into ten distinct clusters. D Expression of key markers identified in the reclustered microglia. E Pseudotime trajectory analysis of microglial cells. F Visualization of ten microglial subclusters, each represented by a distinct color. Microglial subsets with significant differences in oxidative phosphorylation pathways ( G subcluster 0, 2, 3, 4, 7) and glycolysis pathways ( H subcluster 2, 3, 4, 7) identified through GSEA analysis. I CellChat analysis showing interactions between glycolysis-differentiated microglia (subcluster 2, 3, 4, 7) and other cell types. J PCA of bulk mRNA transcriptomics in primary microglial cells. K Heatmap illustrating the results of mRNA sequencing analysis. GSEA analysis of glycolysis-related ( L ) and oxidative phosphorylation-related ( M ) differences between flox and cKO groups. N PCA of metabolomic profiling data. O , P Comparative analysis of glycolysis and TCA cycle metabolic changes between cKO and flox groups. RhoA deletion decreases ATP production ( Q ), accompanied by reduced ECAR ( R ), OCR ( S ), and glucose consumption in the culture medium ( T ). Data are presented as mean ± SD; each dot represents an individual mouse. Statistical significance: *** p < 0.001.

    Techniques Used: Expressing, Phospho-proteomics, Sequencing

    Related Articles

    Expressing:

    Article Title: Loss of RhoA in microglia disables glycolytic adaptation and impairs spinal cord injury recovery through Arhgap25/HIF-1α pathway
    Article Snippet: RhoA flox/flox and Cx3cr1 Cre mice (provided by Cyagen, Suzhou, China) were intercrossed to obtain RhoA cKO mice with genotype of RhoA flox/flox ; Cx3cr1 Cre , as previously described [ ].

    Immunostaining:

    Article Title: Loss of RhoA in microglia disables glycolytic adaptation and impairs spinal cord injury recovery through Arhgap25/HIF-1α pathway
    Article Snippet: RhoA flox/flox and Cx3cr1 Cre mice (provided by Cyagen, Suzhou, China) were intercrossed to obtain RhoA cKO mice with genotype of RhoA flox/flox ; Cx3cr1 Cre , as previously described [ ].

    Phospho-proteomics:

    Article Title: Loss of RhoA in microglia disables glycolytic adaptation and impairs spinal cord injury recovery through Arhgap25/HIF-1α pathway
    Article Snippet: RhoA flox/flox and Cx3cr1 Cre mice (provided by Cyagen, Suzhou, China) were intercrossed to obtain RhoA cKO mice with genotype of RhoA flox/flox ; Cx3cr1 Cre , as previously described [ ].

    Sequencing:

    Article Title: Loss of RhoA in microglia disables glycolytic adaptation and impairs spinal cord injury recovery through Arhgap25/HIF-1α pathway
    Article Snippet: RhoA flox/flox and Cx3cr1 Cre mice (provided by Cyagen, Suzhou, China) were intercrossed to obtain RhoA cKO mice with genotype of RhoA flox/flox ; Cx3cr1 Cre , as previously described [ ].



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    Aberrant AKT/mTORC2 signaling axis activation mediates TiO 2 NPs-induced F-actin disassembly and plasma membrane injury. (a, b) Western blot (a) and densitometric quantification of the p -AKT/AKT ratio (b), confirming TiO 2 NPs-induced activation of the AKT/mTORC2 axis. (c) Quantification of <t>RhoA</t> expression, showing TiO 2 NPs-mediated suppression of RhoA-associated cytoskeletal regulation. (d) Representative confocal fluorescence images of F-actin stained with phalloidin (green) and DAPI (blue), visualizing the disruption of cytoskeletal architecture following TiO 2 NPs exposure. (e) Quantitative analysis of relative F-actin fluorescence intensity. (f, g) Western blot (f) and densitometric analysis of the p -AKT/AKT ratio (g), demonstrating the inhibitory effect of Torin-1 on TiO 2 NPs-induced AKT hyper-phosphorylation. (h) Quantification of F-actin fluorescence intensity, showing the restoration of cytoskeletal integrity by Torin-1 intervention. (i) Quantification of RhoA levels, indicating the rescue of TiO 2 NPs-suppressed RhoA by Torin-1. (j, k) CCK-8 cell viability (j) and LDH release (k) assays assessing the impact of Torin-1 on mitigating TiO 2 NPs-induced cytotoxicity and plasma membrane rupture. (l) Representative phalloidin-stained confocal images displaying the recovery of cytoskeletal morphology in the TiO 2 NPs + Torin-1 group. (m) Intracellular GSH content, revealing that Torin-1 intervention partially mitigates TiO 2 NPs-induced depletion of antioxidant reserves. Experimental groups: Control, Torin-1, TiO 2 NPs, and TiO 2 NPs + Torin-1. Data are presented as Mean ± SEM (n ≥ 3). Statistical significance is denoted by brackets and asterisks: * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)
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    Aberrant AKT/mTORC2 signaling axis activation mediates TiO 2 NPs-induced F-actin disassembly and plasma membrane injury. (a, b) Western blot (a) and densitometric quantification of the p -AKT/AKT ratio (b), confirming TiO 2 NPs-induced activation of the AKT/mTORC2 axis. (c) Quantification of RhoA expression, showing TiO 2 NPs-mediated suppression of RhoA-associated cytoskeletal regulation. (d) Representative confocal fluorescence images of F-actin stained with phalloidin (green) and DAPI (blue), visualizing the disruption of cytoskeletal architecture following TiO 2 NPs exposure. (e) Quantitative analysis of relative F-actin fluorescence intensity. (f, g) Western blot (f) and densitometric analysis of the p -AKT/AKT ratio (g), demonstrating the inhibitory effect of Torin-1 on TiO 2 NPs-induced AKT hyper-phosphorylation. (h) Quantification of F-actin fluorescence intensity, showing the restoration of cytoskeletal integrity by Torin-1 intervention. (i) Quantification of RhoA levels, indicating the rescue of TiO 2 NPs-suppressed RhoA by Torin-1. (j, k) CCK-8 cell viability (j) and LDH release (k) assays assessing the impact of Torin-1 on mitigating TiO 2 NPs-induced cytotoxicity and plasma membrane rupture. (l) Representative phalloidin-stained confocal images displaying the recovery of cytoskeletal morphology in the TiO 2 NPs + Torin-1 group. (m) Intracellular GSH content, revealing that Torin-1 intervention partially mitigates TiO 2 NPs-induced depletion of antioxidant reserves. Experimental groups: Control, Torin-1, TiO 2 NPs, and TiO 2 NPs + Torin-1. Data are presented as Mean ± SEM (n ≥ 3). Statistical significance is denoted by brackets and asterisks: * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

    Journal: Materials Today Bio

    Article Title: Digestive-transformed titanium dioxide nanoparticles disrupt intestinal barrier via mitoxyperilysis mediated by mTOR-cytoskeleton axis dysregulation

    doi: 10.1016/j.mtbio.2026.103674

    Figure Lengend Snippet: Aberrant AKT/mTORC2 signaling axis activation mediates TiO 2 NPs-induced F-actin disassembly and plasma membrane injury. (a, b) Western blot (a) and densitometric quantification of the p -AKT/AKT ratio (b), confirming TiO 2 NPs-induced activation of the AKT/mTORC2 axis. (c) Quantification of RhoA expression, showing TiO 2 NPs-mediated suppression of RhoA-associated cytoskeletal regulation. (d) Representative confocal fluorescence images of F-actin stained with phalloidin (green) and DAPI (blue), visualizing the disruption of cytoskeletal architecture following TiO 2 NPs exposure. (e) Quantitative analysis of relative F-actin fluorescence intensity. (f, g) Western blot (f) and densitometric analysis of the p -AKT/AKT ratio (g), demonstrating the inhibitory effect of Torin-1 on TiO 2 NPs-induced AKT hyper-phosphorylation. (h) Quantification of F-actin fluorescence intensity, showing the restoration of cytoskeletal integrity by Torin-1 intervention. (i) Quantification of RhoA levels, indicating the rescue of TiO 2 NPs-suppressed RhoA by Torin-1. (j, k) CCK-8 cell viability (j) and LDH release (k) assays assessing the impact of Torin-1 on mitigating TiO 2 NPs-induced cytotoxicity and plasma membrane rupture. (l) Representative phalloidin-stained confocal images displaying the recovery of cytoskeletal morphology in the TiO 2 NPs + Torin-1 group. (m) Intracellular GSH content, revealing that Torin-1 intervention partially mitigates TiO 2 NPs-induced depletion of antioxidant reserves. Experimental groups: Control, Torin-1, TiO 2 NPs, and TiO 2 NPs + Torin-1. Data are presented as Mean ± SEM (n ≥ 3). Statistical significance is denoted by brackets and asterisks: * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

    Article Snippet: Intracellular RhoA activity was quantified utilizing the RhoA G-LISA Activation Assay Kit (Cytoskeleton; supplied by Jianglai Biotechnology, Shanghai, China; cat. no. CSK-BK124-S).

    Techniques: Activation Assay, Clinical Proteomics, Membrane, Western Blot, Expressing, Cytoskeletal, Confocal, Fluorescence, Staining, Disruption, Analysis, Phospho-proteomics, CCK-8 Assay, Morphology, Control