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NF-κB is a ubiquitously expressed transcription factor composed of varied combinations of five subunits: p65/RelA, RelB, c-Rel, p105/p50, and p100/p52.1,2,3 The NF-κB p50 subunit is a truncated version of p105 that lacks ankyrin repeat domains.2 The p105 subunit can be phosphorylated by GSK3β, which prevents p105 processing and degradation in resting cells.3 In TNF-α-stimulated cells, GSK3β phosphorylation induces processing of p105 into p50, which forms a heterodimer with p65 and is translocated to the nucleus to initiate the transcription of a variety of genes involved in innate and adaptive immunity. The p105 subunit can also be phosphorylated by the IKKβ complex downstream of TNF receptor 1 (TNFR1), inducing processing of p105 into p50, or by tumor progression locus 2 (TPL2) downstream of toll-like receptor 4 (TLR4) activation by LPS. Increased protein levels of NF-κB, irrespective of cytoplasmic or nuclear localization, are associated with lower overall survival and disease-free survival in patients with solid tumors.4 Cayman’s NF-κB (p105/p50) Rabbit Monoclonal Antibody (Clone RM299) can be used for immunohistochemistry (IHC) and Western blot (WB) applications.
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1. NF-
2. Shaping the nuclear action of NF-
3. Phosphorylation of NF-
4. NF-