ArticleMolecular and cellular biology2004
Regulation of constitutive p50/c-Rel activity via proteasome inhibitor-resistant IkappaBalpha degradation in B cells.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 36 citations in OpenAlex.
- Acetyl-L-carnitine (ALCAR) for the prevention of chemotherapy-induced peripheral neuropathy in patients with relapsed or refractory multiple myeloma treated with bortezomib, doxorubicin and low-dose dexamethasone: a study from the Wisconsin Oncology Network.Cancer chemotherapy and pharmacology · 2014Trial
- Ectopic CH60 mediates HAPLN1-induced cell survival signaling in multiple myeloma.Life science alliance · 2023Article
- Vitamin D receptor absence does not enhance intestinal tumorigenesis in ApcPirc/+rats.Biology open · 2022Article
- HAPLN1 confers multiple myeloma cell resistance to several classes of therapeutic drugs.PloS one · 2022Article
- Hyaluronan and proteoglycan link protein 1 (HAPLN1) activates bortezomib-resistant NF-κB activity and increases drug resistance in multiple myeloma.The Journal of biological chemistry · 2018Article
- Prognostic impact of c-Rel nuclear expression and REL amplification and crosstalk between c-Rel and the p53 pathway in diffuse large B-cell lymphoma.Oncotarget · 2015Article
- Identification of new IκBα complexes by an iterative experimental and mathematical modeling approach.PLoS computational biology · 2014Article
- Fibromodulin suppresses nuclear factor-kappaB activity by inducing the delayed degradation of IKBA via a JNK-dependent pathway coupled to fibroblast apoptosis.The Journal of biological chemistry · 2011Article
- Nuclear export of the NF-κB inhibitor IκBα is required for proper B cell and secondary lymphoid tissue formation.Immunity · 2011Article
- Bone marrow stromal cells from multiple myeloma patients uniquely induce bortezomib resistant NF-kappaB activity in myeloma cells.Molecular cancer · 2010Article
- MAGUK-controlled ubiquitination of CARMA1 modulates lymphocyte NF-kappaB activity.Molecular and cellular biology · 2010Article
- Altered BAFF-receptor signaling and additional modifier loci contribute to systemic autoimmunity in A/WySnJ mice.European journal of immunology · 2009Article
- RNAi-mediated c-Rel silencing leads to apoptosis of B cell tumor cells and suppresses antigenic immune response in vivo.PloS one · 2009Article
- Bortezomib-resistant nuclear factor-kappaB activity in multiple myeloma cells.Molecular cancer research : MCR · 2008Article
- Prevalence of bortezomib-resistant constitutive NF-kappaB activity in mantle cell lymphoma.Molecular cancer · 2008Article
- Systemic autoimmunity in BAFF-R-mutant A/WySnJ strain mice.European journal of immunology · 2008Article
- NF-kappaB activation by combinations of NEMO SUMOylation and ATM activation stresses in the absence of DNA damage.Oncogene · 2007Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Constitutive NF-kappaB activity has emerged as an important cell survival component of physiological and pathological processes, including B-cell development. In B cells, constitutive NF-kappaB activity includes p50/c-Rel and p52/RelB heterodimers, both of which are critical for proper B-cell development. We previously reported that WEHI-231 B cells maintain constitutive p50/c-Rel activity via selective degradation of IkappaBalpha that is mediated by a proteasome inhibitor-resistant, now termed PIR, pathway. Here, we examined the mechanisms of PIR degradation by comparing it to the canonical pathway that involves IkappaB kinase-dependent phosphorylation and beta-TrCP-dependent ubiquitylation of the N-terminal signal response domain of IkappaBalpha. We found a distinct consensus sequence within this domain of IkappaBalpha for PIR degradation. Chimeric analyses of IkappaBalpha and IkappaBbeta further revealed that the ankyrin repeats of IkappaBalpha, but not IkappaBbeta, contained information necessary for PIR degradation, thereby explaining IkappaBalpha selectivity for the PIR pathway. Moreover, we found that PIR degradation of IkappaBalpha and constitutive p50/c-Rel activity in primary murine B cells were maintained in a manner different from B-cell-activating-factor-dependent p52/RelB regulation. Thus, our findings suggest that nonconventional PIR degradation of IkappaBalpha may play a physiological role in the development of B cells in vivo.
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