Pdgfrb

Manufactured by Santa Cruz Biotechnology

Sourced in United States

PDGFRB is a protein-coding gene that provides instructions for making a receptor protein involved in cellular signaling. This receptor is found on the surface of many cell types and plays a role in processes such as cell growth and division. As a research tool, this gene product can be used to study cellular pathways and regulation.

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Anti-PDGFRb (6 citations)

4 protocols using pdgfrb

Western Blot Analysis of Protein Signaling

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Whole cell lysates were harvested using the PRO-PREPTM Protein Extraction Solution (iNtRON, Sungnam, Korea). Western blot analysis was performed as described previously [21 (link),22 (link)]. Blots were incubated with anti-PDGFRA (sc-398206, 1:1000, Santa Cruz Biotechnology, Inc., Santa Cruz, CA, USA), PDGFRB (sc-374573, 1:1000, Santa Cruz), p-STAT3 (ab76315, 1:100000, Abcam), p-ERK (sc-7383, 1:1000, Santa Cruz), t-STAT3 (sc-8019, 1:1000, Santa Cruz), t-ERK (#9102, 1:1000, Cell signaling technology, Danvers, MA, USA), t-HER2 (sc-33684, 1:5000, Santa Cruz), or β-actin (LF-PA0207, 1:5000, AbFrontier Co. Ltd., Seoul) antibodies in 1% Tris-buffered saline with 0.01% Tween-20 (TBST) at 4 °C overnight (O/N). Blots were washed 3–4 times in TBST and incubated with appropriate secondary antibodies in TBST buffer for 1 h at room temperature. Blots were washed 3–4 times with TBST buffer and visualized with the ECL™ Western Blotting Detection Reagent (GE Healthcare, Chicago, IL, USA).

Kim S., Kim H., Jeong Y., You D., Yoon S.Y., Lo E., Nam S.J., Lee J.E, & Kim S.W. (2023). Suppression of Platelet-Derived Growth Factor Receptor-Alpha Overcomes Resistance to Trastuzumab through STAT3-Dependent IL-6 Reduction in HER2-Positive Breast Cancer Cells. Biomedicines, 11(3), 675.

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Quantification of Autophagic Flux by Western Blot

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Extracted proteins were analyzed by western blot. Antibodies used were: SQSTM1/p62 (Cell Signaling, 1/1000), LC3B [MAP1LC3B] (Cell Signaling, 1/1000), ATG7 (Cell signaling, 1/1000), αSMA [ACTA2] (Sigma, 1/1000), PDGFRB (Santa Cruz, 1/500), total eNOS [NOS3] (BD Bioscience, 1/1000), eNOS phos-phorylated Ser1177 (Cell Signaling, 1/1000), HMOX1 (Enzo Life Sciences, 1/1000), NQO1 (Abcam, 1/1000). GAPDH (Santa Cruz, 1/1000) and β-actin [ACTB] (Sigma, 1/1000) served as house-keeping controls. Images were acquired with a LAS-3000 apparatus (Fujifilm, TDI, Alcobendas, Spain) and measurements made with the Multi Gauge software from Fujifilm following manufacturer’s instructions. Protein ratios were normalized to housekeeping proteins (β-actin or GAPDH) and fold-change was calculated relative to control group.
Autophagy flux: As autophagy is a dynamic process influenced by the degradation activity of the cargo and recycling, autophagic flux was measured using the lysosomal inhibitor chloroquine (CQ) (20 μM) for 2 h. Briefly, CQinhibits degradation of the cargo in the autophagosome leading to the accumulation of autophagic vacuoles that can be measured by quantifying the lipidated form of MAP1LC3B/LC3B (microtubule-associated protein 1 light chain 3 beta) (LC3B11) present in the autophagic vacuole membrane, using western blot.

Ruart M., Chavarria L., Campreciós G., Suárez-Herrera N., Montironi C., Guixé-Muntet S., Bosch J., Friedman S.L., Garcia-Pagán J.C, & Hernández-Gea V. (2018). Impaired endothelial autophagy promotes liver fibrosis by aggravating the oxidative stress response during acute liver injury. Journal of hepatology, 70(3), 458-469.

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Immunofluorescence Analysis of GBM Markers

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Human GBM and normal brain tissues were obtained from the Cooperative Human Tissue Network (CHTN). Anti-FRMD6 (Sigma), -Lats1/2 (Bethyl Lab), -MST1/2, -YAP, -c-Met, -PDGFRA, -PDGFRB, and -merlin (Santa Cruz), -actin (Sigma), -v5 epitope (Invitrogen), -phospho-Lats1, -phospho-YAP (Cell signaling), -phospho-c-Met (Invitrogen and Santa Cruz), and -phospho-PDGFRA/B (Santa Cruz and R & D Systems) antibodies were used in the experiments. Anti-Ki67 was from the Fisher Scientific. Secondary anti-rabbit Alexa Fluor^® 594 and anti-mouse Alexa Fluor^® 488 were from Invitrogen.

Xu Y., Wang K, & Yu Q. (2016). FRMD6 inhibits human glioblastoma growth and progression by negatively regulating activity of receptor tyrosine kinases. Oncotarget, 7(43), 70080-70091.

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Protein expression analysis of frozen tumor samples

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Frozen tumor samples were diced in ice-cold lysis buffer containing protease inhibitors and homogenized for 3 seconds, 3-5 times, on ice. Whole-cell lysates from cell cultures were prepared in lysis buffer. All lysates were cleared by centrifugation at 14,000 rpm for 30 min at 4°C, and protein concentrations were determined using a Bradford protein assay (Bio-Rad Laboratories). Electrophoresis, western blotting and detection were performed using standard techniques.
Primary antibodies were p16 (Cell Signaling #4824), phospho-RB1 Ser795 (Cell Signaling #9301), phospho-RB1 Ser807/811 (Cell Signaling #9308), RB (Cell Signaling #9309), CDK4 (Santa Cruz sc-601), PDGFRB (Santa Cruz, sc-432), phospho-PDGFR (sc-12911), actin (Sigma A4700), Cyclin A (Novocastra NCL-Cyclin A), and Cyclin D1 (Santa Cruz sc-220044). GIST48, which harbors a homozygous CDKN2A deletion and expresses no p16, and GIST882, which retains wild type CDKN2A and expresses p16, were used as controls for p16 staining.

Eilers G., Czaplinski J.T., Mayeda M., Bahri N., Tao D., Zhu M., Hornick J.L., Lindeman N.I., Sicinska E., Wagner A.J., Fletcher J.A, & Mariño-Enriquez A. (2015). CDKN2A/p16 loss implicates CDK4 as a therapeutic target in imatinib-resistant dermatofibrosarcoma protuberans. Molecular cancer therapeutics, 14(6), 1346-1353.

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