Product: RelB Antibody
Catalog: AF6380
Description: Rabbit polyclonal antibody to RelB
Application: WB IF/ICC
Reactivity: Human, Mouse
Prediction: Pig, Bovine, Horse, Sheep, Dog
Mol.Wt.: 70kDa; 62kD(Calculated).
Uniprot: Q01201
RRID: AB_2835221

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 100ul $280 In stock
 200ul $350 In stock

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Product Info

Source:
Rabbit
Application:
WB 1:500-1:2000, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user.
*Tips:

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Reactivity:
Human,Mouse
Prediction:
Pig(90%), Bovine(100%), Horse(100%), Sheep(100%), Dog(100%)
Clonality:
Polyclonal
Specificity:
RelB Antibody detects endogenous levels of total RelB.
RRID:
AB_2835221
Cite Format: Affinity Biosciences Cat# AF6380, RRID:AB_2835221.
Conjugate:
Unconjugated.
Purification:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Storage:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
Alias:

Fold/Unfold

I REL; I-Rel; IREL; Nuclear factor of kappa light polypeptide gene enhancer in B cells 3; relB; RELB_HUMAN; Reticuloendotheliosis viral oncogene homolog B; Transcription factor Rel B; Transcription factor RelB; v rel avian reticuloendotheliosis viral oncogene homolog B; v rel reticuloendotheliosis viral oncogene homolog B;

Immunogens

Immunogen:
Uniprot:
Gene(ID):
Description:
RelB a transcription factor of the nuclear factor-kappaB (NFkB) transcription complex. Stimulates promoter activity in the presence NFkB1/NFkB-p50. Plays role in regulation of apoptosis in hepatocellular carcinoma through activation of downstream target genes.
Sequence:
MLRSGPASGPSVPTGRAMPSRRVARPPAAPELGALGSPDLSSLSLAVSRSTDELEIIDEYIKENGFGLDGGQPGPGEGLPRLVSRGAASLSTVTLGPVAPPATPPPWGCPLGRLVSPAPGPGPQPHLVITEQPKQRGMRFRYECEGRSAGSILGESSTEASKTLPAIELRDCGGLREVEVTACLVWKDWPHRVHPHSLVGKDCTDGICRVRLRPHVSPRHSFNNLGIQCVRKKEIEAAIERKIQLGIDPYNAGSLKNHQEVDMNVVRICFQASYRDQQGQMRRMDPVLSEPVYDKKSTNTSELRICRINKESGPCTGGEELYLLCDKVQKEDISVVFSRASWEGRADFSQADVHRQIAIVFKTPPYEDLEIVEPVTVNVFLQRLTDGVCSEPLPFTYLPRDHDSYGVDKKRKRGMPDVLGELNSSDPHGIESKRRKKKPAILDHFLPNHGSGPFLPPSALLPDPDFFSGTVSLPGLEPPGGPDLLDDGFAYDPTAPTLFTMLDLLPPAPPHASAVVCSGGAGAVVGETPGPEPLTLDSYQAPGPGDGGTASLVGSNMFPNHYREAAFGGGLLSPGPEAT

Predictions

Predictions:

Score>80(red) has high confidence and is suggested to be used for WB detection. *The prediction model is mainly based on the alignment of immunogen sequences, the results are for reference only, not as the basis of quality assurance.

Species
Results
Score
Horse
100
Bovine
100
Sheep
100
Dog
100
Pig
90
Xenopus
0
Zebrafish
0
Chicken
0
Rabbit
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

PTMs - Q01201 As Substrate

Site PTM Type Enzyme
R16 Methylation
S37 Phosphorylation
S50 Phosphorylation
T103 Phosphorylation
S116 Phosphorylation
S217 Phosphorylation
S221 Phosphorylation
K242 Ubiquitination
S254 Phosphorylation
Y293 Phosphorylation
K327 Ubiquitination
S425 Phosphorylation
S472 Phosphorylation O14920 (IKBKB) , O15111 (CHUK)
S573 Phosphorylation P49841 (GSK3B)
T579 Phosphorylation

Research Backgrounds

Function:

NF-kappa-B is a pleiotropic transcription factor which is present in almost all cell types and is involved in many biological processed such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. NF-kappa-B is a homo- or heterodimeric complex formed by the Rel-like domain-containing proteins RELA/p65, RELB, NFKB1/p105, NFKB1/p50, REL and NFKB2/p52. The dimers bind at kappa-B sites in the DNA of their target genes and the individual dimers have distinct preferences for different kappa-B sites that they can bind with distinguishable affinity and specificity. Different dimer combinations act as transcriptional activators or repressors, respectively. NF-kappa-B is controlled by various mechanisms of post-translational modification and subcellular compartmentalization as well as by interactions with other cofactors or corepressors. NF-kappa-B complexes are held in the cytoplasm in an inactive state complexed with members of the NF-kappa-B inhibitor (I-kappa-B) family. In a conventional activation pathway, I-kappa-B is phosphorylated by I-kappa-B kinases (IKKs) in response to different activators, subsequently degraded thus liberating the active NF-kappa-B complex which translocates to the nucleus. NF-kappa-B heterodimeric RelB-p50 and RelB-p52 complexes are transcriptional activators. RELB neither associates with DNA nor with RELA/p65 or REL. Stimulates promoter activity in the presence of NFKB2/p49. As a member of the NUPR1/RELB/IER3 survival pathway, may provide pancreatic ductal adenocarcinoma with remarkable resistance to cell stress, such as starvation or gemcitabine treatment. 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 seen in the presence of NFKB2/p52. Is required for both T and B lymphocyte maturation and function.

PTMs:

Phosphorylation at 'Thr-103' and 'Ser-573' is followed by proteasomal degradation.

Subcellular Location:

Nucleus. Cytoplasm>Cytoskeleton>Microtubule organizing center>Centrosome.
Note: Colocalizes with NEK6 in the centrosome.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Subunit Structure:

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 ARNTL/BMAL1 and the interaction is enhanced in the presence of CLOCK (By similarity).

Family&Domains:

Both N- and C-terminal domains are required for transcriptional activation.

Research Fields

· Environmental Information Processing > Signal transduction > MAPK signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > NF-kappa B signaling pathway.   (View pathway)

· Human Diseases > Infectious diseases: Viral > HTLV-I infection.

· Human Diseases > Infectious diseases: Viral > Epstein-Barr virus infection.

· Organismal Systems > Development > Osteoclast differentiation.   (View pathway)

References

1). Deficient DNASE1L3 facilitates neutrophil extracellular traps-induced invasion via cyclic GMP-AMP synthase and the non-canonical NF-κB pathway in diabetic hepatocellular carcinoma. Clinical & Translational Immunology, 2022 (PubMed: 35474906) [IF=5.8]

Application: WB    Species: Human    Sample: HCC cell

Figure 7 Roles of the non‐canonical NF‐κB pathway in HCC cell invasion. (a–d) Gene expression of NF‐κB pathway subunits NFKB2 (a) and RELB (c) in various HCC stages and adjacent normal tissues (Nor). Influence of these genes on the survival of HCC patients in the TCGA_LIHC cohort (b, d). (e, f) NETs DNA‐induced nuclear translocation of RelB in HCC SMMC7721 cells was observed with immunofluorescence imaging under a confocal microscope (n = 4). (g) RNA interference was applied to knock down RELB expression in SMMC7721 cells (n = 3). (h) NETs DNA‐induced invasion was observed between RELB‐downregulated and control SMMC7721 cells (n = 4). Data are shown as mean ± SD.

Application: IF/ICC    Species: Human    Sample: HCC cell

Figure 7 Roles of the non‐canonical NF‐κB pathway in HCC cell invasion. (a–d) Gene expression of NF‐κB pathway subunits NFKB2 (a) and RELB (c) in various HCC stages and adjacent normal tissues (Nor). Influence of these genes on the survival of HCC patients in the TCGA_LIHC cohort (b, d). (e, f) NETs DNA‐induced nuclear translocation of RelB in HCC SMMC7721 cells was observed with immunofluorescence imaging under a confocal microscope (n = 4). (g) RNA interference was applied to knock down RELB expression in SMMC7721 cells (n = 3). (h) NETs DNA‐induced invasion was observed between RELB‐downregulated and control SMMC7721 cells (n = 4). Data are shown as mean ± SD.

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