| Product Includes | Product # | Quantity | Mol. Wt | Isotype/Source |
|---|---|---|---|---|
| Phospho-NF-κB p65 (Ser536) (93H1) Rabbit mAb | 3033 | 20 µl | 65 kDa | Rabbit IgG |
| Acetyl-NF-κB p65 (Lys310) (D2S3J) Rabbit mAb | 12629 | 20 µl | 65 kDa | Rabbit IgG |
| NF-κB p65 (L8F6) Mouse mAb | 6956 | 20 µl | 65 kDa | Mouse IgG2b |
| NF-κB p65 (D14E12) XP® Rabbit mAb | 8242 | 20 µl | 65 kDa | Rabbit IgG |
| Phospho-NF-κB p65 (Ser468) Antibody | 3039 | 20 µl | 65 kDa | Rabbit |
| Anti-rabbit IgG, HRP-linked Antibody | 7074 | 100 µl | Goat | |
| Anti-mouse IgG, HRP-linked Antibody | 7076 | 100 µl | Horse |
Please visit cellsignal.com for individual component applications, species cross-reactivity, dilutions, protocols, and additional product information.
Description
The NF-κB p65 Antibody Sampler Kit contains reagents to examine NF-κB p65/RelA phosphorylation at Ser468 and Ser536; acetylation at Lys310; and total p65 levels.
Storage
Background
Transcription factors of the nuclear factor κB (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 translocates to the nucleus (9-11).
RelA/p65 is a subunit of the NF-κB transcription complex, which plays a crucial role in inflammatory and immune responses. The complex is composed of various homodimeric and heterodimeric Rel family member combinations, the activity of which is modulated by post-translational modifications including phosphorylation and acetylation. p65 phosphorylation by PKA and/or MSK1 at Ser276 allows for increased interaction with the transcriptional coactivator p300/CBP to enhance transcriptional activity. NF-κB dimer assembly with IκB, as well as its DNA binding and transcriptional activities, are regulated by p300/CBP acetyltransferases that principally target Lys218, Lys221 and Lys310 (12-14). This process is reciprocally regulated by histone deacetylases (HDACs); several HDAC inhibitors have been shown to activate NF-κB (12-14). T-cell co-stimulation and Calyculin A have both been shown to increase Ser468 phosphorylation (15,16). IKKβ (but not IKKα) and GSK-3β both target this site (16,17), which appears to have a negative regulatory role not involving inhibition of nuclear translocation after TNF-α or IL-1β stimulation (17). p65 phosphorylation at Ser536 regulates activation, nuclear localization, protein-protein interactions, transcriptional activity, and apoptosis (18-22).
- Baeuerle, P.A. and Henkel, T. (1994) Annu Rev Immunol 12, 141-79.
- Baeuerle, P.A. and Baltimore, D. (1996) Cell 87, 13-20.
- Haskill, S. et al. (1991) Cell 65, 1281-9.
- Thompson, J.E. et al. (1995) Cell 80, 573-82.
- Whiteside, S.T. et al. (1997) EMBO J 16, 1413-26.
- Traenckner, E.B. et al. (1995) EMBO J 14, 2876-83.
- Scherer, D.C. et al. (1995) Proc Natl Acad Sci USA 92, 11259-63.
- Chen, Z.J. et al. (1996) Cell 84, 853-62.
- Senftleben, U. et al. (2001) Science 293, 1495-9.
- Coope, H.J. et al. (2002) EMBO J 21, 5375-85.
- Xiao, G. et al. (2001) Mol Cell 7, 401-9.
- Ashburner, B.P. et al. (2001) Mol Cell Biol 21, 7065-77.
- Mayo, M.W. et al. (2003) J Biol Chem 278, 18980-9.
- Chen, L.F. et al. (2002) EMBO J 21, 6539-48.
- Mattioli, I. et al. (2004) Blood 104, 3302-4.
- Buss, H. et al. (2004) J Biol Chem 279, 49571-4.
- Schwabe, R.F. and Sakurai, H. (2005) FASEB J 19, 1758-60.
- Doyle, S.L. et al. (2005) J Biol Chem 280, 23496-501.
- Sasaki, C.Y. et al. (2005) J Biol Chem 280, 34538-47.
- Mattioli, I. et al. (2004) J Immunol 172, 6336-44.
- Bae, J.S. et al. (2003) Biochem Biophys Res Commun 305, 1094-8.
- Buss, H. et al. (2004) J Biol Chem 279, 55633-43.
Background References
Trademarks and Patents
限制使用
除非 CST 的合法授书代表以书面形式书行明确同意，否书以下条款适用于 CST、其关书方或分书商提供的书品。 任何书充本条款或与本条款不同的客书条款和条件，除非书 CST 的合法授书代表以书面形式书独接受， 否书均被拒书，并且无效。
专品专有“专供研究使用”的专专或专似的专专声明， 且未专得美国食品和专品管理局或其他外国或国内专管机专专专任何用途的批准、准专或专可。客专不得将任何专品用于任何专断或治专目的， 或以任何不符合专专声明的方式使用专品。CST 专售或专可的专品提供专作专最专用专的客专，且专用于研专用途。将专品用于专断、专防或治专目的， 或专专售（专独或作专专成）或其他商专目的而专专专品，均需要 CST 的专独专可。客专：(a) 不得专独或与其他材料专合向任何第三方出售、专可、 出借、捐专或以其他方式专专或提供任何专品，或使用专品制造任何商专专品，(b) 不得复制、修改、逆向工程、反专专、 反专专专品或以其他方式专专专专专品的基专专专或技专，或使用专品开专任何与 CST 的专品或服专专争的专品或服专， (c) 不得更改或专除专品上的任何商专、商品名称、徽专、专利或版专声明或专专，(d) 只能根据 CST 的专品专售条款和任何适用文档使用专品， (e) 专遵守客专与专品一起使用的任何第三方专品或服专的任何专可、服专条款或专似专专