Phospho-RELB (Ser573) Antibody

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Description

Introduction

The Phospho-RELB (Ser573) Antibody is a rabbit polyclonal antibody specifically designed to detect endogenous levels of the transcription factor RelB when phosphorylated at serine 573. RelB, a member of the NF-κB family, plays critical roles in immune regulation, lymphoid development, and non-canonical signaling pathways . Phosphorylation at Ser573 is a key post-translational modification that regulates RelB activity, stability, and its ability to form heterodimers with other NF-κB subunits .

Key Features of the Antibody

  • Specificity: Detects RelB only when phosphorylated at Ser573 .

  • Applications: Validated for Western blotting (WB), immunohistochemistry (IHC), and immunofluorescence (IF) .

  • Reactivity: Cross-reacts with human, mouse, and rat .

Mechanism of Action

RelB is phosphorylated at Ser573 in response to pro-inflammatory signals, such as TNF-α or LPS, which activate the non-canonical NF-κB pathway . Phosphorylation at this site stabilizes RelB by preventing its degradation via the proteasome . The stabilized RelB forms heterodimers with p50 or p52, translocating to the nucleus to regulate transcription of immune-related genes .

Phosphorylation SiteEffectPathway
Ser573Stabilization of RelBNon-canonical NF-κB
Ser552/T84Degradation of RelBCanonical NF-κB

Applications and Performance

The antibody is optimized for detecting RelB phosphorylation in diverse biological contexts:

ApplicationDilutionSample Type
Western Blotting1:1000Cell lysates
Immunohistochemistry1:100Paraffin sections
Immunofluorescence1:100Fixed cells

Validation Data

  • Western Blot: Detects a ~70 kDa band corresponding to phosphorylated RelB in TNF-α-treated HUVEC cells .

  • IHC: Stains nuclear RelB in human breast carcinoma tissue .

  • IF: Localizes phosphorylated RelB to the nucleus of fixed cells .

Research Relevance

RelB’s phosphorylation at Ser573 has been implicated in:

  • Inflammation: Regulates transcription of pro-inflammatory genes in dendritic cells and monocytes .

  • Immune Tolerance: Modulates endotoxin tolerance by repressing immediate-response genes .

  • Metabolism: Couples with bioenergetic sensors like SIRT1 to integrate inflammation with mitochondrial function .

Disease Implications

  • Autoimmune Disorders: Dysregulation of RelB phosphorylation may contribute to autoimmune diseases like lupus .

  • Cancer: Overexpression of phosphorylated RelB correlates with breast carcinoma progression .

References Cell Signaling Technology. Phospho-RelB (Ser552) Antibody #4999. Thermo Fisher Scientific. Phospho-RelB (Ser573) Polyclonal Antibody, Invitrogen™. Antibodies.com. Anti-RelB (Phospho-Ser573) Antibody (A50466). PMC. RelB: an outlier in leukocyte biology.

Product Specs

Form
Supplied at 1.0 mg/mL in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150 mM NaCl, 0.02% sodium azide and 50% glycerol.
Lead Time
Typically, we can ship the products within 1-3 business days after receiving your orders. Delivery times may vary depending on the purchasing method or location. Please consult your local distributors for specific delivery time details.
Synonyms
I REL antibody; I-Rel antibody; IREL antibody; Nuclear factor of kappa light polypeptide gene enhancer in B cells 3 antibody; relB antibody; RELB_HUMAN antibody; Reticuloendotheliosis viral oncogene homolog B antibody; Transcription factor Rel B antibody; Transcription factor RelB antibody; v rel avian reticuloendotheliosis viral oncogene homolog B antibody; v rel reticuloendotheliosis viral oncogene homolog B antibody
Target Names
Uniprot No.

Target Background

Function
NF-κB is a multifaceted transcription factor found in nearly all cell types. It plays a crucial role in various biological processes including inflammation, immunity, differentiation, cell growth, tumorigenesis, and apoptosis. NF-κB exists as a homo- or heterodimeric complex composed of Rel-like domain-containing proteins such as RELA/p65, RELB, NFKB1/p105, NFKB1/p50, REL, and NFKB2/p52. These dimers bind to κB sites within the DNA of their target genes. Different dimer combinations exhibit distinct preferences for different κB sites, binding with varying affinities and specificities. Moreover, these dimer combinations act as either transcriptional activators or repressors. The activity of NF-κB is regulated by various mechanisms, including post-translational modifications, subcellular compartmentalization, and interactions with other cofactors or corepressors. NF-κB complexes are held in the cytoplasm in an inactive state, bound to members of the NF-κB inhibitor (IκB) family. In a typical activation pathway, IκB is phosphorylated by IκB kinases (IKKs) in response to diverse activators, leading to its subsequent degradation. This liberation allows the active NF-κB complex to translocate to the nucleus. NF-κB heterodimeric RelB-p50 and RelB-p52 complexes function as transcriptional activators. RELB, however, does not associate with DNA or RELA/p65 or REL. It stimulates promoter activity in the presence of NFKB2/p49. As a component of the NUPR1/RELB/IER3 survival pathway, it may confer remarkable resistance to cell stress, such as starvation or gemcitabine treatment, on pancreatic ductal adenocarcinoma. It also regulates the circadian clock by repressing the transcriptional activator activity of the CLOCK-ARNTL/BMAL1 heterodimer in a CRY1/CRY2 independent manner. Increased repression of the heterodimer is observed in the presence of NFKB2/p52. Furthermore, RELB is essential for both T and B lymphocyte maturation and function.
Gene References Into Functions
  1. Results show that GSK3β modulates RelB degradation. PMID: 29358699
  2. Data show that TNF receptor-associated factor 3 (TRAF3) autophagy is driven by RAS and results in activation of transcription factor RelB (RELB). PMID: 29146913
  3. TNF-α-induced expression of transport protein genes in HUVEC cells is associated with enhanced expression of RELB and NFKB2. PMID: 29658079
  4. results suggest that changes in the relative concentrations of RelB, NIK:IKK1, and p100 during noncanonical signaling modulate this transitional complex and are critical for maintaining the fine balance between the processing and protection of p100. PMID: 27678221
  5. Low RELB expression is associated with Prostate Cancer. PMID: 28108513
  6. RelB is processed by CO2 in a manner dependent on a key C-terminal domain located in its transactivation domain. Loss of the RelB transactivation domain alters NF-κB-dependent transcriptional activity, and loss of p100 alters sensitivity of RelB to CO2. PMID: 28507099
  7. EZH2, through a methyltransferase-independent mechanism, promotes the transcriptional activation of the non-canonical NF-κB subunit RelB. PMID: 27764181
  8. The altered expression of anti-apoptotic gene Bcl-2 played critical roles in regulating both spontaneous and radiation-induced apoptosis in the presence of RelB knockdown. For the first time, we showed that RelB knockdown significantly attenuated the migration and invasion of DU145 prostate cancer cells, due to the reduction of integrin β-1. PMID: 27121503
  9. Knockdown of ADGRG2 breast cancer cell lines resulted in a strong reduction in cell adhesion and subsequent cell migration which was associated with a selective reduction in RelB. PMID: 26321231
  10. the role of RelB on lymphocyte development in humans was shown. PMID: 26385063
  11. In conclusion, DECs show a unique hypo-responsive phenotype to the pro-inflammatory stimulus LPS in order to control the inflammatory response at feto-maternal interface. PMID: 26463648
  12. Lung-specific (CC-16) and novel (RelB) biomarkers are associated with systemic cardiovascular changes over time. PMID: 26914709
  13. results suggest that glucocorticoids induce a transcription complex consisting of RelB/p52, CBP, and HDAC1 that triggers a dynamic acetylation-mediated epigenetic change to induce CRH expression in full-term human placenta. PMID: 26307012
  14. HDAC4-RelB-p52 complex maintains repressive chromatin around proapoptotic genes Bim and BMF and regulates multiple myeloma survival and growth. PMID: 26455434
  15. RELB enhances proliferation of human-induced pluripotent stem cells without affecting their pluripotency. RELB interacts with LIN28A and IMP3. PMID: 25794352
  16. In non-small cell lung cancer, RelB expression was identified in proliferating tumor cells. Tumor RelB expression was an independent predictor of lymph node metastasis. PMID: 26147201
  17. Basal expression of RelB was significantly lower in lung cells derived from smokers with and without COPD. PMID: 25943190
  18. RelB may represent a novel marker of health outcomes. PMID: 25409035
  19. the specific Asp205 cleavage of RelB by caspase-3 would be involved in the apoptosis induction by anticancer agents, which would provide the positive feedback mechanism. PMID: 25511695
  20. we demonstrate that SUMOylation of RelB might be one of these post-translational modifications rendering the function of the NF-κB transcription factor RelB. PMID: 24616021
  21. RelB-p52 dimers were found to directly bind to the IDO promoter, leading to IDO expression in MDSCs. PMID: 25063873
  22. Unstimulated monocyte-derived dendritic cells express RelB at low level, However, RelB increases, following stimulation, are attenuated by geldanamycin. PMID: 24524692
  23. CTNNA1 expression is specifically downregulated in basal-like breast cancer subtype, correlates with clinical outcome and inversely correlates with TNF and RELB expression. PMID: 24509793
  24. The NF-κB protein RelB is expressed in a particularly aggressive mesenchymal subtype of glioma. PMID: 23451236
  25. RelB activation is key for promoting multiple myeloma cell survival through the upregulation of anti-apoptotic proteins, in particular, CIAP2. PMID: 23555623
  26. The dimer RelB/p50 rather than the p50/p50 complex inhibits TNF production in lipopolysaccharide-stimulated dendritic cells and macrophages. PMID: 23394901
  27. a novel link between NF-κB and growth-inhibitory pathways involving the RelB-dependent transcriptional upregulation of p53. PMID: 22777360
  28. Kaposi's sarcoma-associated herpesvirus oncoprotein K13 upregulated the expression of NF-κB subunit RelB and blocked the anti-IgM-induced decline in c-Myc and rise in p27(Kip1) that have been associated with growth arrest and apoptosis. PMID: 23236068
  29. The expression of RelB negatively regulates the endogenous expression of maspin in prostate cancer cells in vitro. PMID: 22780967
  30. The RelB subunit of NFkappaB acts as a negative regulator of circadian gene expression. PMID: 22894897
  31. These data show that Hodgkin lymphoma is uniquely dependent on relB. PMID: 22968463
  32. RelB/NF-κB2, is constitutively activated in the human placenta, which binds to a previously undescribed NF-κB enhancer of corticotropin-releasing hormone (CRH) gene promoter to regulate CRH expression. PMID: 22734038
  33. RelB is a CO(2)-sensitive NF-κB family member that may contribute to the beneficial effects of hypercapnia in inflammatory diseases of the lung. PMID: 22396550
  34. RelB plays a critical role in the response of PCa to radiotherapy and the inverse expression of IL-8 and PSA. PMID: 22403723
  35. We propose that RelB is an essential molecule controlling the endogenous and the proteasome inhibitor-induced Maspin expression. PMID: 21856005
  36. a central role for Malt1-dependent RelB cleavage in canonical NF-κB activation and thereby provide a rationale for the targeting of Malt1 in immunomodulation and cancer treatment. PMID: 21873235
  37. AHR overexpression is found among estrogen receptor (ER)α-negative human breast tumors and that its overexpression is positively correlated to that of the NF-κB subunit Rel-B and Interleukin 8. PMID: 21640702
  38. Data show that RelB is inducibly phosphorylated by GSK-3β, indicating a direct substrate-enzyme relationship. PMID: 21217772
  39. epigenetic RELB silencing as a new marker of the progressive disease in males. PMID: 21062507
  40. Bovine foamy virus transactivator BTas interacts with cellular RelB to enhance viral transcription. PMID: 20844054
  41. REQ functions as an efficient adaptor protein between the SWI/SNF complex and RelB/p52 and plays important roles in noncanonical NF-κB transcriptional activation and its associated oncogenic activity. PMID: 20460684
  42. the Tio oncoprotein triggers noncanonical NF-κB signaling through NEMO-dependent up-regulation of p100 precursor and RelB, as well as through NEMO-independent generation of p52 effector. PMID: 20353939
  43. the results suggest that RelB was responsible for the LPS-mediated attachment and may play an important role in the progression of some cancers. PMID: 19903458
  44. Rel activity plays a role in regulation of apoptosis in hepatocellular carcinoma through activation of downstream target genes. PMID: 12365017
  45. During dendritic cell maturation, rapidly activated dimers (e.g., RelA) bound to a subset of target promoters are gradually replaced by slowly activated dimers (e.g., RelB). PMID: 12820969
  46. RelB has an effect on p100 processing, which is possibly regulated in a signal-dependent manner. PMID: 12874295
  47. RelB mediates TNF-induced up-regulation of the human polymeric Ig receptor. PMID: 15265917
  48. RelB overexpression promoted, whereas endogenous RelB inhibition (by p100ΔN) blocked, precursor cell development along this DC subset pathway. PMID: 15315978
  49. induced by cytomegalovirus (CMV) immediate-early 1 protein via activation of JNK and AP-1. PMID: 15596805
  50. RelB expression during dendritic cells differentiation is controlled by protein kinase CβII-mediated regulation of transcriptional initiation and elongation. PMID: 16107733

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Database Links

HGNC: 9956

OMIM: 604758

KEGG: hsa:5971

STRING: 9606.ENSP00000221452

UniGene: Hs.654402

Involvement In Disease
Immunodeficiency 53 (IMD53)
Subcellular Location
Nucleus. Cytoplasm, cytoskeleton, microtubule organizing center, centrosome. Note=Colocalizes with NEK6 in the centrosome.

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