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rabbit anti pp2ac antibody  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc rabbit anti pp2ac antibody
    Rabbit Anti Pp2ac Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 360 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/rabbit+anti+pp2ac/PP2A+C+Subunit+Antibody/pm41841751-111-6-12
    Average 96 stars, based on 360 article reviews
    rabbit anti pp2ac antibody - by Bioz Stars, 2026-10
    96/100 stars

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    Related Articles

    Immunofluorescence:

    Article Title: Conditional Knockout in Mice Reveals the Critical Roles of Ppp2ca in Epidermis Development
    Article Snippet: .. Indirect immunofluorescence staining was carried out on paraffin sections using the following primary antibodies: rabbit anti-PP2Ac (1:100, Cell Signaling); mouse anti-cytokeratin-14 (1:50, Santa Cruz, Dallas, CA, USA); mouse anti-pan-cytokeratin (1:50, AE13, Santa Cruz, Dallas, CA, USA); mouse anti-trichohyalin antibody (1:100,AE15, Abcam, Cambridge, UK); Rabbit anti-Ki67 (1:100, Abcam, Cambridge, UK); secondary antibody kit: Rabbit SP detection kits (KIT-9706) (Maxim, FuZhou, China), mouse SP detection kits(KIT-9701) (Maxim). .. Quantification of fluorescence was performed by a blinded observer using the ImageJ software (National Institute of Mental Health, Bethesda, MD, USA) and depicted as percent of relative expression.

    Staining:

    Article Title: Conditional Knockout in Mice Reveals the Critical Roles of Ppp2ca in Epidermis Development
    Article Snippet: .. Indirect immunofluorescence staining was carried out on paraffin sections using the following primary antibodies: rabbit anti-PP2Ac (1:100, Cell Signaling); mouse anti-cytokeratin-14 (1:50, Santa Cruz, Dallas, CA, USA); mouse anti-pan-cytokeratin (1:50, AE13, Santa Cruz, Dallas, CA, USA); mouse anti-trichohyalin antibody (1:100,AE15, Abcam, Cambridge, UK); Rabbit anti-Ki67 (1:100, Abcam, Cambridge, UK); secondary antibody kit: Rabbit SP detection kits (KIT-9706) (Maxim, FuZhou, China), mouse SP detection kits(KIT-9701) (Maxim). .. Quantification of fluorescence was performed by a blinded observer using the ImageJ software (National Institute of Mental Health, Bethesda, MD, USA) and depicted as percent of relative expression.

    other:

    Article Title: Progestin-inducible EDD E3 ubiquitin ligase binds to α4 phosphoprotein to regulate ubiquitination and degradation of protein phosphatase PP2Ac.
    Article Snippet: 28 29 30 31 32 33 34 35 36 37 38 39 40 Article history: Received 16 July 2013 Received in revised form 20 September 2013 Accepted 26 September 2013 Available online xxxx

    Article Title: Dysfunctional BCAA degradation triggers neuronal damage through disrupted AMPK-mitochondrial axis due to enhanced PP2Ac interaction
    Article Snippet: For staining with chemical dyes, larvae brain tissues were dissected in Schneider’s medium (Sigma-Aldrich, S0146) and incubated with chemical dye added into Schneider’s medium.

    Incubation:

    Article Title: Astrocyte-derived lactoferrin reduces Aβ burden by promoting the interaction of p38 and PP2A in APP/PS1 transgenic mice
    Article Snippet: .. Proteins were separated by SDS/PAGE and then transferred to PVDF membranes to incubated with rabbit anti-Lf (Millipore, 07-685, 1:1000; recognizes mouse and human Lf), rabbit antihuman Lf (Abmart, T59526, 1: 1000), rabbit anti-APP695 (Cell Signaling Technology, 2452, 1: 1000), rabbit anti-C-APP (Sigma, SAB4200535, 1:1000), rabbit anti-BACE1 (Abcam, ab183612, 1: 1000), rabbit anti-AMAD 10 (Cell Signaling Technology, 14194, 1: 1000), rabbit anti-presenilin-1 (PS1; Cell Signaling Technology, 5643, 1: 1000), mouse anti-soluble amyloid precursor α (sAPPα· Immuno-Biological Laboratories, 11088, 1: 500), mouse anti-soluble amyloid precursor β (sAPPβ· Immuno-Biological Laboratories, 10321, 1: 500), mouse anti-insulin-degrading enzyme (IDE; Santa Cruz, sc-514458, 1:500), goat anti-apolipoprotein E (APOE; Santa Cruz, sc-6384, 1: 500), rabbit anti-low-density lipoprotein receptor-related protein 1 (LRP1; Abcam, ab92544, 1: 8000), rabbit anti-advanced glycation end products (RAGE; Sigma, SAB2105049, 1: 1000), rabbit anti-Oligomer (Millipore, AB9234, 1: 1000), mouse anti-tau (Sigma, 577801, 1:5000), rabbit anti-p-tau (Thr181) (Cell Signaling Technology, 62672, 1: 2000), rabbit anti-p-tau (Ser202) (Cell Signaling Technology, 39357, 1: 2000), rabbit anti-p-tau (Thr231) (Cell Signaling Technology, 71429, 1: 2000), rabbit anti-p-tau (Ser396) (sigma, SAB4504557, 1: 2000), rabbit anti-p-tau (Ser404) (Cell Signaling Technology, 35834, 1: 2000), rabbit anti-glycogen synthase kinase 3α/β (GSK3α/β· Cell Signaling Technology, 5676, 1: 3000), rabbit anti-p-GSK3α/β (Ser21/9) (Cell Signaling Technology, 8566, 1: 4000), rabbit anti-p38 (Cell Signaling Technology, 8690, 1: 2000), rabbit anti-p-p38 (Cell Signaling Technology, 4511, 1: 2000), rabbit anti-cyclin-dependent kinase 5 (CDK5; Cell Signaling Technology, 14145, 1: 1000), rabbit anti-p-CDK5 (Cell Signaling Technology, 19051, 1: 1000), rabbit anti-PP2Ac (Cell Signaling Technology, 2038, 1: 1000), rabbit anti-p-Erk1/2 (Cell Signaling Technology, 4370, 1: 1000), rabbit anti-Erk1/2 (Cell Signaling Technology, 4695, 1: 1000) and mouse anti-β-actin (Sigma, A2228, 1: 10000) overnight at 4 °C. ..

    Article Title: Astrocyte-derived lactoferrin reduces β-amyloid burden by promoting the interaction between p38 kinase and PP2A phosphatase in male APP/PS1 transgenic mice.
    Article Snippet: Funding information National Natural Science Foundation of China, Grant/Award Numbers: 92049106, 31970967; China Postdoctoral Science Foundation, Grant/Award Number: 2021MD703901 Abstract Background and Purpose: Overexpression of astrocytic lactoferrin (Lf) was observed in the brain of Alzheimer's disease (AD) patients, whereas the role of astrocytic Lf in AD progression remains unexplored.. In this study, we aimed to evaluate the effects of astrocytic Lf on AD progression.. Experimental Approach: Male APP/PS1 mice with astrocytes overexpressing human Lf were developed to evaluate the effects of astrocytic Lf on AD progression.

    Article Title: Activation of vitamin D receptor inhibits Tau phosphorylation is associated with reduction of iron accumulation in APP/PS1 transgenic mice.
    Article Snippet: Vitamin D deficiency and iron accumulation are prevalent in the brains of Alzheimer’s disease (AD) patients, however, whether Vitamin D has a role in the regulations of iron metabolism in the condition of AD remains unknown.. Our previous studies revealed that vitamin D deficiency promotes β-amyloid (Aβ) deposition in the APP/PS1 mouse brains, while supplemented with a specific agonist of vitamin D receptor (VDR), paricalcitol (PAL), significantly reduced Aβ production via promoting the lysosomal degradation of β-site APP cleavage enzyme 1 (BACE1).. In this study, our data suggested that activation of VDR by PAL significantly reduced the iron accumulation in the cortex and hippocampus of APP/PS1 mice through downregulation of Transferrin receptor (TFR) by reducing iron-regulatory protein 2 (IRP2) expression.

    Western Blot:

    Article Title: Dysfunctional BCAA degradation triggers neuronal damage through disrupted AMPK-mitochondrial axis due to enhanced PP2Ac interaction.
    Article Snippet: .. The following antibodies were used for immunoblotting or immunoprecipitation assay: rabbit anti-Atg8 (Sigma-Aldrich, ABC974-I), rabbit antiRef2p (Abcam, ab178440), rabbit antiphospho-S6K(Thr398) (Cell Signaling, #9209), rabbit anti-phosphor-AMPKα (Cell Signaling, #2535), mouse anti-AMPKα (Millipore, MABS1232), rabbit anti-PP2Ac (Cell Signaling, #2038S), rabbit antiphospho-PP2Ac (Merck, SAB4503975), rabbit antiActin (GeneTex, GTX109639), mouse anti-Actin (DSHB, anti-JLA20), rabbit anti-mCherry (Abcam, ab213511), mouse anti-HA (Cell Signaling, #3724), mouse anti-Flag (Merck, F1804), rabbit anti-GFP (GeneTex, GTX113617). .. The following antibodies were used for immunostaining: rabbit anti-cleaved-caspase3 (Cell Signaling, #9661), rabbit anti-4HNE, (Abcam, ab46545), mouse anti-Total OXPHOS Rodent WB Antibody Cocktail (Abcam, ab110413), mouse anti-Elav (DSHB, 9F8A9) and rabbit anti-GFP (GeneTex, GTX113617).

    Immunoprecipitation:

    Article Title: Dysfunctional BCAA degradation triggers neuronal damage through disrupted AMPK-mitochondrial axis due to enhanced PP2Ac interaction.
    Article Snippet: .. The following antibodies were used for immunoblotting or immunoprecipitation assay: rabbit anti-Atg8 (Sigma-Aldrich, ABC974-I), rabbit antiRef2p (Abcam, ab178440), rabbit antiphospho-S6K(Thr398) (Cell Signaling, #9209), rabbit anti-phosphor-AMPKα (Cell Signaling, #2535), mouse anti-AMPKα (Millipore, MABS1232), rabbit anti-PP2Ac (Cell Signaling, #2038S), rabbit antiphospho-PP2Ac (Merck, SAB4503975), rabbit antiActin (GeneTex, GTX109639), mouse anti-Actin (DSHB, anti-JLA20), rabbit anti-mCherry (Abcam, ab213511), mouse anti-HA (Cell Signaling, #3724), mouse anti-Flag (Merck, F1804), rabbit anti-GFP (GeneTex, GTX113617). .. The following antibodies were used for immunostaining: rabbit anti-cleaved-caspase3 (Cell Signaling, #9661), rabbit anti-4HNE, (Abcam, ab46545), mouse anti-Total OXPHOS Rodent WB Antibody Cocktail (Abcam, ab110413), mouse anti-Elav (DSHB, 9F8A9) and rabbit anti-GFP (GeneTex, GTX113617).



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    IL-17A induces p53, PAI-1, Cav1 and apoptosis, and CSP or CSP7 inhibits IL-17A-induced apoptosis in AECs. ( A ) AECs isolated from uninjured WT and p53 −/− mice were treated with IL-17A (0–100 ng/mL) for 24 h, and the lysates were immunoblotted for p53, PAI-1, Cl./Cas-3 and β-actin. ( B ) WT mice received saline or IL-17A intranasally (0–3 μg in 50 μL saline), as previously described . AECs were isolated 24 h later, and lysates were immunoblotted for p53 and Cl./Cas-3 and β-actin. ( C ) WT mice were exposed to saline or IL-17A (1 μg), as described in ( B ). Lysates of AECs isolated 24 h after treatment with IL-17A were immunoblotted for ACp53, p53, Sirt1, Cav1 and apoptosis. ( D ) AECs isolated from WT mice were treated with PBS or IL-17A (100 ng/mL). Two hours later, IL-17A-stimulated cells were treated with or without CSP or CP (10 µM) and analyzed for p53, PAI-1 and apoptosis by Western blotting (WB). ( E ) AECs isolated from WT mice exposed to IL-17A (100 ng/mL) were treated with CSP, its overlapping deletion fragments, or control peptide (CP) for 24 h in vitro. The lysates were analyzed for ACp53, p53, PAI-1, Sirt1 and Cl. Cas-3 by WB. ( F ) miR-34a fl/fl mice and miR-34acKO mice lacking miR-34a in AECs were exposed to IL-17A (1 μg) with or without CSP7 or CP. Control mice were exposed to saline. Lysates from AECs extracted from these mice were analyzed for p53, PAI-1, Sirt1, Cav1 and apoptosis by WB. ( G ) Lung homogenates or lysates of AECs extracted from WT mice exposed to IL-17A with or without CSP7 or CP were subjected to WB for <t>PP2Ac,</t> pATM and ATM kinase. ( H ) Lung homogenates of IL-17A-exposed mice treated with or without CSP7 or CP were immunoprecipitated (IP) using anti-Cav1 antibody and immunoblotted for p53, mdm2, and PP2Ac. ( I ) Lung homogenates of WT mice exposed to saline or IL-17A with or without CSP7 were analyzed for MPO activity.
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    Image Search Results


    IL-17A induces p53, PAI-1, Cav1 and apoptosis, and CSP or CSP7 inhibits IL-17A-induced apoptosis in AECs. ( A ) AECs isolated from uninjured WT and p53 −/− mice were treated with IL-17A (0–100 ng/mL) for 24 h, and the lysates were immunoblotted for p53, PAI-1, Cl./Cas-3 and β-actin. ( B ) WT mice received saline or IL-17A intranasally (0–3 μg in 50 μL saline), as previously described . AECs were isolated 24 h later, and lysates were immunoblotted for p53 and Cl./Cas-3 and β-actin. ( C ) WT mice were exposed to saline or IL-17A (1 μg), as described in ( B ). Lysates of AECs isolated 24 h after treatment with IL-17A were immunoblotted for ACp53, p53, Sirt1, Cav1 and apoptosis. ( D ) AECs isolated from WT mice were treated with PBS or IL-17A (100 ng/mL). Two hours later, IL-17A-stimulated cells were treated with or without CSP or CP (10 µM) and analyzed for p53, PAI-1 and apoptosis by Western blotting (WB). ( E ) AECs isolated from WT mice exposed to IL-17A (100 ng/mL) were treated with CSP, its overlapping deletion fragments, or control peptide (CP) for 24 h in vitro. The lysates were analyzed for ACp53, p53, PAI-1, Sirt1 and Cl. Cas-3 by WB. ( F ) miR-34a fl/fl mice and miR-34acKO mice lacking miR-34a in AECs were exposed to IL-17A (1 μg) with or without CSP7 or CP. Control mice were exposed to saline. Lysates from AECs extracted from these mice were analyzed for p53, PAI-1, Sirt1, Cav1 and apoptosis by WB. ( G ) Lung homogenates or lysates of AECs extracted from WT mice exposed to IL-17A with or without CSP7 or CP were subjected to WB for PP2Ac, pATM and ATM kinase. ( H ) Lung homogenates of IL-17A-exposed mice treated with or without CSP7 or CP were immunoprecipitated (IP) using anti-Cav1 antibody and immunoblotted for p53, mdm2, and PP2Ac. ( I ) Lung homogenates of WT mice exposed to saline or IL-17A with or without CSP7 were analyzed for MPO activity.

    Journal: International Journal of Molecular Sciences

    Article Title: Interleukin-17A Orchestrates Lung Injury and Remodeling Through p53 and uPA System Crosstalk

    doi: 10.3390/ijms27041841

    Figure Lengend Snippet: IL-17A induces p53, PAI-1, Cav1 and apoptosis, and CSP or CSP7 inhibits IL-17A-induced apoptosis in AECs. ( A ) AECs isolated from uninjured WT and p53 −/− mice were treated with IL-17A (0–100 ng/mL) for 24 h, and the lysates were immunoblotted for p53, PAI-1, Cl./Cas-3 and β-actin. ( B ) WT mice received saline or IL-17A intranasally (0–3 μg in 50 μL saline), as previously described . AECs were isolated 24 h later, and lysates were immunoblotted for p53 and Cl./Cas-3 and β-actin. ( C ) WT mice were exposed to saline or IL-17A (1 μg), as described in ( B ). Lysates of AECs isolated 24 h after treatment with IL-17A were immunoblotted for ACp53, p53, Sirt1, Cav1 and apoptosis. ( D ) AECs isolated from WT mice were treated with PBS or IL-17A (100 ng/mL). Two hours later, IL-17A-stimulated cells were treated with or without CSP or CP (10 µM) and analyzed for p53, PAI-1 and apoptosis by Western blotting (WB). ( E ) AECs isolated from WT mice exposed to IL-17A (100 ng/mL) were treated with CSP, its overlapping deletion fragments, or control peptide (CP) for 24 h in vitro. The lysates were analyzed for ACp53, p53, PAI-1, Sirt1 and Cl. Cas-3 by WB. ( F ) miR-34a fl/fl mice and miR-34acKO mice lacking miR-34a in AECs were exposed to IL-17A (1 μg) with or without CSP7 or CP. Control mice were exposed to saline. Lysates from AECs extracted from these mice were analyzed for p53, PAI-1, Sirt1, Cav1 and apoptosis by WB. ( G ) Lung homogenates or lysates of AECs extracted from WT mice exposed to IL-17A with or without CSP7 or CP were subjected to WB for PP2Ac, pATM and ATM kinase. ( H ) Lung homogenates of IL-17A-exposed mice treated with or without CSP7 or CP were immunoprecipitated (IP) using anti-Cav1 antibody and immunoblotted for p53, mdm2, and PP2Ac. ( I ) Lung homogenates of WT mice exposed to saline or IL-17A with or without CSP7 were analyzed for MPO activity.

    Article Snippet: 17 , PP2Ac , CST , 2259S , 1:1000 , .

    Techniques: Isolation, Saline, Western Blot, Control, In Vitro, Immunoprecipitation, Activity Assay