ArticleCell cycle (Georgetown, Tex.)2013
Cell context in the control of self-renewal and proliferation regulated by MLL1.
Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 12 citations in OpenAlex.
- Clinical immunology in chromatinopathies: a scoping review.Frontiers in immunology · 2026Article
- Histone MethyltransferaseAntioxidants (Basel, Switzerland) · 2022Article
- A chromatin perspective on metabolic and genotoxic impacts on hematopoietic stem and progenitor cells.Cellular and molecular life sciences : CMLS · 2020Review
- Hematopoietic transformation in the absence of MLL1/KMT2A: distinctions in target gene reactivation.Cell cycle (Georgetown, Tex.) · 2019Article
- MLL1 is essential for retinal neurogenesis and horizontal inner neuron integrity.Scientific reports · 2018Article
- MLL1 Promotes IL-7 Responsiveness and Survival during B Cell Differentiation.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- RNA Polymerase II-Dependent Transcription Initiated by Selectivity Factor 1: A Central Mechanism Used by MLL Fusion Proteins in Leukemic Transformation.Frontiers in genetics · 2018Review
- Molecular mechanisms of MLL-associated leukemia.International journal of hematology · 2015Review
- Musashi2 sustains the mixed-lineage leukemia-driven stem cell regulatory program.The Journal of clinical investigation · 2015Article
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 at 2 institutions in 1 country.
Funding
Abstract
Mixed lineage leukemia 1 (MLL1) is a gene that is disrupted by chromosomal translocation characteristically in a large proportion of infant leukemia and also in a fraction of childhood and adult leukemia. MLL1 encodes a chromatin regulatory protein related to the Drosophila Trithorax protein, a well-studied epigenetic factor that functions during development to maintain expression of its target genes. Although tremendous progress has been made understanding the downstream targets of MLL1 fusion oncoproteins and how manipulation of those targets impacts leukemogenesis, very little is known regarding how the initial expression of an MLL1 fusion protein impacts on that cell's behavior, particularly how the cell cycle is affected. Here, we focused on the function of endogenous MLL1 in the stem and progenitor cell types that are likely to be transformed upon MLL1 translocation. Our studies reveal a differential response of stem or progenitor populations to acute loss of MLL1 on proliferation and survival. These data suggest that the effects of MLL1 fusion oncoproteins will initiate the leukemogenic process differentially depending on the differentiation state of the cell type in which the translocation occurs.
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.