Phospho-RelB (Ser552) (D41B9) Rabbit Monoclonal Antibody (SignalFlexTMAlexa Fluor®700 Conjugate)#36461,Cell Signaling Technology (CST),36461
Phospho-RelB (Ser552) (D41B9) XP®Rabbit mAb (SignalFlexTM Alexa Fluor®700 Conjugate) detects endogenous levels of RelB only when phosphorylated at Ser552.
Host
Rabbit
Reactivity
Human, Mouse
Conjugate
SignalFlexTMAlexa Fluor®700 Conjugate
Platform ID
BAB328831494
Cell Signaling Technology (CST)
Contact
Tel: 877-616-2355,978-867-2388
Fax: 877-616-2355
Email:
Specifications
Scientific 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).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).Baeuerle, P.A. and Henkel, T. (1994)Annu Rev Immunol12, 141-79.Baeuerle, P.A. and Baltimore, D. (1996)Cell87, 13-20.Haskill, S. et al. (1991)Cell65, 1281-9.Thompson, J.E. et al. (1995)Cell80, 573-82.Whiteside, S.T. et al. (1997)EMBO J16, 1413-26.Traenckner, E.B. et al. (1995)EMBO J14, 2876-83.Scherer, D.C. et al. (1995)Proc Natl Acad Sci USA92, 11259-63.Chen, Z.J. et al. (1996)Cell84, 853-62.Senftleben, U. et al. (2001)Science293, 1495-9.Coope, H.J. et al. (2002)EMBO J21, 5375-85.Xiao, G. et al. (2001)Mol Cell7, 401-9.Ryseck, R.P. et al. (1992)Mol Cell Biol12, 674-84.Bours, V. et al. (1994)Oncogene9, 1699-702.Weih, F. et al. (1995)Cell80, 331-40.Burkly, L. et al. (1995)Nature373, 531-6.Marienfeld, R. et al. (2001)Oncogene20, 8142-7.Alternate NamesI-Rel; IMD53; IREL; REL-B; RELB; RELB proto-oncogene, NF-kB subunit; Transcription factor RelB; v-rel avian reticuloendotheliosis viral oncogene homolog B (nuclear factor of kappa light polypeptide gene enhancer in B-cells 3); v-rel reticuloendotheliosis viral oncogene homolog B; v-rel reticuloendotheliosis viral oncogene homolog B, nuclear factor of kappa light polypeptide gene enhancer in B-cells 3
Synonyms
I-Rel; IMD53; IREL; REL-B; RELB; RELB proto-oncogene, NF-kB subunit; Transcription factor RelB; v-rel avian reticuloendotheliosis viral oncogene homolog B (nuclear factor of kappa light polypeptide gene enhancer in B-cells 3); v-rel reticuloendotheliosis viral oncogene homolog B; v-rel reticuloendotheliosis viral oncogene homolog B, nuclear factor of kappa light polypeptide gene enhancer in B-cells 3
Category Paths
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