title: Regulation of IkappaB beta in WEHI 231 mature B cells.
abstract: Constitutive activation of NF-kappaB in WEHI 231 early mature B cells resembles the persistent activation of NF-kappaB that is observed upon prolonged stimulation of other cells. In both cases, NF-kappaB DNA binding complexes are found in the nucleus, despite the abundance of cytosolic IkappaB alpha. Recently, we have shown that prolonged activation of 70Z/3 cells with lipopolysaccharide results in the degradation of IkappaB beta, followed by its subsequent resynthesis as a hypophosphorylated protein. This protein was shown to facilitate transport of a portion of NF-kappaB to the nucleus in a manner that protects it from cytosolic IkappaB alpha. We now demonstrate that the most abundant form of IkappaB beta in WEHI 231 cells is a hypophosphorylated protein. This hypophosphorylated IkappaB beta is found in a stable complex with NF-kappaB in the cytosol and is also detected in NF-kappaB DNA binding complexes in the nucleus. It is likely that hypophosphorylated IkappaB beta in WEHI 231 cells also protects NF-kappaB from IkappaB alpha, thus leading to the continuous nuclear import of this transcription factor.
authors.affiliation: Department of Molecular Biophysics and Biochemistry, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut 06520, USA.
authors.forename: R J
authors.initials: RJ
authors.lastname: Phillips
authors.forename: S
authors.initials: S
authors.lastname: Ghosh
mesh_terms: D000111:Acetylcysteine / Q000031:analogs & derivatives / Q000494:pharmacology; D000975:Antioxidants / Q000494:pharmacology; D001402:B-Lymphocytes / Q000378:metabolism*; D001692:Biological Transport; D002460:Cell Line; D002467:Cell Nucleus / Q000378:metabolism; D002918:Chymotrypsin / Q000037:antagonists & inhibitors; D015853:Cysteine Proteinase Inhibitors / Q000494:pharmacology; D003600:Cytosol / Q000378:metabolism; D004247:DNA / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005246:Feedback; D006023:Glycoproteins / Q000494:pharmacology; D008070:Lipopolysaccharides / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism*; D010766:Phosphorylation; D011518:Proto-Oncogene Proteins / Q000032:analysis / Q000378:metabolism*; D020569:Proto-Oncogene Proteins c-rel; D011759:Pyrrolidines / Q000494:pharmacology; D012333:RNA, Messenger / Q000032:analysis; D013859:Thiocarbamates / Q000494:pharmacology; D014108:Tosylphenylalanyl Chloromethyl Ketone / Q000494:pharmacology; D051841:Transcription Factor RelB; D014157:Transcription Factors
chemical_list: D000975:Antioxidants; D015853:Cysteine Proteinase Inhibitors; D004791:Enzyme Inhibitors; D006023:Glycoproteins; D008070:Lipopolysaccharides; D016328:NF-kappa B; D011518:Proto-Oncogene Proteins; D020569:Proto-Oncogene Proteins c-rel; D011759:Pyrrolidines; D012333:RNA, Messenger; D013859:Thiocarbamates; D014157:Transcription Factors; C039304:calpain inhibitors; C067713:lactacystin; D051841:Transcription Factor RelB; C020972:pyrrolidine dithiocarbamic acid; D014108:Tosylphenylalanyl Chloromethyl Ketone; D004247:DNA; D002918:Chymotrypsin; D000111:Acetylcysteine