bs-2766R Search Results


anti foxo4  (Bioss)
90
Bioss anti foxo4
LncIRS1 could rescue skeletal muscle atrophy. (A) Effect of lncIRS1 overexpression on AKT‐FOXO signalling pathway. Chicken primary myotubes isolated from leg muscle of E11 were first treated with dexamethasone for 24 hr to induce atrophy and then transfected with lncIRS1 overexpression plasmid for 48 hr, followed by Western blot analysis. (B–E) Effect of lncIRS1 overexpression on protein phosphorylation level of AKT‐FOXO signalling pathway components, including p‐foxo1 (B), p‐foxo3 (C), <t>p‐foxo4</t> (D), and p‐AKT (E). (F) Effect of lncIRS1 overexpression on protein expression level of Atrogin‐1 during dexamethasone treated myotubes. (G) Effect of lncIRS1 knockdown on AKT‐FOXO signalling pathway. Chicken primary myotubes isolated from leg muscle of E11 were first treated with dexamethasone for 24 hr to induce atrophy and then transfected with si‐lncIRS1 for 48 hr, followed by Western blot analysis. (H–K) Effect of lncIRS1 knockdown on protein phosphorylation level of AKT‐FOXO pathway, contains p‐foxo1 (H), p‐foxo3 (I), p‐foxo4 (J), and p‐AKT (K). (L) Effect of lncIRS1 knockdown on Atrogin‐1 protein expression level during dexamethasone treated myotubes. In all panels, error bars indicate the standard error of the mean. Independent sample t ‐test was used to analysis the statistical differences between groups. * P < 0.05, ** P < 0.01, and *** P < 0.001.
Anti Foxo4, supplied by Bioss, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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LncIRS1 could rescue skeletal muscle atrophy. (A) Effect of lncIRS1 overexpression on AKT‐FOXO signalling pathway. Chicken primary myotubes isolated from leg muscle of E11 were first treated with dexamethasone for 24 hr to induce atrophy and then transfected with lncIRS1 overexpression plasmid for 48 hr, followed by Western blot analysis. (B–E) Effect of lncIRS1 overexpression on protein phosphorylation level of AKT‐FOXO signalling pathway components, including p‐foxo1 (B), p‐foxo3 (C), p‐foxo4 (D), and p‐AKT (E). (F) Effect of lncIRS1 overexpression on protein expression level of Atrogin‐1 during dexamethasone treated myotubes. (G) Effect of lncIRS1 knockdown on AKT‐FOXO signalling pathway. Chicken primary myotubes isolated from leg muscle of E11 were first treated with dexamethasone for 24 hr to induce atrophy and then transfected with si‐lncIRS1 for 48 hr, followed by Western blot analysis. (H–K) Effect of lncIRS1 knockdown on protein phosphorylation level of AKT‐FOXO pathway, contains p‐foxo1 (H), p‐foxo3 (I), p‐foxo4 (J), and p‐AKT (K). (L) Effect of lncIRS1 knockdown on Atrogin‐1 protein expression level during dexamethasone treated myotubes. In all panels, error bars indicate the standard error of the mean. Independent sample t ‐test was used to analysis the statistical differences between groups. * P < 0.05, ** P < 0.01, and *** P < 0.001.

Journal: Journal of Cachexia, Sarcopenia and Muscle

Article Title: LncIRS1 controls muscle atrophy via sponging miR‐15 family to activate IGF1‐PI3K/AKT pathway

doi: 10.1002/jcsm.12374

Figure Lengend Snippet: LncIRS1 could rescue skeletal muscle atrophy. (A) Effect of lncIRS1 overexpression on AKT‐FOXO signalling pathway. Chicken primary myotubes isolated from leg muscle of E11 were first treated with dexamethasone for 24 hr to induce atrophy and then transfected with lncIRS1 overexpression plasmid for 48 hr, followed by Western blot analysis. (B–E) Effect of lncIRS1 overexpression on protein phosphorylation level of AKT‐FOXO signalling pathway components, including p‐foxo1 (B), p‐foxo3 (C), p‐foxo4 (D), and p‐AKT (E). (F) Effect of lncIRS1 overexpression on protein expression level of Atrogin‐1 during dexamethasone treated myotubes. (G) Effect of lncIRS1 knockdown on AKT‐FOXO signalling pathway. Chicken primary myotubes isolated from leg muscle of E11 were first treated with dexamethasone for 24 hr to induce atrophy and then transfected with si‐lncIRS1 for 48 hr, followed by Western blot analysis. (H–K) Effect of lncIRS1 knockdown on protein phosphorylation level of AKT‐FOXO pathway, contains p‐foxo1 (H), p‐foxo3 (I), p‐foxo4 (J), and p‐AKT (K). (L) Effect of lncIRS1 knockdown on Atrogin‐1 protein expression level during dexamethasone treated myotubes. In all panels, error bars indicate the standard error of the mean. Independent sample t ‐test was used to analysis the statistical differences between groups. * P < 0.05, ** P < 0.01, and *** P < 0.001.

Article Snippet: The primary antibodies used were anti‐IRS1 (1:1000; catalogue no. ab5603, Abcam, Cambridge, UK), anti‐phospho‐AKT (1:1000; catalogue no. #4040, Cell Signaling Technology, Danvers, MA, USA), anti‐AKT (1:1000; catalogue no. #9272, Cell Signaling Technology), anti‐MyHC (1:50; catalogue no. B103, Developmental Studies Hybridoma Bank, Iowa City, Iowa, USA), anti‐MyoG (1:1000; catalogue no. orb6492, Biorbyt, Cambridge, UK), anti‐Foxo1 (1:1000; catalogue no. 82358, Thermo Fisher Scientific, Meridian Road, IL, USA), anti‐phospho‐Foxo1 and anti‐phospho‐Foxo4 (1:1000; catalogue no. #9461, Cell Signaling Technology), anti‐Foxo3 (1:1000; catalogue no. NBP2‐24579, Novus Biologicals, Littleton, CO, USA), anti‐phospho‐Foxo3 (1:1000; catalogue no. bs‐3140R, Bioss, China), anti‐Foxo4 (1:1000; catalogue no. bs‐2766R, Bioss), anti‐Fbx32/Atrogin‐1 (1:1000; catalogue no. ab74023, Abcam), and anti‐GAPDH (1:10 000; catalogue no. MB001H, Bioworld, St Louis Park, MN, USA).

Techniques: Over Expression, Isolation, Transfection, Plasmid Preparation, Western Blot, Expressing