ArticleOncogene2006
The tumor suppressor p16Ink4a regulates T lymphocyte survival.
Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
13 citing papers in PubMed, 27 citations in OpenAlex.
- IL-23R is a senescence-linked circulating and tissue biomarker of aging.Nature aging · 2025Article
- The Senescence Markers p16INK4A, p14ARF/p19ARF, and p21 in Organ Development and Homeostasis.Cells · 2022Review
- Photosynthesis-inspired HNature communications · 2020Article
- EBV finds a polycomb-mediated, epigenetic solution to the problem of oncogenic stress responses triggered by infection.Frontiers in genetics · 2013Review
- Induction of p16(INK4a) is the major barrier to proliferation when Epstein-Barr virus (EBV) transforms primary B cells into lymphoblastoid cell lines.PLoS pathogens · 2013Article
- Genetic regulation of thymocyte progenitor aging.Seminars in immunology · 2012Review
- Fibroblast growth factor-7 partially reverses murine thymocyte progenitor aging by repression of Ink4a.Blood · 2012Article
- Bone marrow p16INK4a-deficiency does not modulate obesity, glucose homeostasis or atherosclerosis development.PloS one · 2012Article
- Acute lymphoblastic leukemia cells that survive combination chemotherapy in vivo remain sensitive to allogeneic immune effects.Leukemia research · 2011Article
- Article
- Tumor suppressor mechanisms in immune aging.Current opinion in immunology · 2009Review
- High-risk acute lymphoblastic leukemia cells with bcr-abl and INK4A/ARF mutations retain susceptibility to alloreactive T cells.Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation · 2008Article
- Evidence of accelerated ageing in clinical drug addiction from immune, hepatic and metabolic biomarkers.Immunity & ageing : I & A · 2007Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In contrast to other cell cycle inhibitors, the tumor suppressor p16Ink4a is not detectable or expressed at very low levels in embryonic and adult mouse tissues, and therefore it has often been considered as a specialized checkpoint protein that does not participate in the control of normal cell cycle progression. However, Ink4a-/- mice possess increased thymus size and cellularity, thus suggesting the involvement of p16(Ink4a) in the control of thymocyte proliferation. In this study, we found increased numbers of CD8 and CD4 T lymphocytes in thymus and spleen from Ink4a-/- mice. Unexpectedly, this was not related to an increase in T-cell division rates, which were similar in lymphoid organs of Ink4a-/- and wild-type mice. In contrast, T-cell apoptosis rates were significantly decreased in thymus and spleen from Ink4a-/- mice. Moreover, whereas p16Ink4a-deficient and wild-type T cells were equally sensitive to Fas or TCR-mediated apoptosis, the former were clearly more resistant to apoptosis induced by oxidative stress or gamma irradiation. Our results indicate that p16Ink4a function is associated with T-cell apoptosis, and subsequently contributes to the control of T-cell population size in lymphoid organs.
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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.