Anti-c-Rel (phospho S503) antibody

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.

Activity summary

The c-Rel protein also known as REL is a member of the NF-kappaB (nuclear factor kappa-light-chain-enhancer of activated B cells) family of transcription factors. It has a mass of approximately 65 kDa and is expressed in a variety of tissues with high levels seen in immune cells such as T and B lymphocytes. Being a transcription factor c-Rel regulates the expression of genes involved in immune responses cell proliferation and apoptosis. Its activity depends on its ability to translocate to the nucleus where it binds specific DNA sequences to modulate transcription.

Biological function summary

C-Rel functions to regulate immune system processes and is integral in lymphocyte activation. c-Rel functions as part of both homodimer and heterodimer complexes often partnering with other members of the NF-kappaB family to exert its effects. Through these complexes c-Rel influences the transcription of cytokines growth factors and other molecules critical for immune function. The protein’s role extends to influencing the differentiation and survival of lymphocytes instrumental in mounting adequate immune responses.

Pathways

C-Rel plays a significant role in the regulation of the NF-kappaB signaling pathway and the MAPK (mitogen-activated protein kinase) pathway. The NF-kappaB pathway is activated by inflammatory stimuli and stress which leads to the translocation of c-Rel to the nucleus. Here c-Rel regulates genes important for immune and inflammatory responses alongside other proteins like RelA and p50. In conjunction with the MAPK pathway c-Rel contributes to cellular responses to growth signals and stress collaborating with proteins such as JNK (c-Jun N-terminal kinase) and ERK (extracellular signal-regulated kinase).

Associated diseases and disorders

C-Rel’s dysregulation is associated with autoimmune diseases and lymphoid malignancies. Abnormal c-Rel activity contributes to diseases like rheumatoid arthritis where enhanced expression can lead to excessive inflammation and immune response. In certain lymphomas and leukemias overactive c-Rel promotes uncontrolled cell proliferation and survival. P53 a protein known for its role in tumor suppression may interact with pathways involving c-Rel influencing cancer progression and immune response dynamics. Understanding c-Rel and its interactions offers potential therapeutic targets for these and other related conditions.