Anti-beta Actin ACTB Rabbit Monoclonal Antibody

Western blot analysis of Beta Actin using anti-Beta Actin antibody (M01263).
Electrophoresis was performed on a 5-20% SDS-PAGE gel at 70V (Stacking gel) / 90V (Resolving gel) for 2-3 hours. The sample well of each lane was loaded with 30 ug of sample under reducing conditions.
Lane 1: human GES-1 whole cell lysates,
Lane 2: human Hela whole cell lysates,
Lane 3: human A431 whole cell lysates,
Lane 4: human K562 whole cell lysates,
Lane 5: rat C6 whole cell lysates,
Lane 6: rat PC-12 whole cell lysates,
Lane 7: mouse Neuro-2a whole cell lysates.
After electrophoresis, proteins were transferred to a nitrocellulose membrane at 150 mA for 50-90 minutes. Blocked the membrane with 5% non-fat milk/TBS for 1.5 hour at RT. The membrane was incubated with rabbit anti-Beta Actin antigen affinity purified monoclonal antibody (Catalog # M01263) at 1:5000 overnight at 4°C, then washed with TBS-0.1%Tween 3 times with 5 minutes each and probed with a goat anti-rabbit IgG-HRP secondary antibody at a dilution of 1:500 for 1.5 hour at RT. The signal is developed using an Enhanced Chemiluminescent detection (ECL) kit (Catalog # EK1002) with Tanon 5200 system. A specific band was detected for Beta Actin at approximately 42 kDa. The expected band size for Beta Actin is at 42 kDa.

Immunohistochemical analysis of paraffin-embedded (1) Human heart; (2) Mouse testis; (3) Human bladder cancer; (4) Mouse heart, using beta Actin Antibody.

(A–F) Cisatracurium inhibits metastatic ability of CRC in vivo . (A) Line graph of subcutaneous tumor volume. (B) Weight of subcutaneous tumors in grams. Data are expressed as mean tumor volume or weight ± SE. ∗ p < 0.05. (C–F) Representative densities of tumor viability and migration regulatory proteins (p53, p21 and CD1, SNAI-1, CALD1, E-Cadherin) in tumor tissue samples. β-Actin was used as internal control. The cluster bar chats in (D , F) indicates the levels of viability and migration regulatory proteins in the treatment group. Data are expressed as Mean ± SEM ( n = 3). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 versus control.
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Immunofluorescent analysis using the Antibody at 1:50 dilution.

The expression levels of FTH1 protein in different treated groups over time. The expression levels of FTH1 protein in different treated groups of HFL1 cells over time (Western Blot). The β-actin protein was used as an internal reference protein. The relative expression levels of FTH1 protein quantified by image analysis, and corrected by internal reference protein and control. The trend of levels of FTH1 protein expression were consistent with the results of immunofluorescence after TGF-β1 and DHA treatments. Data are presented as mean ± SEM (n = 3). Compared with the control group, *P < 0.05, **P < 0.01; compared with TGF-β1treatment group, △△P < 0.01, compared with DHA treated group, ##P < 0.01.
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(A–D) Cisatracurium alters migration and invasion regulatory genes transcription and protein expression levels in HCT116 cells. (A) Representative densities of SNAI-1, SLUG, E-Cadherin, CALD1, and β-actin proteins following western blot experiment. (B,C) Cluster bar charts of SNAI-1, SLUG, E-Cadherin, and CALD1 proteins expression and mRNA transcription levels of untreated and cisatracurium-treated (10 or 20 μM) HCT116 cells. β-Actin was used as internal control during western blot and qRT-PCR experiments. (D) Immunofluorescence was performed using FITC-labeled phalloidin, SNAI-1, SLUG, E-Cadherin, and CALD1 were stained with DAPI (Scale bar: 20 μm). Data are expressed as Mean ± SEM ( n = 3). ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 versus untreated (0).
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Increased β-catenin expression in HBV-infected hepatic cells. a Western blot analysis of β-catenin expression in hepatic L02 cells transfected with and without pcDNA3.1-HBV (1.3 and 1.1) or its control pcDNA3.1 for 48 h. β-actin served as a loading control. b Immunofluorescence staining for β-catenin in L02 cells transfected with and without pcDNA3.1-HBV (1.3 and 1.1) or its control pcDNA3.1 for 48 h. White scale bars = 50 µm. c ELISA assay for β-catenin expression in L02 cells transfected with and without pcDNA3.1-HBV (1.3 and 1.1) or its control pcDNA3.1 for 48 h. d LDH assay for LDH from L02 cells transfected with and without pcDNA3.1-HBV (1.3 and 1.1) or its control pcDNA3.1 for 48 h. e Flow cytometry analysis for apoptotic L02 cells transfected with and without pcDNA3.1-HBV (1.3 and 1.1) or its control pcDNA3.1 for 72 h. f Apoptosis index for L02 cells with different treatment. Ns no statistical significance
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MSMP-containing serum inhibited NF-κB pathway in macrophages after LPS induction. (A) Western blot analysis of p-p65, p65 and β-actin; (B) Statistical analysis of the Western blot results for p-p65/β-actin (%); (C) Statistical analysis of the Western blot results for p-p65/p65 (%); Quantification of the proteins was analyzed by the ImageJ software. (D) The immunofluorescence assay shows the blue fluorescence for DAPI, the red fluorescence for p-p65 and finally the merge plot; (E, F) The expression of p-p65 was analyzed by the ImageJ software. Scale bar represents 100 μm (Date are mean ± SD, #### p < 0.0001, versus Control group; *** p < 0.001, **** p < 0.0001, versus LPS group).
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Effects of 1,25 VD3 supplementation on hepatic lipid peroxidation, inflammation and fatty acid metabolizing genes in NASH rats. To assess oxidative stress, hepatic (A) MDA was measured using a thiobarbituric acid kit and (B) TAOC levels measured using the FRAP method. (C) NF-κB expression in liver tissue, analyzed by Western blotting and normalized to β-actin (left panel showing representative blot and right panel showing quantification by densitometry of 65 kDa band). Antibodies used and their dilutions: primary antibodies against NF-κB (anti-rabbit, 1:1000) and β-actin (anti-rabbit, 1:1000), followed by HRP-conjugated secondary antibody (1:2000). (D) PPARα and (E) CPT-1 mRNA levels were quantified by qPCR in liver tissues of indicated groups, and expressed as relative mRNA levels following normalization to GAPDH mRNA levels. Data are presented as mean ± SEM, n=6. *p < 0.05, **p<0.01 and ***p < 0.001 vs CG; ##p < 0.01 and ###p < 0.001 vs CDG.
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