RELB Recombinant Monoclonal Antibody

說明書

中文名稱：

RELB重組抗體
貨號：

CSB-RA130517A0HU
規格：

￥1320
圖片：
Immunofluorescence staining of Hela with CSB-RA130517A0HU at 1:25, counter-stained with DAPI. The cells were fixed in 4% formaldehyde and blocked in 10% normal Goat Serum. The cells were then incubated with the antibody overnight at 4°C. The secondary antibody was Alexa Fluor 507-congugated AffiniPure Goat Anti-Rabbit IgG(H+L).

Overlay Peak curve showing Hela cells stained with CSB-RA130517A0HU (red line) at 1:50. The cells were fixed in 4% formaldehyde and permeated by 0.2% TritonX-100. Then 10% normal goat serum to block non-specific protein-protein interactions followed by the antibody (1μg/1*10⁶cells) for 45min at 4℃. The secondary antibody used was FITC-conjugated Goat Anti-rabbit IgG(H+L) at 1:200 dilution for 35min at 4℃.Control antibody (green line) was rabbit IgG (1μg/1*10⁶cells) used under the same conditions. Acquisition of >10,000 events was performed.
其他：

產品詳情
產品評價
相關產品
靶點詳情

產品詳情

產品描述：

CSB-RA130517A0HU RELB重組單克隆抗體是針對核因子κB家族成員RELB開發的高特異性科研工具。該抗體靶向的RELB蛋白是NF-κB信號通路中的關鍵轉錄因子，在調控免疫應答、炎癥反應及細胞存活等生物學過程中發揮重要作用。本品采用重組表達技術制備，經ELISA、免疫熒光（IF）和流式細胞術（FC）等多平臺嚴格驗證，結果顯示其具有優異的抗原結合能力與低交叉反應性。推薦使用稀釋比例為IF 1:50-1:200、FC 1:50-1:200，可清晰呈現細胞核定位特征及表面標記檢測。適用于探索NF-κB通路活化機制、免疫細胞功能調控、慢性炎癥性疾病模型構建等基礎研究領域，尤其適合在體外實驗體系中分析RELB的亞細胞定位及表達水平變化。該產品具有高批次間一致性，可為免疫信號轉導、腫瘤微環境調控等相關研究提供穩定可靠的技術支持。
Uniprot No.：

Q01201
基因名：

RELB
別名：

Transcription factor RelB (I-Rel), RELB
反應種屬：

Human
免疫原：

A synthesized peptide derived from Human RELB
免疫原種屬：

Homo sapiens (Human)
標記方式：

Non-conjugated
克隆類型：

Monoclonal
抗體亞型：

Rabbit IgG
純化方式：

Affinity-chromatography
克隆號：

9E4
濃度：

It differs from different batches. Please contact us to confirm it.
保存緩沖液：

Rabbit IgG in 10mM phosphate buffered saline , pH 7.4, 150mM sodium chloride, 0.05% BSA, 0.02% sodium azide and 50% glycerol.
產品提供形式：

Liquid
應用范圍：

ELISA, IF, FC

推薦稀釋比：

Application	Recommended Dilution
IF	1:50-1:200
FC	1:50-1:200

Protocols：

ELISA Protocol
Immunofluorescence (IF) Protocol
Flow cytometry (FC) Protocol
儲存條件：

Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.
貨期：

Basically, we can dispatch the products out in 1-3 working days after receiving your orders. Delivery time maybe differs from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
用途：

For Research Use Only. Not for use in diagnostic or therapeutic procedures.

產品評價

靶點詳情

功能：

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.
基因功能參考文獻：
1. Results show that GSK3beta 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-alpha-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-kappaB-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-kappaB 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 b-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-kappaB 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-kappaB 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-kappaB 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-kappaB 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-kappaB2, is constitutively activated in the human placenta, which binds to a previously undescribed NF-kappaB enhancer of corticotropin-releasing hormone (CRH) gene promoter to regulate CRH expression. PMID: 22734038
33. RelB is a CO(2)-sensitive NF-kappaB 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-kappaB 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)alpha-negative human breast tumors and that its overexpression is positively correlated to that of the NF-kappaB subunit Rel-B and Interleukin 8. PMID: 21640702
38. Data show that RelB is inducibly phosphorylated by GSK-3beta, 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-kappaB transcriptional activation and its associated oncogenic activity. PMID: 20460684
42. the Tio oncoprotein triggers noncanonical NF-kappaB 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 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 p100DeltaN) 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 CbetaII-mediated regulation of transcriptional initiation and elongation PMID: 16107733
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相關疾病：

Immunodeficiency 53 (IMD53)
亞細胞定位：

Nucleus. Cytoplasm, cytoskeleton, microtubule organizing center, centrosome. Note=Colocalizes with NEK6 in the centrosome.
數據庫鏈接：

HGNC: 9956

OMIM: 604758

KEGG: hsa:5971

STRING: 9606.ENSP00000221452

UniGene: Hs.654402

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