ReviewEMBO reports2002
Cell-nonautonomous function of the retinoblastoma tumour suppressor protein: new interpretations of old phenotypes.
Review in EMBO reports, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed, 19 citations in OpenAlex.
- Inactivation of Rb in stromal fibroblasts promotes epithelial cell invasion.The EMBO journal · 2012Article
- Article
- The role of the RB tumour suppressor pathway in oxidative stress responses in the haematopoietic system.Nature reviews. Cancer · 2008Review
- Rb intrinsically promotes erythropoiesis by coupling cell cycle exit with mitochondrial biogenesis.Genes & development · 2008Article
- Rb regulates interactions between hematopoietic stem cells and their bone marrow microenvironment.Cell · 2007Article
- The Rb tumor suppressor is required for stress erythropoiesis.The EMBO journal · 2004Article
- PU.1 and pRB interact and cooperate to repress GATA-1 and block erythroid differentiation.Molecular and cellular biology · 2003Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Loss of the retinoblastoma protein (pRb) induces a cell-nonautonomous defect in both erythroid and neuronal differentiation. It has previously been thought that this reflects a requirement for pRb function in cells that normally support erythropoiesis and neurogenesis, rather than in the erythrocytes or neurons themselves. However, recent studies have challenged this interpretation, and it appears that erythrocytes and neurons themselves have the intrinsic requirement for pRb function. This requirement can be bypassed by signals supplied by wild-type erythroid or neuronal cells. The existence of such a signalling mechanism has implications not only in understanding pRb function but also in the interpretation of other cell-nonautonomous phenotypes.
Indexed as
Identifiers
What OpenQuestion holds
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.