抗体

NFkB p65(C20)抗体

MBS440031

0.2毫克

240美元

多克隆

兔

未共轭

人类, 小鼠

免疫印迹, 免疫组化, 免疫沉淀

抗体

NFkB p65(C20)抗体

NFkB p65

NFkB p65

多克隆

兔

小鼠, 大鼠, 人类

NFkB p65 (C20) MBS440031, freacts with NFkB p65 of mouse, rat and human origin by Western Blotting, immunoprecipitation and immunohistchemistry. Western Blotting starting dilution: 1:400-1:1000.

200微克/毫升兔多克隆IgG在1毫升PBS含0.1% 叠氮化钠和0.2% 明胶

0.2毫克/毫升

Store this product at 4 degree C, do not freeze. The product is stable for one year from the date of shipment.

免疫印迹(免疫印迹), 免疫沉淀(免疫沉淀), 免疫组化(免疫组化)

NFkB p65 (C20) DB033 reacts with NFkB p65 of mouse, rat, and human origin by western blotting, immunoprecipitation,immunohistochemistry and EMSA. Western blotting starting dilution: 1:400-1:1000.

Origin: NFkB p65 (C20) is provided as an affinity purified rabbit polyclonal antibody, raised against a peptide mapping to the carboxy terminus of human NFkB p65. Product Details: Each vial contains 200ug/ml of affinity-purified rabbit IgG, NFkB p65 MBS440031, in 1 ml PBS containing 0.1% sodium azide and 0.2% gelatin. Competition Studies: A blocking peptide is also available, MBS443031, for use in competition studies. Each vial contains 100ug of peptide in 0.5ml PBS 0.1% sodium azide and 100 ug BSA.

Members of the rel/NFkB family of transcription factors are involved in the regulation of cellular responses, such as growth, development, and the inflammatory response. They share a structural motif known as the rel homology region (RHR), the C-terminal one third of which mediates protein dimerization (2, 6, 8). Complexes of p50 (NF-kB1) or p52 (NF-kB2) are generated through the processing of p105 and p100 precursors, respectively. These are usually associated with members of the Rel family (p65, c-Rel, Rel B). The homo- and heterodimer formed through combinations of NFkB/Rel proteins bind distinct kB sites to regulate the transcription of different genes (7, 9). In resting cells, NFkB is retained in the cytoplasm bound to inhibitory proteins of the IkB family. Degradation of IkB proteins occurs with cell activation, via of variety of signals, including inflammatory cytokines and bacterial lipopolysaccharides (LPS) as well as oxidative and fluid mechanical stress. This results in nuclear translocation of NFkB and the transcriptional gene activation of proinflammatory genes (1, 9). It has been suggested that NFkB plays a role in the development of numerous pathological states. Activation of NFkB induces gene programs leading to transcription of factors that promote inflammation, such as leukocyte adhesion molecules, cytokines, and chemokines. It is also thought that there are some substances with possible anti-inflammatory effects that are also NFkB regulated. There is some evidence indicating NFkB as a key factor in the pathophysiology of cardiac ischemia-reperfusion injury as well as the development of insulin dependent Diabetes Mellitus (4, 3).

1.) Leitch D, Barrans SL, Jack AS, Owen RG. 2003. Dysregulation of apoptosis in Waldenstrom's macroglobulinemia does not involve nuclear factor kappa B activation. Semin Oncol. Apr;30(2):161-4.2.) Stjernholm-Vladic Y, Stygar D, Mansson C, Masironi B, Akerberg S, Wang H, Ekman-Ordeberg G, and Sahlin L. 2004. Factors involved in the inflammatory events of cervical ripening in humans. Reproductive Biology & Endocrinology 2:74.3.) Lee KW, Lee Y, Kwon HJ and Kim DS. 2005. Sp1-associated activation of macrophage inflammatory protein-2 promoter by CpG-oligodeoxynucleotide and lipopolysaccharide. Cell and Molecular Life Sciences 62:188-198. 4.)Joo SS, Won TJ, Lee do I. Potential role of ursodeoxycholic acid in suppression of nuclear factor kappa B in microglial cell line (BV-2). Arch Pharm Res. 2004 Sep;27(9):954-60. 5.) Popov Y, Patsenker E, Bauer M, Niedobitek E, Schulze-Krebs A, Schuppan D. 2006. Halofuginone induces matrix metalloproteinases in rat hepatic stellate cells via activation of p38 and NFkappaB. J Biol Chem. 281(22):15090-8.6.) Longpré F, Garneau P, Christen Y, Ramassamy C. 2006. Protection by EGb 761 against beta-amyloid-induced neurotoxicity: involvement of NF-kappaB, SIRT1, and MAPKs pathways and inhibition of amyloid fibril formation. Free Radic Biol Med. Dec 15;41(12):1781-94. 7.) Kang HB, Kim YE, Kwon HJ, Sok DE, Lee Y. 2007. Enhancement of NF-kappaB expression and activity upon differentiation of human embryonic stem cell line SNUhES3. Stem Cells Dev. 2007 Aug;16(4):615-23.8.) Lee KW, Lee Y, Kim DS, Kwon HJ. 2006. Direct role of NF-kappaB activation in Toll-like receptor-triggered HLA-DRA expression. Eur J Immunol. May;36(5):1254-66.9.) Fan Z, Söder S, Oehler S, Fundel K, Aigner T. 2007. Activation of interleukin-1 signaling cascades in normal and osteoarthritic articular cartilage. Am J Pathol. Sep;171(3):938-46. 1. Lentsch AB, Ward PA. The NFkappaBb/IkappaB system in acute inflammation. Arch Immunol Ther Exp (Warsz). 48(2): 59-63. 2. Hatada EN, Krappmann D, Scheidereit C. NF-kappaB and the innate immune response. Curr Opin Immunol. 2000 Feb; 12(1): 52-8 3. Ho E, Bray TM. Antioxidants, NFkappaB activation, and diabetogenesis. Proc Soc Exp Biol Med. 1999 Dec; 222(3): 205-13.4. Valen G, Yan ZQ, Hansson GK. Nuclear factor kappa-B and the heart. J Am Coll Cardiol. 2001 Aug; 38(2): 307-14.5. Chen FE, Kempiak S, Huang DB, Phelps C, Ghosh G. Construction, expression, purification and functional analysis of recombinant NFkappaB p50/p65 heterodimer. Protein Eng. 1999 May; 12(5): 423-8.6. Sengchanthalangsy LL, Datta S, Huang DB, Anderson E, Braswell EH, Ghosh G. Characterization of the dimer interface of transcription factor NFkappaB p50 homodimer. J Mol Biol. 1999 Jun 18; 289(4): 1029-40.7. Huang DB, Huxford T, Chen YQ, Ghosh G. The role of DNA in the mechanism of NFkappaB dimer formation: crystal structures of the dimerization domains of the p50 and p65 subunits. Structure. 1997 Nov 15; 5(11): 1427-36.8. Magnani M, Crinelli R, Bianchi M, Antonelli A. The ubiquitin-dependent proteolytic system and other potential targets for the modulation of nuclear factor-kB (NF-kB). Curr Drug Targets. 2000 Dec; 1(4): 387-99.

0.2毫克

240美元