RelB is a member of the nuclear factor-kappa B (NF-κB) family of transcription factors, which play crucial roles in regulating immune responses, inflammation, cell proliferation, and survival. Unlike other NF-κB family members, RelB primarily forms heterodimers with the p52 subunit, and together they function as transcriptional activators of genes involved in immune regulation, tissue development, and stress responses. RelB activation occurs through canonical and non-canonical NF-κB signaling pathways, which are triggered by distinct cellular stimuli and involve different upstream signaling molecules and regulatory mechanisms. In the canonical pathway, activation of NF-κB typically involves the phosphorylation and subsequent degradation of the inhibitor of kappa B (IκB) proteins, leading to the release and nuclear translocation of NF-κB dimers such as RelA:p50 complexes. However, RelB activation primarily occurs through the non-canonical pathway, which is initiated by the activation of specific receptors such as lymphotoxin beta receptor (LTβR), B-cell activating factor receptor (BAFFR), or receptor activator of NF-κB (RANK), among others.
Upon ligand binding, these receptors activate a cascade of signaling events that culminate in the activation of the NF-κB-inducing kinase (NIK) and subsequent processing of the p100 precursor protein to generate the active p52 subunit. The p52 subunit then forms heterodimers with RelB and translocates to the nucleus, where it regulates the expression of target genes involved in immune and inflammatory responses, lymphoid organ development, and cellular homeostasis. Additionally, RelB activation can be modulated by various post-translational modifications, including phosphorylation, acetylation, and ubiquitination, which regulate its stability, subcellular localization, and interactions with coactivators or corepressors.
| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
IMD 0354 | 978-62-1 | sc-203084 | 5 mg | $199.00 | 3 | |
IMD-0354 is an inhibitor of IKKβ, a kinase involved in the phosphorylation and degradation of IκBα. By inhibiting IKKβ, IMD-0354 indirectly activates RelB through the non-canonical NF-κB pathway. The disruption of IKKβ-mediated signaling leads to altered RelB activity, influencing gene expression associated with immune responses and inflammation. | ||||||
ML 120B Dihydrochloride | 783348-36-7 (free base) | sc-487759 | 5 mg | $380.00 | ||
MLN120B is a selective IKKβ inhibitor, disrupting the NF-κB signaling pathway. By inhibiting IKKβ, MLN120B indirectly activates RelB through the non-canonical NF-κB pathway. The modulation of RelB activity by MLN120B influences downstream gene expression patterns associated with immune responses and inflammation. MLN120B's specificity for IKKβ positions it as a valuable tool for investigating the non-canonical NF-κB pathway and its role in regulating RelB activation. | ||||||
IKK-2 Inhibitor IV | 507475-17-4 | sc-203083 | 500 µg | $133.00 | 12 | |
TPCA-1 is an inhibitor of IKK2, a key component of the classical NF-κB pathway. By inhibiting IKK2, TPCA-1 indirectly activates RelB through the non-canonical NF-κB pathway. The disruption of IKK2-mediated signaling alters RelB activity, influencing gene expression patterns associated with immune responses and inflammation. | ||||||
IKK 16 | 1186195-62-9 | sc-204009 sc-204009A | 10 mg 50 mg | $223.00 $942.00 | 2 | |
IKK-16 is an inhibitor of IKKα and IKKβ, key components of the classical NF-κB pathway. By inhibiting both IKKα and IKKβ, IKK-16 indirectly activates RelB through the non-canonical NF-κB pathway. The disruption of IKK-mediated signaling alters RelB activity, influencing gene expression patterns associated with immune responses and inflammation. | ||||||
SC514 | 354812-17-2 | sc-205504 sc-205504A | 5 mg 10 mg | $67.00 $91.00 | 13 | |
SC-514 is a selective COX-2 inhibitor, impacting the prostaglandin pathway. By inhibiting COX-2, SC-514 indirectly activates RelB through mechanisms involving the non-canonical NF-κB pathway. The modulation of RelB activity by SC-514 influences downstream gene expression patterns associated with inflammation and immune responses. | ||||||
Withaferin A | 5119-48-2 | sc-200381 sc-200381A sc-200381B sc-200381C | 1 mg 10 mg 100 mg 1 g | $130.00 $583.00 $4172.00 $20506.00 | 20 | |
Withaferin A, found in Withania somnifera, is a natural compound that inhibits IKKβ activity. By inhibiting IKKβ, Withaferin A indirectly activates RelB through the non-canonical NF-κB pathway. The disruption of IKKβ-mediated signaling alters RelB activity, influencing gene expression patterns associated with immune responses and inflammation. | ||||||
MLN 4924 | 905579-51-3 | sc-484814 | 1 mg | $286.00 | 1 | |
MLN4924 is an inhibitor of NEDD8-activating enzyme (NAE), impacting the ubiquitin-proteasome pathway. By inhibiting NAE, MLN4924 indirectly activates RelB through mechanisms involving the non-canonical NF-κB pathway. The disruption of NAE-mediated signaling alters RelB activity, influencing gene expression patterns associated with immune responses and inflammation. | ||||||
Bortezomib | 179324-69-7 | sc-217785 sc-217785A | 2.5 mg 25 mg | $135.00 $1085.00 | 115 | |
Bortezomib is a proteasome inhibitor that impacts NF-κB signaling by preventing the degradation of IκBα. By inhibiting the proteasome, Bortezomib indirectly activates RelB through the non-canonical NF-κB pathway. The disruption of proteasome-mediated signaling alters RelB activity, influencing gene expression patterns associated with immune responses and inflammation. | ||||||