ArticleMolecular and cellular biology2006
p27Kip1 and p130 cooperate to regulate hematopoietic cell proliferation in vivo.
Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- A replicative self-renewal model for long-lived plasma cells: questioning irreversible cell cycle exit.Frontiers in immunology · 2013Review
- p27Kip1 represses transcription by direct interaction with p130/E2F4 at the promoters of target genes.Oncogene · 2012Article
- Cyclin D1 and cdk4 mediate development of neurologically destructive oligodendroglioma.Cancer research · 2011Article
- Chemical genetics approach to restoring p27Kip1 reveals novel compounds with antiproliferative activity in prostate cancer cells.BMC biology · 2010Article
- PIM1 kinase is destabilized by ribosomal stress causing inhibition of cell cycle progression.Oncogene · 2010Article
- Single round of antigen receptor signaling programs naive B cells to receive T cell help.Immunity · 2010Article
- Development of a malignancy-associated proteomic signature for diffuse large B-cell lymphoma.The American journal of pathology · 2009Article
- Regulation of B-cell proliferation and differentiation by pre-B-cell receptor signalling.Nature reviews. Immunology · 2009Review
- Many forks in the path: cycling with FoxO.Oncogene · 2008Review
- Promiscuous and lineage-specific roles of cell cycle regulators in haematopoiesis.Cell division · 2007Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
Abstract
To investigate the potential functional cooperation between p27Kip1 and p130 in vivo, we generated mice deficient for both p27Kip1 and p130. In p27Kip1-/-; p130-/- mice, the cellularity of the spleens but not the thymi is significantly increased compared with that of their p27Kip1-/- counterparts, affecting the lymphoid, erythroid, and myeloid compartments. In vivo cell proliferation is significantly augmented in the B and T cells, monocytes, macrophages, and erythroid progenitors in the spleens of p27Kip1-/-; p130-/- animals. Immunoprecipitation and immunodepletion studies indicate that p130 can compensate for the absence of p27Kip1 in binding to and repressing CDK2 and is the predominant CDK-inhibitor associated with the inactive CDK2 in the p27Kip1-/- splenocytes. The finding that the p27Kip1-/-; p130-/- splenic B cells are hypersensitive to mitogenic stimulations in vitro lends support to the concept that the hyperproliferation of splenocytes is not a result of the influence of their microenvironment. In summary, our findings provide genetic and molecular evidence to show that p130 is a bona fide cyclin-dependent kinase inhibitor and cooperates with p27Kip1 to regulate hematopoietic cell proliferation in vivo.
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Registered trials
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.