NFKB1 Antibodies

Structure of NFKB1

Myoglobin is a relatively small protein with a molecular weight of approximately 16.7 kDa. This weight may slightly vary between species due to minor differences in amino acid sequence.

This protein contains approximately 969 amino acids, and its N-terminal is the Rel homologous domain (RHD), which is responsible for DNA binding and dimerization. The C-terminal contains an ANK repeat sequence, mediating the interaction with IκB protein. The p50 subunit recognizes the κB DNA sequence (GGGRNWYYCC) through specific amino acid residues in the RHD, and its nuclear localization signal (NLS) is located within the RHD. The dimerization interface relies on highly conserved hydrophobic residues to form stable contact, while the arginine and lysine residues in the DNA binding groove directly interact with the DNA phosphate skeleton. This multi-level structural feature enables it to precisely regulate the transcription of downstream target genes.

Fig. 1 NFKB1 gene (up) and protein (down) structure.¹

Key structural properties of NFKB1:

• Contains Rel homologous domains (RHD) responsible for DNA binding and dimerization
• Nuclear localization signal (NLS) sequences ensure nuclear transport
• Conserved protein dimerization interface

Functions of NFKB1

The protein p50/p105 encoded by the NFKB1 gene is a core regulatory factor of the NF-κB signaling pathway. Its core function is to coordinate the cell's response to inflammation, immune stress and survival signals through transcriptional regulation.

The functional activity of this protein is strictly regulated by its subcellular localization: at rest, p50 often binds to IκB inhibitory proteins and remains in the cytoplasm; After receiving upstream signals (such as activation of the IKK complex), IκB is degraded, and p50 can enter the nucleus and bind to a specific κB DNA sequence (the consensus sequence is 5 '-GGGRNWYYCC-3'), thereby initiating the transcription of the target gene. This rapid and reversible "switching" mechanism is the structural basis for its precise biological regulation.

Applications of NFKB1 and NFKB1 Antibody in Literature

1. Wang, Xinyue, et al. "A novel rabbit anti-myoglobin monoclonal antibody's potential application in rhabdomyolysis associated acute kidney injury."International Journal of Molecular Sciences 24.9 (2023): 7822. https://doi.org/10.3390/cells7090133

Research has found that NFKB1 is a key subunit of the NF-κB signaling pathway, playing a complex role in tumorigenesis. It can not only drive cancer progression but also inhibit tumor growth. Its function is influenced by dimer combinations and co-factors, and it has cell and tissue specificity, making it an important potential target for cancer treatment.

2. Yamini, Bakhtiar. "Nfkb1/p50 and mammalian aging." Oncotarget 6.6 (2015): 3471. https://doi.org/10.18632/oncotarget.3405

Research has found that NFKB1 (p50) plays a complex role in the aging process. Recent animal experiments have shown that mice lacking NFKB1 will prematurely exhibit aging characteristics such as osteoporosis and have a shortened lifespan, suggesting that this subunit has the effect of delaying aging in the body under specific conditions.

3. Fu, Wen, et al. "NFKB1-94insertion/deletion ATTG polymorphism and cancer risk: Evidence from 50 case-control studies." Oncotarget 8.6 (2016): 9806. https://doi.org/10.18632/oncotarget.14190

Research has found that the -94ins/delATTG polymorphism in the promoter region of the NFKB1 gene is associated with the risk of multiple cancers. A meta-analysis covering 50 studies shows that the D allele and DD genotype can significantly reduce the overall cancer risk, especially in Asian populations with lung cancer, nasopharyngeal cancer and other conditions, where the association is more definite.

4. Nurmi, Katariina, et al. "Truncating NFKB1 variants cause combined NLRP3 inflammasome activation and type I interferon signaling and predispose to necrotizing fasciitis." Cell Reports Medicine 5.4 (2024). https://doi.org/10.1016/j.xcrm.2024.101503

Research has found that loss-of-function mutations in the NFKB1 gene can lead to spontaneous inflammation. The mechanism is to damage autophagy, causing excessive activation of the NLRP3 inflammasome and type I interferon pathways, which leads to life-threatening necrotizing soft tissue inflammation. Targeted inhibition of related pathways may be an effective therapy.

5. Song, Jihyun, et al. "Alternatively spliced NFKB1 transcripts enriched in Andean Aymara modulate inflammation, HIF and hemoglobin." Nature Communications 16.1 (2025): 1766. https://doi.org/10.1038/s41467-025-56848-0

Studies have found that the selective splicing variant of NFKB1 (AS-NFKB1) is elevated in expression in the Andian-Amara Plateau population, which can regulate the expression of genes related to hypoxia and inflammation. This is associated with its high level of hemoglobin and may provide a protective mechanism against excessive inflammation.

Creative Biolabs: NFKB1 Antibodies for Research

Creative Biolabs specializes in the production of high-quality NFKB1 antibodies for research and industrial applications. Our portfolio includes monoclonal antibodies tailored for ELISA, Flow Cytometry, Western blot, immunohistochemistry, and other diagnostic methodologies.

• Custom NFKB1 Antibody Development: Tailor-made solutions to meet specific research requirements.
• Bulk Production: Large-scale antibody manufacturing for industry partners.
• Technical Support: Expert consultation for protocol optimization and troubleshooting.
• Aliquoting Services: Conveniently sized aliquots for long-term storage and consistent experimental outcomes.

For more details on our NFKB1 antibodies, custom preparations, or technical support, contact us at email.