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RelA/NFkB p65

Killing two birds with one stone: Treating inflammation and cancer by inhibiting prolyl-4-hydroxylase-1

The effect of antioxidants and the NFkB p65 pathway in inflammation

NFkB is a transcription factor that plays a role in the expression of genes involved in immune response, inflammation, metastasis, cell survival and more. RelA (p65) is one member of the NFkB mammalian family, alongside other subunits.

The subunit RelA(p65) mediates NF-kB signal transduction in multiple ways

RelA (also known as p65) is an NF-kB family member and a subunit of the NF-kB transcription factor complex.  The mammalian NF-kB family has five members (NF-kB1, NF-kB2, RelA (p65), RelB, and c-Rel), each of which contains an N-terminal Rel homology domain. Active NF-kB protein complexes are dimeric (hetero- or homo-), and are made up of two family members. NF-kB signaling is activated in response to many different types of stimuli and modulates transcription of numerous downstream targets.

NFkB3-p65: Say that three times fast!

NF-kappa-B is a ubiquitous transcription factor involved in several biological processes such as inflammation, immunity, differentiation, cell growth, tumor genesis and apoptosis. Unlike the majority of transcription factors that reside in the nucleus, NFkB is predominantly bound to IkBs protein inhibitors and is located in the cytoplasm. There are two major signaling pathways involved in the activation of NFkB, canonical and non-canonical. [1] In the canonical NF-kB pathway, NF-kB activation is dependent on the inducible degradation of IkBs, particularly IkBa.