RelB Antibody (YA1852)
(Synonyms: RELB; Transcription factor RelB; I-Rel)RelB Antibody (YA1852) is a Rabbit-derived and non-conjugated IgG monoclonal antibody, targeting to RelB.
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Host:
Rabbit
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Isotype:
IgG
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Application:
WB, IP
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Reactivity :
Human, Mouse, Rat
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Formulation:
Supplied in 50mM Tris-Glycine(pH 7.4), 0.15M NaCl, 40% Glycerol, 0.01% Sodium azide and 0.05% BSA
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Conjugation:
Non-conjugated
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Applications
| Application |
WB
WB: Western Blot
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IP
IP: Immunoprecipitation
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|---|---|---|
| Dilution Ratio | 1:500-1:1000 | 1:20 |
Product Details
RelB Antibody (YA1852) is a Rabbit-derived and non-conjugated IgG monoclonal antibody, targeting to RelB.
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Host Rabbit
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Clonality Recombinant,Monoclonal
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Species ReactivityHuman, Mouse, Rat
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Observed Molecular WeightObserved band size: 62 kDa
Note: Due to possible protein modifications or aggregation, the molecular weight should be confirmed by actual measurement, and the predicted value is for reference only.
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Calculated Molecular Weight Predicted band size: 62 kDa
Entrez Gene: 5971 Human ; 19698 Mouse ; 100360982 Rat
SwissProt: Q01201 Human ; Q04863 Mouse ;
OMIM: 617585 Human
A synthetic peptide of human Rel B
Endogenous
Affinity Purified
Non-conjugated
Unmodified
IgG
Product Properties
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Appearance
Solution
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Formulation
Supplied in 50mM Tris-Glycine(pH 7.4), 0.15M NaCl, 40% Glycerol, 0.01% Sodium azide and 0.05% BSA
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Storage & Stability
Stored at -20°C for 1 year. Avoid repeated freeze / thaw cycles.
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Shipping
Shipping with blue ice.
Background
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Function
RelB is a member of the NF-κB transcription factor family and functions as a key regulator of immune homeostasis, antigen-presenting cell activity, and lymphoid tissue organization[4][1]. Mechanistically, RelB is the principal transcriptional component of the non-canonical NF-κB pathway, where NF-κB-inducing kinase (NIK) and IKKα promote processing of p100 into p52, leading to formation and nuclear translocation of RelB:p52 heterodimers that regulate distinct target genes involved in lymphoid organogenesis, lymphocyte trafficking, and immune regulation[1][5]. In dendritic cells, RelB is highly expressed and is required for dendritic cell maturation, antigen presentation, and T-cell activation, highlighting its central role in adaptive immune responses[2]. Disease relevance arises from the broad involvement of non-canonical NF-κB signaling in inflammatory, autoimmune, and malignant disorders, while RelB-dependent transcriptional programs contribute to the regulation of immune response genes and maintenance of immune homeostasis[1][3][6]. Compared with the closely related NF-κB subunit RelA (p65), which predominantly mediates canonical NF-κB signaling through p50:RelA dimers, RelB preferentially forms transcriptionally active complexes with p52 and controls a distinct set of genes associated with developmental and homeostatic immune functions[1][5]. Experimental studies further indicate that RelB can modulate inflammatory gene expression by competing with RelA for κB-binding sites, providing a mechanistic basis for functional divergence among NF-κB family members[6]. For research applications, pharmacological strategies targeting NF-κB signaling, including inhibitors of upstream kinases and nuclear NF-κB activity, are widely used to investigate RelB-regulated pathways in immunity, inflammation, and cancer models[3].
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Subcellular Localization
Nucleus; Cytoplasm, cytoskeleton, microtubule organizing center, centrosome
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Expression
Induction:Up-regulated by mitogens and NUPR1 -
Subunit
Component of the NF-kappa-B RelB-p50 complex. Component of the NF-kappa-B RelB-p52 complex. Self-associates; the interaction seems to be transient and may prevent degradation allowing for heterodimer formation with p50 or p52. Interacts with NFKB1/p50, NFKB2/p52 and NFKB2/p100. Interacts with NFKBID. Interacts with BMAL1 and the interaction is enhanced in the presence of CLOCK (By similarity)
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SwissProt ID
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Synonyms
RELB; Transcription factor RelB; I-Rel
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Research Field
Cell Biology
Documentation
[1]. Sun SC. The non-canonical NF-kappaB pathway in immunity and inflammation. Nat Rev Immunol. 2017;17(9):545-558. [Content Brief]
[2]. Shih VFS, et al. Control of RelB during dendritic cell activation integrates canonical and noncanonical NF-kappaB pathways. Nat Immunol. 2012;13(12):1162-1170. [Content Brief]
[3]. Guo Q, et al. NF-κB in biology and targeted therapy: new insights and translational implications. Signal Transduct Target Ther. 2024 Mar 4;9(1):53. [Content Brief]
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