Cell Signaling Technology

Product Pathways - NF-kB Signaling

Phospho-RelB (Ser552) Antibody #4999

No. Size Price
4999S 100 µl ( 10 western blots ) ¥3,900.00 现货查询 购买询价
4999 carrier free & custom formulation / quantityemail request
Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
W 1:1000 Human,Mouse, Endogenous 70 Rabbit
IP 1:100
F 1:400
IF-IC 1:200

Species cross-reactivity is determined by western blot.

Applications Key: W=Western Blotting, IP=Immunoprecipitation, F=Flow Cytometry, IF-IC=Immunofluorescence (Immunocytochemistry),


Species predicted to react based on 100% sequence homology: Rat, Monkey, Bovine, Dog,

Specificity / Sensitivity

Phospho-RelB (Ser552) Antibody detects endogenous levels of RelB only when phosphorylated at Ser552.

Phospho-RelB (Ser552) Antibody只能检测内源的在Ser552位点磷酸化的RelB蛋白。

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Ser552 of mouse RelB. Antibodies are purified by protein A and peptide affinity chromatography.

此多克隆抗体是通过合成鼠源对应的RelB Ser552位点周围的磷肽段来免疫动物而获得。抗体是通过protein A和多肽亲和层析纯化。

Flow Cytometry

Flow Cytometry

Flow cytometric analysis of Raji cells, untreated (blue) or TPA-treated (green), using Phospho-RelB (Ser552) Antibody.流式细胞仪分析未经处理(蓝色) 或经TPA (绿色)处理的Raji细胞。所用抗体为 Phospho-RelB (Ser552) Antibody。



Confocal immunofluorescent analysis of Raji cells, serum-starved (left), treated with TPA (Phorbol-12-Myristate-13-Acetate) #9905 (center) or λ phosphatase-treated (right), using Phospho-RelB (Ser552) Antibody (green). Blue pseudocolor = DRAQ5® #4084 (fluorescent DNA dye).共聚焦免疫荧光分析Raji 细胞,经血清饥饿(左图), TPA (Phorbol-12-Myristate-13-Acetate) #9905 处理(中间图)或 λ phosphatase处理 (右图),所用抗体为Phospho-RelB (Ser552) Antibody (绿色)。Blue pseudocolor = DRAQ5® #4084 (DNA荧光染料)

Western Blotting

Western Blotting

Western blot analysis of extracts from A20 and CTTL2 cells, untreated or treated with TPA #4174 (200nM, 30 minutes) alone or with λ phosphatase, using Phospho-RelB (Ser552) Antibody.Western免疫印迹。用 Phospho-RelB (Ser552) Antibody研究未经处理的和经TPA #4174 (200nM, 30 min) 或经TPA #4174 (200nM, 30 min)与 λ phosphatase共处理的 A20 和 CTTL2 细胞的细胞提取液。


Transcription factors of the nuclear factor κ B (NF-κB)/Rel family play a pivotal role in inflammatory and immune responses (1,2). There are five family members in mammals: RelA, c-Rel, RelB, NF-κB1 (p105/p50), and NF-κB2 (p100/p52). Both p105 and p100 are proteolytically processed by the proteasome to produce p50 and p52, respectively. Rel proteins bind p50 and p52 to form dimeric complexes that bind DNA and regulate transcription. In unstimulated cells, NF-κB is sequestered in the cytoplasm by IκB inhibitory proteins (3-5). NF-κB-activating agents can induce the phosphorylation of IκB proteins, targeting them for rapid degradation through the ubiquitin-proteasome pathway and releasing NF-κB to enter the nucleus where it regulates gene expression (6-8). NIK and IKKα (IKK1) regulate the phosphorylation and processing of NF-κB2 (p100) to produce p52, which is then translocated to the nucleus (9-11).

核因子κ B(NF-κB)/Rel 家族的转录调控因子在炎症反应和免疫反应中发挥了至关重要的作用(1,2)。在哺乳动物中一共有5个家族成员: RelA, c-Rel, RelB, NF-κB1 (p105/p50) 和 NF-κB2 (p100/p52)。 p105 和 p100 在蛋白水解酶的作用下分别形成p50 和 p52。Rel与p50和p52形成二聚体,此复合体能够结合到DNA上调控转录。在未刺激的状态下, NF-κB 在IκB抑制剂作用下在细胞质中处于非活性状态(3-5)。 NF-κB激活因子能够诱导 IκB 蛋白的磷酸化, 这就使IκB能够快速的经过泛素化-蛋白酶通路降解从而释放 NF-κB,激活的NF-κB入核调控基因的表达(6-8)。 NIK 和 IKKα (IKK1) 调节磷酸化并促使NF-κB2 (p100) 生成p52, p52之后会入核发挥功能(9-11)。

RelB, which is generally activated by non-canonical signaling, forms heterodimers with either p50 or p52 NF-κB subunits to regulate transcription (12,13). RelB null mice are significantly impaired in inflammatory responses and hematopoietic differentiation (14,15). Phosphorlyation at Thr84 and Ser552 results in proteosomal degradation (16).

RelB通常是通过不固定形式的信号通路激活,与p50 或 p52 NF-κB 亚单元形成二聚体而调控转录(12,13)。RelB缺失的大鼠的炎症反应和血细胞的分化也严重的缺陷(14,15)。在Thr84 和 Ser552位点的磷酸化导致其通过蛋白酶体的降解(16)。

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  2. Baeuerle, P.A. and Baltimore, D. (1996) Cell 87, 13-20.
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  4. Thompson, J.E. et al. (1995) Cell 80, 573-82.
  5. Whiteside, S.T. et al. (1997) EMBO J 16, 1413-26.
  6. Traenckner, E.B. et al. (1995) EMBO J 14, 2876-83.
  7. Scherer, D.C. et al. (1995) Proc Natl Acad Sci USA 92, 11259-63.
  8. Chen, Z.J. et al. (1996) Cell 84, 853-62.
  9. Senftleben, U. et al. (2001) Science 293, 1495-9.
  10. Coope, H.J. et al. (2002) EMBO J 21, 5375-85.
  11. Xiao, G. et al. (2001) Mol Cell 7, 401-9.
  12. Ryseck, R.P. et al. (1992) Mol Cell Biol 12, 674-84.
  13. Bours, V. et al. (1994) Oncogene 9, 1699-702.
  14. Weih, F. et al. (1995) Cell 80, 331-40.
  15. Burkly, L. et al. (1995) Nature 373, 531-6.
  16. Marienfeld, R. et al. (2001) Oncogene 20, 8142-7.

Application References

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