cPLA2 (D49A7) Rabbit mAb 5249T from Cell Signaling Technology

Published Figures

Register or Sign In to View Figures.

Scientific Reports
January 03 2024

Fig 1: Atp10A deletion perturbs liver insulin signaling in female mice fed a HFD. (a, d) Representative blots for total and/or phosphorylated (a) DGAT1, DGAT2, AMPKα, ACC, and (d) IRβ, IRS-1, Akt, GSK-3β, and cPLA2. (b) For DGAT1 and DGAT2 quantitation, total protein was normalized to β-actin levels. (c, e) The phosphoproteins were normalized to their respective total protein and β-actin levels. Mean measurements of 4–6 independent experiments are shown. P value by (b, c) unpaired t-test or (e) 2-way ANOVA with Sidak’s multiple comparison test. (a–c, 10A+/+ n = 7, 10A−/− n = 7, b: **P = 0.0050; c: *P = 0.0229, *P = 0.0481; d, e, 10A+/+ n = 8, 10A−/− n = 8, **P = 0.0044, ***P = 0.0007, **P = 0.0038, ****P=\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$<$$\end{document}< 0.0001,). (a) Original blots are shown in Supplemental Fig. 7B (DGAT 1 and DGAT 2) and Supplemental Fig. 7C (ACC, p-AMPKαT172, p-ACCS79, AMPKα, β-actin. (b) Original blots are shown in Supplemental Fig. 7D (p-IRβ1146, p-IRβ1150/51), Supplemental Fig. 7E (p-GSK-3βS9, p-cPLA2S505, cPLA2, IRβ), Supplemental Fig. 7F (p-IRS-1S612, IRS-1), Supplemental Fig. 7G (p-AktS473/T308, Akt, GSK-3β), Supplemental Fig. 7H (β-actin). (f) Schematic adapted from65 and created using Biorender.com. The illustration shows insulin binding to the insulin receptor and the resulting downstream signaling events that stimulate LysoPC production, AA metabolism, changes to glucose and lipid metabolism; including the promotion of lipogenesis. MAPK = mitogen-activated protein kinase, cPLA2 = cytosolic phospholipase 2, IRS-1 = insulin receptor substrate 1, PI3K = phosphoinositide 3-kinase, PIP2 = phosphatidylinositol 4,5-bisphosphate, PIP3 = phosphatidylinositol 3,4,5-triphosphate, PDK1 = pyruvate dehydrogenase kinase 1, GSK-3β = glycogen synthase kinase-3 beta, LKB1 = liver kinase B1, AMPKα = AMP-activated protein kinase alpha, MCD = malonyl-CoA decarboxylase, ACC1 = acetyl-CoA carboxylase, SCD1 = stearoyl-CoA desaturase 1, MGAT = monoglycerol acyltransferase, DGAT = diglyceride acyltransferase.
Register or Sign In to View Figures.

Frontiers in Cell and Developmental Biology
February 13 2024

Fig 2: Atp10A deficiency results in changes to signaling pathways in the testes. Total tissue lysates from testes from the 10A+/+ and 10A−/− mice were subjected to Western immunoblot analysis. (A, D) Representative blots for (A) total FSHR and LHR, (D) and total and phosphorylated ERK1/2, p38, cPLA2, and Akt. (B, C) For FSHR and LHR quantitation, total protein was normalized to β-actin levels and total protein from 10A+/+ samples. (E, F, G, and H) The phosphoproteins were normalized to their respective total protein, β-actin levels, and total protein from 10A+/+ samples. Mean measurements of 4-6 independent experiments are shown. p-value by unpaired t-test. (B, 10A+/+ n = 8, 10A−/− n = 8, **p = 0.0012; C, 10A+/+ n = 8, 10A−/− n = 7, *p = 0.0448; E,F,G, 10A+/+ n = 8, 10A−/− n = 8, (E) ****p < 0.0001, (F)**p = 0.0020, (G)**p = 0.0058; H, 10A+/+ n = 7, 10A−/− n = 6, (H): ****p < 0.0001).
Register or Sign In to View Figures.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)
March 01 2025

Fig 3: MIF changes arachidomic acid metabolism and causes dysfunction of platelet and immune regulation. A). qPCR analysis of selected genes in THP‐1 cells after stimulation with vehicle, dxms, MIF, and the combination of MIF and dxms (ANXA1, n = 8 per group; PTGS2, n = 9 per group; LAT4H, n = 8 per group; PTGES2, n = 8 per group). B). Bubble plot of arachidomic acid metabolism associated gene expression in monocytes from patients with ITP versus healthy donors. C). Heatmap of differentially expressed proteins. Differences of protein abundance between resistin‐treated THP‐1 cells, MIF‐treated THP‐1 cells, and untreated controls were assessed by proteomic profiling. D). Arachidomic acid metabolomics of BM plasma samples from patients with ITP and HDs. Plasma samples were stored at ‐80 °C after platelet removal for further metabolomics. E). Abundance differences of ALOX5 and PTGDS between ITP patient BM plasma samples and healthy donor BM plasma samples assessed by proteomic profiling. Data represent the mean or the mean with SD. P values: ns, P > 0.05; *, P < 0.05. F). The protein levels of cPLA2 and p‐cPLA2 were detected by western blotting. G). MIF reprograms AA metabolism by altering the expression patterns of ANXA1, PTGS2, and PTGES2, which are resistant to GC therapy. Dysfunctional AA metabolism affects platelet function and immunological homeostasis.

Be the first to write a review!

Citations:

(6)

Figures:

$153.00 Inquire

from
Cell Signaling Technology for
cPLA2 (D49A7) Rabbit mAb

The cPLA2 (D49A7) Rabbit mAb Antibody from Cell Signaling Technology is a Rabbit Monoclonal antibody to PLA2G4A. This antibody recognizes Homo Sapiens, Human, and Mouse antigen. The cPLA2 (D49A7) Rabbit mAb Antibody has been shown to work in the following applications: Precipitation, Immunoprecipitation, and Western Blot.

Scientific Reports

Frontiers in Cell and Developmental Biology

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

cPLA2 (D49A7) Rabbit mAb from Cell Signaling Technology

Cell Signaling Technology

Citations (6)

Reviews

cPLA2 (D49A7) Rabbit mAb from Cell Signaling Technology

About Biocompare

Advertise with Us

Specialized Search Tools

Site Map