Cell Signaling Technology

Product Pathways - NF-kB Signaling

Toll-like Receptor 8 (D3Z6J) Rabbit mAb #11886

No. Size Price
11886S 100 µl ( 10 western blots ) ¥3,250.00 现货查询 购买询价
11886 carrier free & custom formulation / quantityemail request
Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
W 1:1000 Human, Endogenous 150 Rabbit IgG

Species cross-reactivity is determined by western blot.

Applications Key: W=Western Blotting,

Homology

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

Specificity / Sensitivity

TLR8 (D3Z6J) Rabbit mAb recognizes endogenous levels of total TLR8 protein. This antibody cross-reacts with a 30 kDa protein and a 37 kDa protein of unknown origin.

TLR8 (D3Z6J) Rabbit mAb抗体能识别内源性TLR8 总蛋白水平。此抗体与来源不明的30kDa和37kDa的蛋白有交叉反应。

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro141 of human TLR8 protein.

此单克隆抗体通过用合成肽免疫动物制备,该合成肽是人TLR8蛋白Pro141周围的残基。

Western Blotting

Western Blotting

Western blot analysis of extracts from THP-1 cells differentiated with TPA #4174 (80 nM, 16 hr), untreated (-) or treated with Human Interferon-γ (hIFN-γ) #8901 (20 ng/mL, 8 hr; +), using TLR8 (D3Z6J) Rabbit mAb (upper) or β-Actin (D6A8) Rabbit mAb #8457 (lower).Western blot分析TPA #4174诱导分化(80 nM, 16 小时)的THP-1细胞的提取物,未处理(-)或Human Interferon-γ (hIFN-γ) #8901 (20 ng/mL, 8小时; +)处理。使用的抗体是:TLR8 (D3Z6J) Rabbit mAb(上图)、β-Actin (D6A8) Rabbit mAb #8457(下图)。

Western Blotting

Western Blotting

Western blot analysis of extracts from 293T cells, mock transfected (-) or transfected with a construct expressing HA-tagged full-length human TLR8 (hTLR8-HA; +), using TLR8 (D3Z6J) Rabbit mAb.Western blot分析293T细胞的提取物,对照转染(-)或用HA标记的全长的人TLR8(hTLR8-HA; +)转染。使用的抗体是:TLR8 (D3Z6J) Rabbit mAb。

Background

Members of the Toll-like receptor (TLR) family, named for the closely related Toll receptor in Drosophila, play a pivotal role in innate immune responses (1-4). TLRs recognize conserved motifs found in various pathogens and mediate defense responses (5-7). Triggering of the TLR pathway leads to the activation of NF-κB and subsequent regulation of immune and inflammatory genes (4). The TLRs and members of the IL-1 receptor family share a conserved stretch of approximately 200 amino acids known as the Toll/Interleukin-1 receptor (TIR) domain (1). Upon activation, TLRs associate with a number of cytoplasmic adaptor proteins containing TIR domains, including myeloid differentiation factor 88 (MyD88), MyD88-adaptor-like/TIR-associated protein (MAL/TIRAP), Toll-receptor-associated activator of interferon (TRIF), and Toll-receptor-associated molecule (TRAM) (8-10). This association leads to the recruitment and activation of IRAK1 and IRAK4, which form a complex with TRAF6 to activate TAK1 and IKK (8,11-14). Activation of IKK leads to the degradation of IκB, which normally maintains NF-κB in an inactive state by sequestering it in the cytoplasm.Toll样受体(TLR)家族成员是对果蝇中密切相关的一系列Toll样受体的命名,它们在先天免疫反应中发挥着举足轻重的作用(1-4)。TLRs能识别各种病原体中的保守基序和调解防御反应(5-7)。TLR通路的触发往往导致NF-κB的活化及随后的免疫和炎症基因的调控(4)。TLRs和白介素1受体家族成员共享一个约200个氨基酸的保守区域,称为Toll/IL-1受体(TIR)结构域(1)。激活后,TLRs与许多细胞质(包含TIR结构域)的接头蛋白相关,包括髓样分化因子88(MyD88)、MyD88样接头蛋白/TIR结构域接头蛋白(MAL/TIRAP)、Toll受体相关的干扰素活化剂(TRIF)和Toll受体相关的分子(TRAM)(8-10)。这种关联导致IRAK1和IRAK4的补充和活化,能与TRAF6形成复合物激活TAK1和IKK(8,11-14)。IKK的活化能导致IκB的降解,通常情况下,IκB使NF-κB以失活状态存在于细胞质中。

TLR8 is an intracellular TLR localized to the endoplasmic reticulum, endosomes, lysosomes, and endolysosomes (4). It is activated by single-stranded viral RNA, as well as synthetic imidazoquinoline compounds including R-848 (5). TLR8 expression is highest in the lung and in myeloid cells (6,7). In addition, expression is upregulated by IFN-γ in monocyte-like leukemic THP-1 cells that have been differentiated with TPA (7).

TLR8是一种细胞内的TLR,位于内质网、内涵体、溶酶体和内吞溶酶体(4)。它能被单链病毒RNA和合成的咪唑喹啉类化合物(包括R-848)激活(5)。TLR8的表达在肺和髓系细胞中最高(6,7)。另外,TLR8可由单核细胞样白血病THP-1细胞(受TPA诱导向单核系方向分化)中的IFN-γ引起表达上调(7)。

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  3. Dunne, A. and O'Neill, L.A. (2003) Sci STKE 2003, re3.
  4. Medzhitov, R. et al. (1997) Nature 388, 394-7.
  5. Schwandner, R. et al. (1999) J Biol Chem 274, 17406-9.
  6. Takeuchi, O. et al. (1999) Immunity 11, 443-51.
  7. Alexopoulou, L. et al. (2001) Nature 413, 732-8.
  8. Zhang, F.X. et al. (1999) J Biol Chem 274, 7611-4.
  9. Horng, T. et al. (2001) Nat Immunol 2, 835-41.
  10. Oshiumi, H. et al. (2003) Nat Immunol 4, 161-7.
  11. Muzio, M. et al. (1997) Science 278, 1612-5.
  12. Wesche, H. et al. (1997) Immunity 7, 837-47.
  13. Suzuki, N. et al. (2002) Nature 416, 750-6.
  14. Irie, T. et al. (2000) FEBS Lett 467, 160-4.
  15. Heil, F. et al. (2003) Eur J Immunol 33, 2987-97.
  16. Jurk, M. et al. (2002) Nat Immunol 3, 499.
  17. Chuang, T.H. and Ulevitch, R.J. (2000) Eur Cytokine Netw 11, 372-8.
  18. Zarember, K.A. and Godowski, P.J. (2002) J Immunol 168, 554-61.

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Cell Signaling Technology is a trademark of Cell Signaling Technology, Inc.

Cell Signaling Technology® is a trademark of Cell Signaling Technology, Inc.

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