Gapdh 2118l

Manufactured by Cell Signaling Technology

GAPDH (2118L) is a primary antibody that recognizes the glyceraldehyde-3-phosphate dehydrogenase (GAPDH) protein. GAPDH is a key enzyme involved in the glycolytic pathway and is commonly used as a loading control or reference protein in various biochemical and cell biology applications.

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Lab products found in correlation

Ub sc 8017, by Santa Cruz Biotechnology (1 mentions) Nanog ab109250, by Abcam (1 mentions) Complete lysis buffer, by Merck Group (1 mentions) Dc protein assay, by Bio-Rad (1 mentions) Protease and phosphatase inhibitor cocktail, by Roche (1 mentions) Enos 610297, by BD (1 mentions) Nitrocellulose membrane, by Cytiva (1 mentions) Enhanced chemiluminescence detection system, by Merck Group (1 mentions) Anti atg5 nb110 53818, by Novus Biologicals (1 mentions) Beclin 1, by Abcam (1 mentions)

3 protocols using gapdh 2118l

Multiparametric Antibody Detection Protocol

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SOX2 (2748), MEK1 (12671), phospho-MEK1 (2338), Ki-67 (8D5) (9449) and GAPDH (2118L) antibodies were purchased from Cell Signaling Technology. SIRT1 (H-300) (sc-15404), c-Myc (9E10) (sc-40) and Ub (sc-8017) antibodies were purchase from Santa Cruz. GFP (ab290), OCT4 (ab19857) and Nanog (ab109250) antibodies were purchased from abcam. ERK1/2 (05-1152) and phospho- ERK1/2 (05-797R) were purchased from Millpore. Alexa Flour 647 (A31571) antibody was purchased from life technologies.

Cheng J., Liu C., Liu L., Chen X., Shan J., Shen J., Zhu W, & Qian C. (2016). MEK1 signaling promotes self-renewal and tumorigenicity of liver cancer stem cells via maintaining SIRT1 protein stabilization. Oncotarget, 7(15), 20597-20611.

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Western Blot Analysis of Epithelial-Mesenchymal Markers

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Cell lysates were prepared using complete lysis buffer (EMD Millipore, San Diego, CA) with protease and phosphatase inhibitor cocktails (Roche Diagnostics, Indianapolis, IN). Protein quantification was performed using DC protein assay from Bio-Rad (Hercules, and CA). Western blot analysis was performed as described previously (Abdalla et al., 2013 (link); Al-Azayzih et al., 2015 (link)). Antibodies used include N-cadherin (4061), VE-cadherin (2158S), phosphorylated p-38 MAPK (9211S), total p38-MAPK (9212S), phosphorylated Smad2/3 (8828S), total Smad2/3 (8685S), FoxC2 (12974S), Snail (3879S), and GAPDH (2118L) from Cell Signaling Technology (Danvers, MA), αSMA (A2547) and β-actin (A5441) from Sigma (St. Louis, MO), eNOS (610297) from BD Pharmingen (San Diego, CA), and TGFβ2 (MAB612) from R&D (Minneapolis, MN). Band densitometry was done using NIH Image J software.

Sabbineni H., Verma A, & Somanath P.R. (2018). Isoform-Specific Effects of Transforming Growth Factor-β on Endothelial to Mesenchymal Transition. Journal of cellular physiology, 233(11), 8418-8428.

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Western Blot Analysis of Autophagy Proteins

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Cells were lysed on ice for 30 min in lysis buffer containing 50 mM Tris-HCl, pH 7.4, 150 mM NaCl, 1% Nonidet P-40, and 0.1% SDS supplemented with protease inhibitors (10 m g/ml leupeptin, 10 m g/ml
pepstatin A, and 10 m g/ml aprotinin). For western analysis, 15μg of sample was resolved by 12% SDS-PAGE and electro-transferred onto nitrocellulose membranes (Whatman, Piscataway, NJ). The primary antibodies used were anti-ULK-1 (NBP2-24738, Novus Biologicals); anti-ATG-5 (NB110-53818, Novus Biologicals); anti-Bcl-2 (2876S, Cell Signaling Technology); LC3 (SAB1306673, Sigma-Aldrich); Beclin-1 (ab55878, Abcam) at a dilution of 1:500. To normalize protein loading, a GAPDH (2118L, Cell Signaling Technology) antibody was used at 1:2,000 dilution. HRP-conjugated secondary antibodies were used at a 1:2,000 dilution. The antigen-antibody complexes were visualized using an enhanced chemiluminescence detection system (Millipore, Billerica, MA) as recommended by the manufacturer.

Zhang F., Wang J., Chu J., Yang C., Xiao H., Zhao C., Sun Z., Gao X., Chen G., Han Z., Zou W, & Liu T. (2015). MicroRNA-146a Induced by Hypoxia Promotes Chondrocyte Autophagy through Bcl-2. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, 37(4).

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