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Rel Oncogene

Rel Oncogene: A proto-oncogene that plays a crucial role in the regulation of cell growth, differentiation, and survival.
It is a member of the Rel/NF-kappa B transcription factor family and is involved in various cellular processes, including immune response, inflammation, and cancer development.
Rel Oncogene is an important target for research aimed at understanding the molecular mechanisms underlying its contribution to disease pathogenesis and identifying potential therapeutic interventions.
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Most cited protocols related to «Rel Oncogene»

pMSCV has been described previously (Gilmore et al., 2003 (link)). pMSCV-RELΔTAD1 was created by subcloning a BglII to XhoI fragment containing the RELΔTAD1 cDNA into pMSCV.
Human A293T cells and BJAB or Daudi lymphoma cells were maintained in Dulbecco’s modified Eagle’s medium (DMEM) supplemented with 10 or 20% fetal bovine serum (Biologos, Montgomery, IL), respectively, as described (Starczynowski et al., 2005 (link)). Virus stocks were generated by transfecting A293T cells with pMSCV or pMSCV-RELΔTAD1 plus helper plasmid pcL10a1, essentially as described previously (Gilmore et al., 2003 (link)). Approximately two days later, virus was harvested. One ml of virus (in the presence of 4 μg/ml polybrene) was used to infect 106 BJAB or Daudi cells using the spin infection method (Gilmore et al., 2003 (link)). Two days later, cells were selected with 2.5 μg/ml puromycin (Sigma) for 2-4 weeks.
Publication 2009
Cells DNA, Complementary Eagle Fetal Bovine Serum Homo sapiens Infection Lymphoma Plasmids Polybrene Puromycin Virus
Representative areas with the highest percentage of tumor cells were selected for tissue microarray (TMA) construction as described previously (5 (link)). Immunohistochemical (IHC) studies for various markers were performed; B-cell lymphoma 2 (BCL2), B-cell lymphoma 6 (BCL6), cyclin D1, CD10, CD30, Forkhead box protein P1 (FOXP1), Germinal Center B cell-expressed Transcript-1 (GCET1), Multiple Myeloma Oncogene 1 (MUM1), MYC, Nuclear factor-κB (NF-κB) components (p50, p52, p65, and c-Rel), p53, phosphorylated protein kinase B (pAKT), and phosphorylated signal transducer and activator of transcription 3 (pSTAT3). Receiver-operating characteristic (ROC) curves and X-tile analyses were utilized to assess a cutoff (5 (link)). When an optimal cutoff could not be determined by ROC curve and X-tile analyses, a conventional cutoff value for individual markers was decided based on previous reports in the literature. The cutoff scores for these markers were as follows: 10% for cyclin D1; 20% for CD30 and p53; 30% for CD10, and BCL6, 40% for MYC; 50% for pSTAT3; 60% for GCET1, MUM1 and FOXP1; and 70% for AKT and BCL2. All markers except cyclin D1 were determined by ROC curve. Any nuclear expression of each NF-κB component was considered positive.
Publication 2014
AKT1 Protein Kinase B-Cell Lymphomas B-Lymphocytes BCL6 protein, human Cells Cyclin D1 Forkhead Transcription Factors Germinal Center interferon regulatory factor 4, human Microarray Analysis Neoplasms NF-kappa B rel Oncogene STAT3 Protein Tissues
Transfections for reporter assays using RID deletion mutants in A293 and mouse 3T3 cells using Superfect and in DF1 cells using DMSO/polybrene were carried out as described previously (Kalaitzidis and Gilmore, 2002 (link); Starczynowski et al., 2007 (link)). Transfections using the Superfect reagent were performed according to the manufacturer's recommendations (Qiagen, Valencia, CA, USA). Transfections of A293 cells for EMSAs or reporter assays with REL splice variant isoforms were performed using PEI (polyethylenimine; Polysciences Inc., Warrington, PA, USA). A293 cells were seeded to be 40-60% confluent on the day of transfection. On the day of transfection, cells were incubated with DNA/PEI at a ratio of 3:1 in serum-free media (300 μl for a 60 mm plate) for 15min at room temperature. Following incubation, 4.7ml of DMEM/10% FBS was added to the DNA mixture, and this mixture was added to cells. Twenty-four hours later, the media was replaced with 5ml of fresh DMEM/10% FBS. The following day, the cells were harvested.
After lysing the cells, luciferase activity was measured using the Luciferase Assay System according to the manufacturer's recommendations (Promega, Madison, WI, USA). Luciferase values were normalized to βgal levels in all assays, as described previously (Kalaitzidis et al., 2002 (link)).
Yeast reporter gene assays were carried out as previously described (Epinat et al., 2000 (link)).
Publication 2008
3T3 Cells Biological Assay Cells Culture Media, Serum-Free Deletion Mutation Electrophoretic Mobility Shift Assay Genes, Reporter Luciferases Mus Polybrene Polyethyleneimine Promega Protein Isoforms Sulfoxide, Dimethyl Transfection Yeast, Dried
Total RNA from cells was extracted using TRIzol (Invitrogen). Two microgram of RNA was reverse-transcribed using M-MLV reverse transcriptase (Promega) and cDNA was resuspended in 40 μl of RNase-free water. PCR was then performed with 2μl of cDNA, using the conditions and primers described in Supplemental Material.
Publication 2008
Cells DNA, Complementary Endoribonucleases Oligonucleotide Primers Promega RNA-Directed DNA Polymerase trizol
For soft agar assays, equal numbers of the indicated BJAB or Daudi cells (250, 500, 1000 or 2000 cells) were placed in soft agar containing DMEM, 20% FBS and 0.3% bacto agar (Difco, Franklin Lakes, NJ), and plates were placed at 37°C in a humid incubator with 5% CO2. To confirm cell counts, total cell protein assays (Bio-Rad) were performed on the cell dilutions used for plating. Macroscopic soft agar colonies were counted 14 days after plating.
Tumor studies were performed essentially as described previously (Yamamoto et al., 2000 (link); Gapuzan et al., 2002 (link)). 5 × 106 cells were injected subcutaneously into SCID mice (Taconic Farms, Germantown, NY). Once tumors appeared, mice were monitored 3× weekly and animals were sacrificed when tumors reached 2.25 mm2. All animal studies were performed in accordance with NIH guidelines and with approval of the Boston University Institutional Animal Care and Use Committee.
Publication 2009
Agar Animals Biological Assay Cells Institutional Animal Care and Use Committees Mus Neoplasms Proteins SCID Mice Technique, Dilution

Most recents protocols related to «Rel Oncogene»

The data of lung cancer gene comparison was from TCGA data curated by UALCAN database (http://ualcan.path.uab.edu/cgi-bin/ualcan-res.pl), cBioPortal for Cancer Genomics (https://www.cbioportal.org/mutation_mapper) and human protein atlas (https://www.proteinatlas.org/).
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Publication 2024
The C57BL/6 mice used in this study were bred and housed in a specific pathogen-free animal facility at Sun Yat-Sen University. The mice were kept in a controlled 12-hour light and 12-hour dark cycle. Random assignment of the mice to different experimental groups was done for follow-up experiments. All animal procedures conducted in this study were performed in compliance with the guidelines for the treatment of laboratory animals and approved by the Institutional Animal Care and Use Committee of Sun Yat-Sen University.
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Publication 2024
Lung tissues were fixed in 1% PFA for 1 hour, and then embedded in paraffin for sectioning. H&E staining were performed for histopathological analysis.
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Publication 2024
Cell climbing was placed in the 24-well plate, and 2 × 105 cells were inoculated into the 24-well plate and cultured overnight. 2 hours before harvest, we added EdU solution (10 μM/ml) and incubated for 20 minutes. In accordance with the manufacturer's directions, EdU Imaging Kits (K1075, Apexbio) was used to stain the proliferative cells.
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Publication 2024
The specimens of surgically excised tumors were procured from the Guangzhou First People's Hospital situated in China. The patients included in this study had not undergone any form of treatment prior to surgery, thus ensuring the purity of the tissue samples and the integrity of our findings. The study protocol adhered strictly to the ethical guidelines set forth by the esteemed Ethics Committee of the School of Medicine at Sun Yat-Sen University. Moreover, prior to participating in the study, each patient provided informed consent.
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Publication 2024

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More about "Rel Oncogene"

Rel oncogene, also known as c-Rel, is a critical proto-oncogene that plays a pivotal role in regulating cell growth, differentiation, and survival.
As a member of the Rel/NF-κB transcription factor family, it is involved in a variety of cellular processes, including immune response, inflammation, and cancer development.
Optimizing your Rel oncogene research is crucial, and PubCompare.ai, the AI-driven platform, can enhance the reproducibility and accuracy of your studies.
The platform allows you to easily locate the best protocols from literature, preprints, and patents, using intelligent comparisons.
This can help you discover the most reliable and effective methods to advance your Rel oncogene studies with confidence.
To further enhance your research, you can incorporate related terms, such as B-cell lymphoma (BL505A), β-actin (a common housekeeping gene), and GAPDH (another popular housekeeping gene).
Techniques like inverted bright field microscopy (Axio Observer 7) and High-Capacity cDNA Reverse Transcription Kit can also be useful in your investigations.
Additionally, considering the involvement of Rel oncogene in the NF-κB pathway, you may want to explore the regulation of the pathway, including the phosphorylation of IκBα (P-IκBα) and the use of protease inhibitor cocktails.
Leveraging the power of AI-driven analysis provided by PubCompare.ai can take your Rel oncogene research to new heights, enabling you to make groundbreaking discoveries and advance the understanding of this crucial proto-oncogene.