phospho pi3k p85 tyr458 (Cell Signaling Technology Inc)

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Cell Signaling Technology Inc phospho pi3k p85 tyr458

ARHGAP40 associates with RhoA and is accompanied by reduced RhoA activity, <t>PI3K/AKT</t> signaling, and altered glutamine-related/redox measures. (A) Flag-based co-immunoprecipitation showing association of ARHGAP40 with RhoA. (B) Endogenous immunoprecipitation of RhoA followed by immunoblotting for ARHGAP40. (C) RhoA activity assay using a conformation-specific anti-RhoA-GTP antibody, with representative GTP-RhoA and total RhoA blots and quantification of the GTP-RhoA/total RhoA ratio. (D) Representative western blots and densitometric analyzes of p -AKT/AKT and p -PI3K/PI3K. (E) Intracellular glutamate levels. (F) Intracellular glutamine levels. (G) GSH/GSSG ratios. (H) Representative ROS flow-cytometry histograms and mean fluorescence intensity. Quantitative analyzes used n = 3 independent biological replicates and are shown as mean ± SEM. Two-group comparisons were performed using two-tailed Student's t-test. * P < 0.05, ** P < 0.01, *** P < 0.001.

Phospho Pi3k P85 Tyr458, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 2057 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+pi3k/Phospho-PI3+Kinase+p85+(Tyr458)%2Fp55+(Tyr199)+Antibody/pmc13652080-111-41-44
Average 96 stars, based on 2057 article reviews

phospho pi3k p85 tyr458 - by Bioz Stars, 2026-10

96/100 stars

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1) Product Images from "ARHGAP40 suppresses clear cell renal cell carcinoma progression and is associated with altered glutamine-related metabolism and redox balance"

Article Title: ARHGAP40 suppresses clear cell renal cell carcinoma progression and is associated with altered glutamine-related metabolism and redox balance

Journal: Cancer Biology & Therapy

doi: 10.1080/15384047.2026.2746137

ARHGAP40 associates with RhoA and is accompanied by reduced RhoA activity, PI3K/AKT signaling, and altered glutamine-related/redox measures. (A) Flag-based co-immunoprecipitation showing association of ARHGAP40 with RhoA. (B) Endogenous immunoprecipitation of RhoA followed by immunoblotting for ARHGAP40. (C) RhoA activity assay using a conformation-specific anti-RhoA-GTP antibody, with representative GTP-RhoA and total RhoA blots and quantification of the GTP-RhoA/total RhoA ratio. (D) Representative western blots and densitometric analyzes of p -AKT/AKT and p -PI3K/PI3K. (E) Intracellular glutamate levels. (F) Intracellular glutamine levels. (G) GSH/GSSG ratios. (H) Representative ROS flow-cytometry histograms and mean fluorescence intensity. Quantitative analyzes used n = 3 independent biological replicates and are shown as mean ± SEM. Two-group comparisons were performed using two-tailed Student's t-test. * P < 0.05, ** P < 0.01, *** P < 0.001.

Figure Legend Snippet: ARHGAP40 associates with RhoA and is accompanied by reduced RhoA activity, PI3K/AKT signaling, and altered glutamine-related/redox measures. (A) Flag-based co-immunoprecipitation showing association of ARHGAP40 with RhoA. (B) Endogenous immunoprecipitation of RhoA followed by immunoblotting for ARHGAP40. (C) RhoA activity assay using a conformation-specific anti-RhoA-GTP antibody, with representative GTP-RhoA and total RhoA blots and quantification of the GTP-RhoA/total RhoA ratio. (D) Representative western blots and densitometric analyzes of p -AKT/AKT and p -PI3K/PI3K. (E) Intracellular glutamate levels. (F) Intracellular glutamine levels. (G) GSH/GSSG ratios. (H) Representative ROS flow-cytometry histograms and mean fluorescence intensity. Quantitative analyzes used n = 3 independent biological replicates and are shown as mean ± SEM. Two-group comparisons were performed using two-tailed Student's t-test. * P < 0.05, ** P < 0.01, *** P < 0.001.

Techniques Used: Activity Assay, Co-Immunoprecipitation Assay, Immunoprecipitation, Western Blot, Flow Cytometry, Fluorescence, Two Tailed Test

Incubation:

Article Title: Long noncoding RNA SRRM2-AS1 mediates coronary artery damage in Kawasaki disease by promoting endothelial-to-mesenchymal transition
Article Snippet: .. After being blocked with BSA, the membranes were incubated overnight at 4 °C with the following primary antibodies: anti-ZO1 (1:1000, Cat. No. 5406 S, Cell Signaling Technology, Danvers, MA), anti-N-cadherin (1:1000, Cat. No. 4061 S, Cell Signaling Technology, Danvers, MA), anti-Vimentin (1:1000, Cat. No. 5741T, Cell Signaling Technology), anti-GAPDH (1:1000; Cat. No. 5174T, Cell Signaling Technology), anti-SRRM2 (1:1000, Cat. No. ab182251, Abcam), anti-UBC (1:200, Cat. No. NBP2-54692, Novus Biologicals, Littleton, CO), anti-PI3K (1:100, Cat. No. 4249 S, Cell Signaling Technology), anti-Phospho-Akt (1:1000, Cat. No. 4060 S, Cell Signaling Technology), anti-Akt (1:1000, Cat. No. 4691 S, Cell Signaling Technology), anti-GSK-3β (1:1000, Cat. No. 12456 S, Cell Signaling Technology), anti-β-catenin (1:1000, Cat. No. 8480 S, Cell Signaling Technology). .. The membranes were washed with Tris-buffered saline/0.1% Tween 20 (TBST) and incubated with secondary antibodies at 25 °C for 1 h. Hybridization signals were assessed using PierceTM ECL Western Blotting Substrate (Thermo Fisher Scientific, Waltham, MA).

Article Title: Activation of the PI3K/AKT pathway by EDIL3 induces EMT and promotes tumor progression in clear cell renal cell carcinoma.
Article Snippet: tumor microenvironment, which collectively contribute to its aggressive biological behavior, Despite recent advances in imaging techniques (Shuch et al. 2024), many patients are diagnosed at advanced stages, resulting in a poor prognosis (Rathmell et al. 2022). this highlights a critical need to identify key regulators (Rosellini et al. 2023) that drive ccRCC initiation and progression and to elucidate the molecular mechanisms underlying tumor cell proliferation, invasion, and metastasis.. A deeper understanding of these processes is essential not only for improving early diagnosis but also for uncovering novel targets for mechanism-based therapeutic intervention.. Epithelial-mesenchymal transition (EMT) is a biological process in which cells change from an epithelial phenotype to a mesenchymal phenotype (Singh et al. 2018).

Article Title: Norepinephrine promotes colorectal cancer liver metastasis via mechanisms dependent on Kupffer cells.
Article Snippet: The mechanisms underlying colorectal cancer liver metastasis (CRLM) remain incompletely understood.. Increasing evidence suggests that stress-associated catecholamines may influence tumor progression.. However, how norepinephrine (NE) influences the hepatic immune microenvironment during CRLM progression remains poorly characterized.

Blocking Assay:

other:

Article Title: BCR::ABL1 tyrosine kinase inhibitors induce ribosome collisions to activate ZAK-dependent ribotoxic stress and apoptosis in chronic myeloid leukemia.
Article Snippet: Protein band intensities were measured from individual lanes using ImageJ software, subtracted by background signals, and then normalized to controls.

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