What is the Difference Between NFkb1 and NFkb2?
🆚 Go to Comparative Table 🆚The NFKB1 and NFKB2 proteins, also known as p105 and p100, are part of the NF-κB signaling system, which plays a crucial role in controlling transcription of DNA, cytokine production, and cell survival. They are both involved in the regulation of immune responses against infection and other cellular responses to stimuli such as stress, cytokines, free radicals, heavy metals, ultraviolet irradiation, oxidized LDL, and bacterial or viral antigens.
The key difference between NFKB1 and NFKB2 lies in their gene encoding:
- NFKB1: This protein is encoded by the NFKB1 gene in humans.
- NFKB2: This protein is encoded by the NFKB2 gene in humans.
In addition to their role in the NF-κB signaling system, NFKB1 and NFKB2 proteins have distinct functions:
- NFKB1: The full-length form of NFKB1, known as P105, cotranslates into the active form P50.
- NFKB2: The full-length form of NFKB2, known as P100, cotranslates into the active form P52.
Despite their similarities, some studies have revealed differences in their transcriptional activity, with NFKB1 and NFKB2 having distinct roles in both canonical and non-canonical NF-κB signaling pathways.
Comparative Table: NFkb1 vs NFkb2
NFkb1 and NFkb2 are proteins in humans encoded by the NFkb1 and NFkb2 genes, respectively. They are part of the NF-κB (nuclear factor κB) protein complex, which controls the transcription of DNA, cytokine production, and cell survival. Here is a table highlighting the differences between NFkb1 and NFkb2:
Feature | NFkb1 | NFkb2 |
---|---|---|
Gene | NFkb1 | NFkb2 |
Full-length protein | P105 (active form: P50) | P100 (active form: P52) |
Function | Controls transcription of DNA, cytokine production, and cell survival | Controls transcription of DNA, cytokine production, and cell survival |
Both NFkb1 and NFkb2 are involved in immune cell biology and play crucial roles in regulating immune responses against infections. Some differences have been observed in mutant mice, where NFkb1-deficient mice exhibit multiple defects in both innate and adaptive immunity, while NFkb2-deficient mice suffer from thymic medullary hypoplasia and autoimmune diseases. Additionally, rare mutations in NFKB2 have been linked to an autosomal dominant human syndrome of hypogammaglobulinemia and organ-specific autoimmunity.