Rabbit Recombinant Monoclonal NF-kB p65 phospho S536 antibody - conjugated to FITC. Suitable for Flow Cyt and reacts with Human samples. Cited in 1 publication. Immunogen corresponding to Synthetic Peptide within Human RELA phospho S536.
Preservative: 0.09% Sodium azide
Constituents: 99.71% PBS, 0.2% BSA
Flow Cyt | |
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Human | Tested |
Species | Dilution info | Notes |
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Species Human | Dilution info 5 µL for 106 Cells | Notes - |
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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).
NFKB3, RELA, Transcription factor p65, Nuclear factor NF-kappa-B p65 subunit, Nuclear factor of kappa light polypeptide gene enhancer in B-cells 3
Rabbit Recombinant Monoclonal NF-kB p65 phospho S536 antibody - conjugated to FITC. Suitable for Flow Cyt and reacts with Human samples. Cited in 1 publication. Immunogen corresponding to Synthetic Peptide within Human RELA phospho S536.
Preservative: 0.09% Sodium azide
Constituents: 99.71% PBS, 0.2% BSA
This product is a recombinant monoclonal antibody, which offers several advantages including:
For more information, read more on recombinant antibodies.
NF-kB p65 also known as RelA is a significant component of the NF-kB protein complex. This complex usually involves a molecular weight for p65 of approximately 65 kDa. NF-kB p65 is mechanistically a transcription factor that regulates genes involved in inflammation cell survival and immune response. Expression of p65 is widely seen in various cell types including immune cells and epithelial cells suggesting its role in numerous physiological processes.
NF-kB p65 acts as part of the larger NF-kB complex usually forming a heterodimer with other family members like p50. This complex translocates to the nucleus upon activation where it binds specific DNA sequences to regulate gene expression. The p65 subunit is essential for transactivating target genes involved in immune and inflammatory responses. Its regulation is important for proper cellular functioning especially in the maintenance of immune homeostasis and inflammatory response.
NF-kB p65 participates in critical pathways like the NF-kB signaling and Toll-like receptor pathways. These pathways are fundamental for initiating immune responses and contribute to the regulation of apoptosis and cellular stress responses. In the context of these pathways the IKK complex plays a pivotal role in NF-kB activation leading to the phosphorylation and subsequent degradation of inhibitors that retain NF-kB p65 in the cytoplasm therefore allowing its movement to the nucleus.
NF-kB p65 is implicated in conditions such as cancer and autoimmune diseases. Its dysregulation can lead to persistent activation of inflammatory pathways contributing to tumorigenesis and chronic inflammation. In the context of these diseases proteins such as the p50 subunit and the IKK complex are often involved reflecting the importance of tight regulation of NF-kB signaling in preventing pathological conditions.
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Flow cytometric analysis of HeLa cells unstained and untreated as negative control (blue) or untreated (red) or treated with TNFa plus CalA (green) and stained using ab278631.
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