Anti-NF-κB p105 Antibody detects endogenous levels of total NF-κB p105 protein.
The gene NFκB1(nuclear factor κ B subunit 1) is mapped to human chromosome 4q24. It codes for κB p105/p50 isoforms.
Immunogen
The antiserum was produced against synthesized peptide derived from human NF-kappaB p105/p50.
Immunogen Range: 860-909
Biochem/physiol Actions
NF-κB (nuclear factor κ B) is an important transcription factor that regulates the process of apoptosis, immune response and cell-growth control genes. It is associated with a number of human disorders including inflammatory diseases and cancers. NF-κB signaling cascade is known to be stimulated by many genotoxic stresses and also DNA damage. NF-κB is involved in bone metabolism. Downregulation of NF-κB mediates GPER (G-protein coupled estrogen receptor) specific agonist G-1 induced EMT (epithelial mesenchymal transition) suppression. Thereby, it prevents the motility of triple-negative breast cancer cells in vitro.
Features and Benefits
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Physical form
Rabbit IgG in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.
Human molecular genetics, 13(1), 35-45 (2003-11-14)
Nuclear Factor-kappaB (NF-kappaB) is a major transcription regulator of immune response, apoptosis and cell-growth control genes, and is upregulated in inflammatory bowel disease (IBD), both ulcerative colitis (UC) and Crohn's disease. The NFKB1 gene encodes the NF-kappaB p105/p50 isoforms. Genome-wide
The targeted therapy for triple-negative breast cancer (TNBC) is a great challenge due to our poor understanding on its molecular etiology. In the present study, our clinical data showed that the expression of G-protein coupled estrogen receptor (GPER) is negatively
Given the involvement of telomerase activation and dysregulated metabolism in glioma progression, the connection between these two critical players was investigated. Pharmacological inhibition of human Telomerase reverse transcriptase (hTERT) by Costunolide induced glioma cell apoptosis in a reactive oxygen species
Previously we reported that Src-associated-substrate-during-mitosis-of-68kDa (Sam68/KHDRBS1) is pivotal for DNA damage-stimulated NF-κB transactivation of anti-apoptotic genes (Fu et al., 2016). Here we show that Sam68 is critical for genotoxic stress-induced NF-κB activation in the γ-irradiated colon and animal and that
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