ArticleGenesis (New York, N.Y. : 2000)2010
p89c-Myb is not required for fetal or adult hematopoiesis.
Article in Genesis (New York, N.Y. : 2000), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 6 citations in OpenAlex.
- SRSF1 plays a critical role in invariant natural killer T cell development and function.Cellular & molecular immunology · 2021Article
- Physiological and Aberrant γ-Globin Transcription During Development.Frontiers in cell and developmental biology · 2021Review
- MYB - A regulatory factor in hematopoiesis.Gene · 2018Review
- Expression of p89(c-Mybex9b), an alternatively spliced form of c-Myb, is required for proliferation and survival of p210BCR/ABL-expressing cells.Blood cancer journal · 2012Article
- Myb proteins: angels and demons in normal and transformed cells.Frontiers in bioscience (Landmark edition) · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The c-myb gene encodes two proteins, termed p75 and p89. Of these, the larger isoform is transcribed from an alternatively spliced message that contains an additional exon, exon 9A. Disruption of the c-myb locus in mice results in embryonic lethality due to defective hematopoiesis and in the adult, tissue-specific inactivation of c-myb in hematopoietic tissues blocks differentiation along several lineages. The c-myb knock-out mouse models described thus far result in the disruption of both the p75 and p89 isoforms, making it impossible to assign a definitive role to p89(c-Myb) in development and hematopoiesis. We have therefore generated a null-mutant mouse where exon 9A has been systemically deleted that results in the absence of only the p89-myb transcript and protein. Unlike disruption of both forms of the c-myb gene, loss of only the p89-encoding isoform does not have any deleterious effects on mammalian hematopoiesis and development.
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.