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RELA protein, human

The RELA protein, also known as NF-kappa-B p65 subunit, is a crucial transcription factor involved in regulating inflammatory and immune responses.
It is a member of the NF-kB family and plays a central role in activating genes related to cell survival, proliferation, and immune function.
The RELA protein binds to DNA and interacts with other transcription factors to modulate gene expression.
It has been implicated in the pathogenesis of various diseases, including cancer, autoimmune disorders, and neurodegenerative conditions.
Reserach on the RELA protein is crucial for understanding its role in health and disease, as well as developing targeted therapeis.
Experieence the future of scientific discovery with PubCompare.ai, an AI-driven platform that helps optimize RELA protein research by locating the best protocols and enabling reproducibility through intelligent comparisons.

Most cited protocols related to «RELA protein, human»

1
Genome-wide RNAi Screens Identify KRAS-NF-κB Signaling
Cited 1026 times
Large-scale, arrayed format RNAi screens to identify genes essential for proliferation/viability were performed as described3 (link),14 (link). The effect of introducing each of the 5002 shRNAs (targeting 957 genes) was determined in 19 cell lines, and normalized using the B-score metric4 (link). Feature selection of shRNA B-score data was performed using the Comparative Marker Application Suite in GenePattern5 (link) and was independently analyzed using RIGER analysis6 (link) to compute NES for each gene. Secondary screen viability data was normalized using a percent of control statistic, given the biased nature of the candidate shRNA plate. Expression profiling was used to generate a signature that correlates with KRAS activation and implicated NF-κB signaling in cell lines and tumors dependent on KRAS. Regulation of NF-κB by TBK1 was shown using biochemical and cell biological approaches. Details of the analytical methods are provided in the Full Methods.
Barbie D.A., Tamayo P., Boehm J.S., Kim S.Y., Moody S.E., Dunn I.F., Schinzel A.C., Sandy P., Meylan E., Scholl C., Fröhling S., Chan E.M., Sos M.L., Michel K., Mermel C., Silver S.J., Weir B.A., Reiling J.H., Sheng Q., Gupta P.B., Wadlow R.C., Le H., Hoersch S., Wittner B.S., Ramaswamy S., Livingston D.M., Sabatini D.M., Meyerson M., Thomas R.K., Lander E.S., Mesirov J.P., Root D.E., Gilliland D.G., Jacks T, & Hahn W.C. (2009). Systematic RNA interference reveals that oncogenic KRAS-driven cancers require TBK1. Nature, 462(7269), 108-112.
Publication 2009
Biopharmaceuticals Cell Lines Cells Genes K-ras Genes Neoplasms RELA protein, human RNA Interference Short Hairpin RNA TBK1 protein, human
2
Genome-wide RNAi Screens Identify KRAS-NF-κB Signaling
Cited 922 times
Large-scale, arrayed format RNAi screens to identify genes essential for proliferation/viability were performed as described3 (link),14 (link). The effect of introducing each of the 5002 shRNAs (targeting 957 genes) was determined in 19 cell lines, and normalized using the B-score metric4 (link). Feature selection of shRNA B-score data was performed using the Comparative Marker Application Suite in GenePattern5 (link) and was independently analyzed using RIGER analysis6 (link) to compute NES for each gene. Secondary screen viability data was normalized using a percent of control statistic, given the biased nature of the candidate shRNA plate. Expression profiling was used to generate a signature that correlates with KRAS activation and implicated NF-κB signaling in cell lines and tumors dependent on KRAS. Regulation of NF-κB by TBK1 was shown using biochemical and cell biological approaches. Details of the analytical methods are provided in the Full Methods.
Barbie D.A., Tamayo P., Boehm J.S., Kim S.Y., Moody S.E., Dunn I.F., Schinzel A.C., Sandy P., Meylan E., Scholl C., Fröhling S., Chan E.M., Sos M.L., Michel K., Mermel C., Silver S.J., Weir B.A., Reiling J.H., Sheng Q., Gupta P.B., Wadlow R.C., Le H., Hoersch S., Wittner B.S., Ramaswamy S., Livingston D.M., Sabatini D.M., Meyerson M., Thomas R.K., Lander E.S., Mesirov J.P., Root D.E., Gilliland D.G., Jacks T, & Hahn W.C. (2009). Systematic RNA interference reveals that oncogenic KRAS-driven cancers require TBK1. Nature, 462(7269), 108-112.
Publication 2009
Biopharmaceuticals Cell Lines Cells Genes K-ras Genes Neoplasms RELA protein, human RNA Interference Short Hairpin RNA TBK1 protein, human
3
MicroRNA Regulation of Atherosclerosis Development
Cited 30 times
Pre-miR miRNA precursor molecules negative (nonspecific) control #1 (AM17110) and Hsa-miR-181b-5p Pre-miR miRNA precursor (PM12442) were used from Ambion. Real-time quantitative polymerase chain reaction was performed with the Mx3000P real-time polymerase chain reaction system (Stratagene) following the manufacturer's instructions. NF-κB promoter with GFP/luciferase fusion reporter (NGL) mice fully backcrossed into C57BL/6 were crossed with homozygous ApoE−/− mice to generate ApoE−/−/NGL transgenic mice. To induce atherosclerosis, 8-week-old male ApoE−/− mice were fed a high-fat diet (HFD) from Research Diets Inc (D12108Ci) for 12 weeks. Aortas were carefully excised from mice and examined for immunohistology and characterization of atherosclerotic lesions.
For detailed experimental methods, please see the Online Data Supplement.
Sun X., He S., Wara A.K., Icli B., Shvartz E., Tesmenitsky Y., Belkin N., Li D., Blackwell T.S., Sukhova G.K., Croce K, & Feinberg M.W. (2013). Systemic Delivery of MicroRNA-181b Inhibits Nuclear Factor-κB Activation, Vascular Inflammation, and Atherosclerosis in Apolipoprotein E–Deficient Mice. Circulation research, 114(1), 32-40.
Publication 2013
Aorta Apolipoproteins E Atherosclerosis Diet Diet, High-Fat Dietary Supplements Homozygote Luciferases Males Mice, Laboratory Mice, Transgenic MicroRNAs miR-181b, human pre-miRNA Real-Time Polymerase Chain Reaction RELA protein, human
4
Two-Step Chromatin Immunoprecipitation Protocol
Cited 26 times
An overview of the two-step ChIP protocol is shown in Fig. 1. The selection of the cross-linker should be undertaken with some understanding of the chemistry and effective cross-linking length. We have had success with DSG, an irreversible cross-linking agent that cross-links NHS esters with an effective radius of approximately 7Å. This agent has been useful for highly efficient cross-linking of NF-κB, STAT3, p300/CBP, RNA Pol II and CDK9 where stimulus – inducible chromatin interactions can be seen (4 (link);5 (link)). A summary of the types of useful cross-linkers, their chemistries, spacing arms, and methods for reversal is shown in Table III. Some demonstrations of their application have been previously reported (2 (link);8 ).
Selection of the appropriate negative control for the immunoprecipitation is an important consideration. We typically include a tube of chromatin immunoprecipitated using pre-immune IgG. This control is important in some approaches for quantification using quantitative real-time genomic PCR (Q-RT-gPCR).
Another critical parameter in the design of the experimental protocol is to decide which type of target identification assay will be employed (Schematically diagrammed in Fig. 1). For downstream analysis using qualitative- or quantitative real-time genomic PCR (Q-RT-gPCR), fragmentation of the chromatin into 500–1000 bp fragments is optimal. However, for downstream analysis using next generation sequencing, fragmentation into smaller 300–500 bp fragments is preferred. These fragmentation methods are described as alternate protocols (Section 3.5). Similarly, the method of decross-linking is different for ChIP-Seq applications, and requires selection of one of the alternate protocols (Section 3.9).
Tian B., Yang J, & Brasier A.R. (2012). Two-step Crosslinking for Analysis of Protein-Chromatin Interactions. Methods in molecular biology (Clifton, N.J.), 809, 105-120.
Publication 2012
Arm, Upper Biological Assay CDK9 protein, human Chromatin Chromatin Immunoprecipitation Sequencing DNA Chips EP300 protein, human Esters Genome Immunoprecipitation Radius Real-Time Polymerase Chain Reaction RELA protein, human RNA Polymerase II STAT3 Protein Vision
5
Lentiviral Vector Transduction of 3T3 Cells
Cited 24 times

Protocol full text hidden due to copyright restrictions

Open the protocol to access the free full text link

Publication 2014
Anti-Infective Agents Cell Lines Cells Cloning Vectors Glutamine hygromycin A Lentivirus NIH 3T3 Cells Penicillins Plasmids Proteins Puromycin RELA protein, human Streptomycin

Most recents protocols related to «RELA protein, human»

1
NF-κB Activation by Enterococcus Flagellin
Not available on PMC !

Example 10

The ability of the bacterial strain MRx0518 to activate NF-κB was investigated. The results are presented in FIG. 18. MRx0518 supernatant was the most potent activator of NF-κB. The activation of NF-κB was eliminated after treatment with trypsin.

These data show that flagellin from the genus Enterococcus and in particular from MRx0518 produce a very strong NF-κB response, and so may be useful in therapy.

US11857614B2. Enterococcus gallinarum flagellin polypeptides (2024-01-02). CJ BIOSCIENCE, INC. [KR]. Inventors: Imke Elisabeth Mulder [GB], Emma Raftis [GB], Emma Elizabeth Clare Hennessy [GB], Delphine Louise Claudette Laute-Caly [GB], Philip Cowie [GB].
Full text: Click here
Patent 2024
Aftercare Bacteria Enterococcus Flagellin RELA protein, human Strains Therapeutics Trypsin
2
MALT1 Inhibitor Impacts T Cell Activation
Not available on PMC !

Example 3

In addition to antigen receptors in B cells, MALT1 also affects signaling downstream of the TCR. Because of the central role of MALT1 in NF-κB signaling, which has been described to be important in the activation of T cells, we investigated the effects of increasing concentrations of the MALT1 inhibitor on T cell activation in both CLL-derived and healthy T cells. Activation and proliferation upon stimulation with soluble anti-CD3/CD28 antibodies was significantly reduced upon MALT1 inhibition in both CD4 and CD8 T cells (FIG. 3A-C). There appeared to be no difference between CLL patients and healthy donors. Additionally, CD107a (LAMP-1) expression as a parameter for T cell degranulation was reduced upon MALT1 inhibition (FIG. 3D). Furthermore, MALT1 inhibition significantly inhibited IFNγ and TNFα cytokine secretion (FIG. 3E). These results suggest that the MALT1 inhibitor impairs various aspects of in vitro T cell activation, when applied at concentrations >1 μM.

US11872220B2. Methods and compositions for treating B-cell malignancies (2024-01-16). Janssen Pharmaceutica NV [BE]. Inventors: Eric Frederik Eldering [NL], Karoline Kielbassa [NL], Ulrike Philippar [BE], Andrew Steele [US], Marco Vincent Haselager [NL], A. P. Kater [NL].
Full text: Click here
Patent 2024
Anti-Antibodies CD8-Positive T-Lymphocytes Cell Degranulation Cytokine Donors Immunomodulation Interferon Type II lysosomal-associated membrane protein 1, human MALT1 protein, human Patients Psychological Inhibition Receptors, Antigen, B-Cell RELA protein, human secretion T-Lymphocyte Tumor Necrosis Factor-alpha
3
Exosome-Mediated NF-κB Delivery
Not available on PMC !

Example 16

The binding of CIBN and CRY2 in cells expressing CIBN-EGFP-CD9 and NF-κB-mCherry-Cry2 at 488 nm wavelength blue light, and the loading of NF-κB within the exosome is evaluated.

For the massive production of NF-κB-loaded exosomes, cells stably expressing CIBN-EGFP-CD9 gene and NF-κB-mCherry-CRY2 gene are established, and exosomes are isolated and purified by Tangential Flow Filtration (TFF) method from culture supernatant.

Functional analysis of NF-κB-loaded exosomes is performed in target cells:

Target cells are treated with the NF-κB-loaded exosomes to show the functional activity.

Animal models are administered with the NF-κB-loaded exosomes by i.p. or i.v. to show therapeutic effect.

US11872193B2. Compositions containing protein loaded exosome and methods for preparing and delivering the same (2024-01-16). ILIAS BIOLOGICS INC. [KR]. Inventors: Chulhee Choi [KR], Nambin Yim [KR], Won Do Heo [KR], Seung-Wook Ryu [KR], Hojun Choi [KR], Kyungsun Choi [KR].
Full text: Click here
Patent 2024
Animal Model Cells Exosomes Filtration Genes Light RELA protein, human Therapeutic Effect
4
Peptide Synthesis Reagents and Cell Culture Protocols
Not available on PMC !

Example 1

Reagents for peptide synthesis were purchased from Chem-Impex (Wood Dale, IL), NovaBiochem (La Jolla, CA), or Anaspec (San Jose, CA). Rink amide resin LS (100-200 mesh, 0.2 mmol/g) was purchased from Advanced ChemTech. Cell culture media, fetal bovine serum, penicillin-streptomycin, 0.25% trypsin-EDTA, and DPBS were purchased from Invitrogen (Carlsbad, CA). Methyl 3,5-dimethylbenzoiate, N-bromosuccinimide, diethyl phosphite, 2,2′-dipyridyl disulfide, and other organic reagents/solvents were purchased from Sigma-Aldrich (St. Louis, MO). Anti-GST-Tb and streptavidin-d2 were purchased from Cisbio (Bedford, MA). The NF-κB reporter (Luc)-HEK293 cell line and One-Step™ luciferase assay system were purchased from BPS Bioscience (San Diego, CA).

[Figure (not displayed)]

US11878046B2. Di-sulfide containing cell penetrating peptides and methods of making and using thereof (2024-01-23). Ohio State Innovation Foundation [US]. Inventors: Dehua Pei [US], Ziqing Qian [US].
Full text: Click here
Patent 2024
Anabolism Biological Assay Bromosuccinimide Cell Culture Techniques Cells Culture Media Disulfides Edetic Acid Fetal Bovine Serum HEK293 Cells Luciferases Penicillins Peptide Biosynthesis Phosphite RELA protein, human Rink amide resin Solvents Streptavidin Streptomycin Trypsin
5
Molecular Cloning of Engineered Lentiviral Constructs
pSIV3+, psPAX2, HXB2 env, CMV-VSVG, pTRIP-SFFV-GFP, and pTRIP-SFFV-GFPIRF3 were previously described (Manel et al., 2010 (link)). pTRIP-SFFV-GFP-RELA was obtained by PCR cloning of RELA (#23255; Addgene) into the pTRIP-SFFV-GFP backbone. RELA K5R and RELA K5Q mutants were generated by subcloning DNA fragments (Twist Biosciences) into the pTRIP-SFFV-GFP-RELA plasmid, resulting in pTRIP-SFFV-GFP-RELA K5R and pTRIP-SFFV-GFP-RELA K5Q. RELA K310R mutant was generated by overlapping PCR mutagenesis in pTRIP-SFFV-GFPRELA plasmid resulting in pTRIP-SFFV-GFP-RELA K310R. pLKO.1-puro-IRF7sh1 (IRF7sh1, 5′-CCC​GAG​CTG​CAC​GTT​CCT​ATA-3′), pLKO.1-puroIRF7sh5 (IRF7sh5, 5′-CGC​AGC​GTG​AGG​GTG​TGT​CTT-3′), and pLKO.1puro-shLacZ (LacZsh) were previously described (Döring et al., 2021 (link)). HIV-mTagBFP2 and HIV-2 ROD9 ∆env∆nef mTagBFP2+ were previously described (Bhargava et al., 2021 (link)). pTRIP-SFFV-GFP (control), pTRIP-SFFV-EGFP-FLAG-cGAS (cGAS), pTRIP-SFFV-EGFP-NLS (NLS), and pTRIP-SFFV-EGFP-NLS-FLAG-cGAS (NLS-cGAS) were previously described (Gentili et al., 2019 (link)). pTRIP-SFF-tagBFP-2A, pTRIP-SFFV–tagBFP-2A-STING, IFNB-pGL3, and pTRH1-NFkB-dscGFP have been previously described (Cerboni et al., 2017 (link)). pTRIP-SFFV-tagBFP-2A-ZebrafishSTING was subcloned from pCOM37_pcDNA4 ZFish STING (de Oliveira Mann et al., 2019 (link)). Human CD19 cDNA (NCBI accession no. NM_001178098; Genescript) was cloned into the pCDH-CMV-MCS-EF1-Puro plasmid (System Biosciences) to create pCDH-CMV-CD19 puro.
Jeremiah N., Ferran H., Antoniadou K., De Azevedo K., Nikolic J., Maurin M., Benaroch P, & Manel N. (2023). RELA tunes innate-like interferon I/III responses in human T cells. The Journal of Experimental Medicine, 220(5), e20220666.
Publication 2023
Chromogranin A DNA, Complementary HIV-2 Homo sapiens Interferon, beta Mutagenesis NF-kappa B Paragangliomas 3 Plasmids RELA protein, human Spleen Focus-Forming Virus Vertebral Column

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Lipofectamine 2000 is a cationic lipid-based transfection reagent designed for efficient and reliable delivery of nucleic acids, such as plasmid DNA and small interfering RNA (siRNA), into a wide range of eukaryotic cell types. It facilitates the formation of complexes between the nucleic acid and the lipid components, which can then be introduced into cells to enable gene expression or gene silencing studies.
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More about "RELA protein, human"

RELA, NF-kappa-B p65 subunit, NF-κB, transcription factor, inflammatory response, immune response, cell survival, cell proliferation, immune function, DNA binding, disease pathogenesis, cancer, autoimmune disorders, neurodegenerative conditions, Dual-Luciferase Reporter Assay System, Lipofectamine 2000, Western blotting, PVDF membranes, β-actin, GAPDH, TRIzol reagent, Luciferase Assay System, FBS