ArticleGenesis (New York, N.Y. : 2000)2011
A new allele of Lyl1 confirms its important role in hematopoietic stem cell function.
Article in Genesis (New York, N.Y. : 2000), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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
5 citing papers in PubMed, 11 citations in OpenAlex.
- LYL1 is critical for adult hematopoietic stem cell-derived B and T lymphopoiesis.Scientific reports · 2026Article
- The response to kidney injury is epigenetically regulated through the activation of bivalent genes.American journal of physiology. Renal physiology · 2026Article
- Lyl1-deficiency promotes inflammatory responses and increases mycobacterial burden in response toFrontiers in immunology · 2022Article
- Article
- The transcription factor Lyl-1 regulates lymphoid specification and the maintenance of early T lineage progenitors.Nature immunology · 2012Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Lyl1 codes for a bHLH protein that is an important regulator of hematopoietic stem cell function. An existing mutant allele of Lyl1 features a lacZ gene inserted in-frame into the fourth exon, leaving behind the N-terminus and the DNA-binding basic region, resulting in a translated chimeric protein. Here, we have generated a null allele, which allowed us to examine residual function of the N-terminus in the absence of a bHLH region. The new Lyl1-/- mouse model exhibited a reduced ability to generate lymphoid lineages and a somewhat more severe hematopoietic repopulation defect when transplanting purified hematopoietic stem cells. Our data show that in the absence of the HLH but presence of the N-terminus, residual function of the Lyl1 is detectable but relatively minor. The new model may be of use for studies of Lyl1 in which a null allele is required, or for which presence of the LacZ may complicate the combined use of additional mouse models bearing the lacZ marker.
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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.