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> home > Products > Primary Antibodies > Antibody Collections > GPCR Antibodies > Anti-RELA / NFKB p65 Antibody (clone 8G3)
Anti-RELA / NFKB p65 Antibody (clone 8G3)
Mouse Anti Human Monoclonal Antibody
- SPECIFICATION
- CITATIONS: 1
- PROTOCOLS
- BACKGROUND
Application 
| WB, IHC-P, IF, E |
|---|---|
| Primary Accession | Q04206 |
| Predicted | Human |
| Host | Mouse |
| Clonality | Monoclonal |
| Isotype | IgG1,l |
| Clone Names | 8G3 |
| Calculated MW | 60219 Da |
| Dilution | ELISA, IF (35 µg/ml), IHC-P (10 µg/ml), WB |
| Gene ID | 5970 |
|---|---|
| Alias Symbol | RELA |
| Other Names | RELA, NF-kappa-B p65delta3, NFKB3, p65, Transcription factor p65 |
| Target/Specificity | Human RELA / NFKB p65 |
| Reconstitution & Storage | Protein A purified |
| Precautions | Anti-RELA / NFKB p65 Antibody (clone 8G3) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | RELA |
|---|---|
| Synonyms | NFKB3 |
| Function | NF-kappa-B is a pleiotropic transcription factor present in almost all cell types and is the endpoint of a series of signal transduction events that are initiated by a vast array of stimuli related to many biological processes such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. NF-kappa-B is a homo- or heterodimeric complex formed by the Rel-like domain- containing proteins RELA/p65, RELB, NFKB1/p105, NFKB1/p50, REL and NFKB2/p52. The heterodimeric RELA-NFKB1 complex appears to be most abundant one. The dimers bind at kappa-B sites in the DNA of their target genes and the individual dimers have distinct preferences for different kappa-B sites that they can bind with distinguishable affinity and specificity. Different dimer combinations act as transcriptional activators or repressors, respectively. The NF-kappa-B heterodimeric RELA-NFKB1 and RELA-REL complexes, for instance, function as transcriptional activators. NF-kappa-B is controlled by various mechanisms of post-translational modification and subcellular compartmentalization as well as by interactions with other cofactors or corepressors. NF-kappa-B complexes are held in the cytoplasm in an inactive state complexed with members of the NF-kappa-B inhibitor (I- kappa-B) family. In a conventional activation pathway, I-kappa-B is phosphorylated by I-kappa-B kinases (IKKs) in response to different activators, subsequently degraded thus liberating the active NF-kappa-B complex which translocates to the nucleus. The inhibitory effect of I- kappa-B on NF-kappa-B through retention in the cytoplasm is exerted primarily through the interaction with RELA. RELA shows a weak DNA- binding site which could contribute directly to DNA binding in the NF- kappa-B complex. Beside its activity as a direct transcriptional activator, it is also able to modulate promoters accessibility to transcription factors and thereby indirectly regulate gene expression. Associates with chromatin at the NF-kappa-B promoter region via association with DDX1. Essential for cytokine gene expression in T- cells (PubMed:15790681). The NF-kappa-B homodimeric RELA-RELA complex appears to be involved in invasin-mediated activation of IL-8 expression. Key transcription factor regulating the IFN response during SARS-CoV-2 infection (PubMed:33440148). |
| Cellular Location | Nucleus. Cytoplasm. Note=Nuclear, but also found in the cytoplasm in an inactive form complexed to an inhibitor (I-kappa-B) (PubMed:1493333). Colocalized with DDX1 in the nucleus upon TNF-alpha induction (PubMed:19058135). Colocalizes with GFI1 in the nucleus after LPS stimulation (PubMed:20547752). Translocation to the nucleus is impaired in L.monocytogenes infection (PubMed:20855622) |
Research Areas
- Primary Antibodies
- Cancer
- Cardiovascular
- Cell Biology
- Immunology
- Metabolism
- Microbiology
- Neuroscience
- Signal Transduction
- Antibody Collections
- GPCR Antibodies
- Host-virus interaction
- Inflammasome
- RIG-l-like Receptor
- Toll receptor signaling
- Toll-Like Receptor
- Toll-Like receptor signaling
- B cell receptor signaling
- Immune system process
- T cell receptor signaling
- Chemokine signaling
- Inflammation mediated by chemokine and cytokine signaling
- Apoptosis
- Apoptosis signaling
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