ArticleMolecular and cellular biology2002
NF-kappaB1 can inhibit v-Abl-induced lymphoid transformation by functioning as a negative regulator of cyclin D1 expression.
Article in Molecular and cellular biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- NFKB1 as a key player in Tumor biology: from mechanisms to therapeutic implications.Cell biology and toxicology · 2025Pooled it
- p50 mono-ubiquitination and interaction with BARD1 regulates cell cycle progression and maintains genome stability.Nature communications · 2020Article
- Reduced miR-3127-5p expression promotes NSCLC proliferation/invasion and contributes to dasatinib sensitivity via the c-Abl/Ras/ERK pathway.Scientific reports · 2014Article
- Plasmacytomagenesis in Eμ-v-abl transgenic mice is accelerated when apoptosis is restrained.Blood · 2014Article
- Prevalence of bortezomib-resistant constitutive NF-kappaB activity in mantle cell lymphoma.Molecular cancer · 2008Article
- Viral induction of AID is independent of the interferon and the Toll-like receptor signaling pathways but requires NF-kappaB.The Journal of experimental medicine · 2007Article
- Expression of the NF-kappaB-responsive gene BTG2 is aberrantly regulated in breast cancer.Oncogene · 2004Article
- The transcription factors c-rel and RelA control epidermal development and homeostasis in embryonic and adult skin via distinct mechanisms.Molecular and cellular biology · 2004Article
- To be, or not to be: NF-kappaB is the answer--role of Rel/NF-kappaB in the regulation of apoptosis.Oncogene · 2003Review
- Article
- Long-term culture of keratinocyte-like cells derived from mouse embryonic stem cells.In vitro cellular & developmental biology. AnimalArticle
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mounting evidence implicates deregulated Rel/NF-kappaB signaling as a common feature of lymphoid malignancies. Despite the fact that they promote the survival and proliferation of normal lymphocytes, the underlying mechanisms by which various Rel/NF-kappaB proteins with different transcriptional regulatory capacities might facilitate transformation remain to be established. Here we show that the proliferation and tumorigenicity of Abelson murine leukemia virus (A-MuLV)-transformed pre-B cells are enhanced in the absence of NF-kappaB1 and that this coincides with elevated levels of cyclin D1. Support for a link between cyclin D1 expression and v-Abl transformation came from the finding that proliferation of transformed pre-B cells was reduced in the absence of cyclin D1, while enforced cyclin D1 expression increased the proliferation and tumorigenicity of wild-type transformants. A reduction in endogenous cyclin D1 levels that coincided with NF-kappaB1 transgene reversal of enhanced nfkb1(-/-) pre-B-cell transformation, coupled with NF-kappaB1 inhibition of v-Abl-induced kappaB-dependent murine cyclin D1 transcription, lends support to a model in which v-Abl-induced cyclin D1 transcription in transformed pre-B cells is controlled by Rel/NF-kappaB dimers with different activities.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.