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rabbit anti phospho pi3k  (Bioss)


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    Structured Review

    Bioss rabbit anti phospho pi3k
    Rabbit Anti Phospho Pi3k, supplied by Bioss, used in various techniques. Bioz Stars score: 95/100, based on 90 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti phospho pi3k/product/Bioss
    Average 95 stars, based on 90 article reviews
    rabbit anti phospho pi3k - by Bioz Stars, 2026-02
    95/100 stars

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    Cell Signaling Technology Inc rabbit anti p pi3k tyr458 antibody
    Akk improves hepatic lipid metabolism via <t>PI3K/Akt</t> pathway in obese mice (A–C) Akk significantly affected mouse liver protein network interaction pathways, significantly regulated pathways and differential proteins by proteomic analysis. (D–J) Western blot in the PI3K/Akt pathway in mouse liver: p-PI3K/PI3K, p -AMPK/AMPK, p -Akt/Akt, PPARγ/GAPDH, and SREBP-1c/GAPDH. (K) mRNA levels of genes related to lipogenesis (ACC1, FASN, SCD1, and PPARγ), lipid oxidation (CPT1α), and lipid uptake (SREBP-1c) in mouse liver. Data are expressed as mean ± SD (n = 6–8), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, compared with the Mod group, and p value was calculated using Dunnet’s post hoc test in one-way ANOVA.
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    Cell Signaling Technology Inc rabbit polyclonal anti phospho pi3k p pi3k antibodies
    Fig. 2. MβCD increases <t>PI3K</t> phosphorylation, while inhibition of S1PR or NOS impairs MβCD-induced tyrosine phosphorylation. Spermatozoa were incubated for 3.5 h at 37 ◦C under various conditions: untreated (−), treated with 10 % v/v fetal cord serum ultrafiltrate (FCSu), treated with 0.5 mM methyl- β-cyclodextrin (MβCD), and treated with MβCD in combination with (a) 40 μM VPC 23019 (S1PR1/3 inhibitor) or (b) L-NAME (Nitric Oxide Synthase inhibitor). (a) Immunoblotting analysis revealed that VPC 23019 at 40 μM decreased PI3K phosphorylation <t>(P-PI3K)</t> in spermatozoa incubated with 0.5 mM of MβCD. (b) Immunoblotting showed that L-NAME treatment decreased tyrosine phosphorylation (P-Tyr) in sperm samples treated with FCSu and MβCD. The signal intensity for each lane was normalized to the silver-stain optical density value for accurate quantification. α-Tubulin loading controls were performed for direct comparison with the silver stain loading controls. The data represent sperm samples from four different healthy donors (n = 4). Statistical analysis was performed using ANOVA with Tukey’s test: *p ≤0.05, **p ≤0.01, and ***p ≤0.001.
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    Cell Signaling Technology Inc anti phospho pi3k
    Fig. 2. MβCD increases <t>PI3K</t> phosphorylation, while inhibition of S1PR or NOS impairs MβCD-induced tyrosine phosphorylation. Spermatozoa were incubated for 3.5 h at 37 ◦C under various conditions: untreated (−), treated with 10 % v/v fetal cord serum ultrafiltrate (FCSu), treated with 0.5 mM methyl- β-cyclodextrin (MβCD), and treated with MβCD in combination with (a) 40 μM VPC 23019 (S1PR1/3 inhibitor) or (b) L-NAME (Nitric Oxide Synthase inhibitor). (a) Immunoblotting analysis revealed that VPC 23019 at 40 μM decreased PI3K phosphorylation <t>(P-PI3K)</t> in spermatozoa incubated with 0.5 mM of MβCD. (b) Immunoblotting showed that L-NAME treatment decreased tyrosine phosphorylation (P-Tyr) in sperm samples treated with FCSu and MβCD. The signal intensity for each lane was normalized to the silver-stain optical density value for accurate quantification. α-Tubulin loading controls were performed for direct comparison with the silver stain loading controls. The data represent sperm samples from four different healthy donors (n = 4). Statistical analysis was performed using ANOVA with Tukey’s test: *p ≤0.05, **p ≤0.01, and ***p ≤0.001.
    Anti Phospho Pi3k, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 97 stars, based on 1 article reviews
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    Image Search Results


    Akk improves hepatic lipid metabolism via PI3K/Akt pathway in obese mice (A–C) Akk significantly affected mouse liver protein network interaction pathways, significantly regulated pathways and differential proteins by proteomic analysis. (D–J) Western blot in the PI3K/Akt pathway in mouse liver: p-PI3K/PI3K, p -AMPK/AMPK, p -Akt/Akt, PPARγ/GAPDH, and SREBP-1c/GAPDH. (K) mRNA levels of genes related to lipogenesis (ACC1, FASN, SCD1, and PPARγ), lipid oxidation (CPT1α), and lipid uptake (SREBP-1c) in mouse liver. Data are expressed as mean ± SD (n = 6–8), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, compared with the Mod group, and p value was calculated using Dunnet’s post hoc test in one-way ANOVA.

    Journal: iScience

    Article Title: Akkermansia muciniphila ameliorates fatty liver through microbiota-derived α-ketoisovaleric acid metabolism and hepatic PI3K/Akt signaling

    doi: 10.1016/j.isci.2025.112458

    Figure Lengend Snippet: Akk improves hepatic lipid metabolism via PI3K/Akt pathway in obese mice (A–C) Akk significantly affected mouse liver protein network interaction pathways, significantly regulated pathways and differential proteins by proteomic analysis. (D–J) Western blot in the PI3K/Akt pathway in mouse liver: p-PI3K/PI3K, p -AMPK/AMPK, p -Akt/Akt, PPARγ/GAPDH, and SREBP-1c/GAPDH. (K) mRNA levels of genes related to lipogenesis (ACC1, FASN, SCD1, and PPARγ), lipid oxidation (CPT1α), and lipid uptake (SREBP-1c) in mouse liver. Data are expressed as mean ± SD (n = 6–8), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, compared with the Mod group, and p value was calculated using Dunnet’s post hoc test in one-way ANOVA.

    Article Snippet: Rabbit anti-p-PI3K (Tyr458) antibody , Cell Signaling Technology , Cat# 4228, RRID: AB_659940.

    Techniques: Western Blot

    α-ketoisovaleric acid is the key metabolite in improving hepatic lipid metabolism via PI3K/Akt pathway in obese mice (A) Flowchart of α-ketoisovaleric acid compensation experiment. All mice, except for the Con group, were fed an HFHCD from week 1 to week 8. α-ketoisovaleric acid group was orally administered α-ketoisovaleric acid every day, while the Con and Mod groups were given saline. (B) Representative photographs of mouse livers from each group. (C–H) Western blot in the PI3K/Akt pathway in mouse liver: p-PI3K/PI3K, p -AMPK/AMPK, p -Akt/Akt, PPARγ/GAPDH, and SREBP-1c/GAPDH. (I) mRNA levels of genes related to lipogenesis (ACC1, FASN, and PPARγ), lipid oxidation (CPT1α), and lipid uptake (SREBP-1c) in mouse liver. (J) Akk improves hepatic lipid metabolism via PI3K/Akt pathway through α-ketoisovaleric acid. Data are expressed as mean ± SD (n = 6–8), ∗ p < 0.05, ∗∗ p < 0.01, compared with the Mod group, and p value was calculated using Dunnet’s post hoc test in one-way ANOVA. Scale bars: 1 cm.

    Journal: iScience

    Article Title: Akkermansia muciniphila ameliorates fatty liver through microbiota-derived α-ketoisovaleric acid metabolism and hepatic PI3K/Akt signaling

    doi: 10.1016/j.isci.2025.112458

    Figure Lengend Snippet: α-ketoisovaleric acid is the key metabolite in improving hepatic lipid metabolism via PI3K/Akt pathway in obese mice (A) Flowchart of α-ketoisovaleric acid compensation experiment. All mice, except for the Con group, were fed an HFHCD from week 1 to week 8. α-ketoisovaleric acid group was orally administered α-ketoisovaleric acid every day, while the Con and Mod groups were given saline. (B) Representative photographs of mouse livers from each group. (C–H) Western blot in the PI3K/Akt pathway in mouse liver: p-PI3K/PI3K, p -AMPK/AMPK, p -Akt/Akt, PPARγ/GAPDH, and SREBP-1c/GAPDH. (I) mRNA levels of genes related to lipogenesis (ACC1, FASN, and PPARγ), lipid oxidation (CPT1α), and lipid uptake (SREBP-1c) in mouse liver. (J) Akk improves hepatic lipid metabolism via PI3K/Akt pathway through α-ketoisovaleric acid. Data are expressed as mean ± SD (n = 6–8), ∗ p < 0.05, ∗∗ p < 0.01, compared with the Mod group, and p value was calculated using Dunnet’s post hoc test in one-way ANOVA. Scale bars: 1 cm.

    Article Snippet: Rabbit anti-p-PI3K (Tyr458) antibody , Cell Signaling Technology , Cat# 4228, RRID: AB_659940.

    Techniques: Saline, Western Blot

    Fig. 2. MβCD increases PI3K phosphorylation, while inhibition of S1PR or NOS impairs MβCD-induced tyrosine phosphorylation. Spermatozoa were incubated for 3.5 h at 37 ◦C under various conditions: untreated (−), treated with 10 % v/v fetal cord serum ultrafiltrate (FCSu), treated with 0.5 mM methyl- β-cyclodextrin (MβCD), and treated with MβCD in combination with (a) 40 μM VPC 23019 (S1PR1/3 inhibitor) or (b) L-NAME (Nitric Oxide Synthase inhibitor). (a) Immunoblotting analysis revealed that VPC 23019 at 40 μM decreased PI3K phosphorylation (P-PI3K) in spermatozoa incubated with 0.5 mM of MβCD. (b) Immunoblotting showed that L-NAME treatment decreased tyrosine phosphorylation (P-Tyr) in sperm samples treated with FCSu and MβCD. The signal intensity for each lane was normalized to the silver-stain optical density value for accurate quantification. α-Tubulin loading controls were performed for direct comparison with the silver stain loading controls. The data represent sperm samples from four different healthy donors (n = 4). Statistical analysis was performed using ANOVA with Tukey’s test: *p ≤0.05, **p ≤0.01, and ***p ≤0.001.

    Journal: Redox biology

    Article Title: Dysregulation of sphingolipid and cholesterol homeostasis imposes oxidative stress in human spermatozoa.

    doi: 10.1016/j.redox.2025.103669

    Figure Lengend Snippet: Fig. 2. MβCD increases PI3K phosphorylation, while inhibition of S1PR or NOS impairs MβCD-induced tyrosine phosphorylation. Spermatozoa were incubated for 3.5 h at 37 ◦C under various conditions: untreated (−), treated with 10 % v/v fetal cord serum ultrafiltrate (FCSu), treated with 0.5 mM methyl- β-cyclodextrin (MβCD), and treated with MβCD in combination with (a) 40 μM VPC 23019 (S1PR1/3 inhibitor) or (b) L-NAME (Nitric Oxide Synthase inhibitor). (a) Immunoblotting analysis revealed that VPC 23019 at 40 μM decreased PI3K phosphorylation (P-PI3K) in spermatozoa incubated with 0.5 mM of MβCD. (b) Immunoblotting showed that L-NAME treatment decreased tyrosine phosphorylation (P-Tyr) in sperm samples treated with FCSu and MβCD. The signal intensity for each lane was normalized to the silver-stain optical density value for accurate quantification. α-Tubulin loading controls were performed for direct comparison with the silver stain loading controls. The data represent sperm samples from four different healthy donors (n = 4). Statistical analysis was performed using ANOVA with Tukey’s test: *p ≤0.05, **p ≤0.01, and ***p ≤0.001.

    Article Snippet: Rabbit polyclonal anti-phospho-PI3K (P-PI3K) antibodies were purchased from Cell Signaling (#4228) (Beverly, MA, USA).

    Techniques: Phospho-proteomics, Inhibition, Incubation, Western Blot, Silver Staining, Comparison