ArticleMolecular and cellular biology2001
Functional analysis of the leukemia protein ELL: evidence for a role in the regulation of cell growth and survival.
Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 36 citations in OpenAlex.
- Decoding adipocyte heterogeneity through single-nucleus transcriptomics unveils subtype-specific adipocytes orchestrate immunosuppressive niches in breast cancer.Journal for immunotherapy of cancer · 2026Article
- EAF2: a tumor suppressor gene with multi-aspect functions.Frontiers in pharmacology · 2024Review
- Sequence, structural and functional conservation among the human and fission yeast ELL and EAF transcription elongation factors.Molecular biology reports · 2022Article
- Atypical Rearrangements in APL-Like Acute Myeloid Leukemias: Molecular Characterization and Prognosis.Frontiers in oncology · 2022Review
- ELL2 Is Required for the Growth and Survival of AR-Negative Prostate Cancer Cells.Cancer management and research · 2020Article
- A Meta-Analysis of Genome-Wide Association Studies of Growth Differentiation Factor-15 Concentration in Blood.Frontiers in genetics · 2018Article
- Article
- Selective expression of the transcription elongation factor ELL3 in B cells prior to ELL2 drives proliferation and survival.Molecular immunology · 2017Article
- Ell3 stimulates 5-FU resistance in a breast cancer cell line.Oncology letters · 2017Article
- ELL targets c-Myc for proteasomal degradation and suppresses tumour growth.Nature communications · 2016Article
- Krüppel-like factor 9 is a circadian transcription factor in human epidermis that controls proliferation of keratinocytes.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Ell3 enhances differentiation of mouse embryonic stem cells by regulating epithelial-mesenchymal transition and apoptosis.PloS one · 2012Article
- Identification of PITX1 as a TERT suppressor gene located on human chromosome 5.Molecular and cellular biology · 2011Article
- ELL is an HIF-1alpha partner that regulates and responds to hypoxia response in PC3 cells.The Prostate · 2010Article
- AFF4, a component of the ELL/P-TEFb elongation complex and a shared subunit of MLL chimeras, can link transcription elongation to leukemia.Molecular cell · 2010Article
- Elongation factor ELL (Eleven-Nineteen Lysine-rich Leukemia) acts as a transcription factor for direct thrombospondin-1 regulation.The Journal of biological chemistry · 2009Article
- FB1, an E2A fusion partner in childhood leukemia, interacts with U19/EAF2 and inhibits its transcriptional activity.Cancer letters · 2007Article
- Apoptosis induction and growth suppression by U19/Eaf2 is mediated through its ELL-binding domain.The Prostate · 2007Article
- Mutational analysis of an RNA polymerase II elongation factor in Drosophila melanogaster.Molecular and cellular biology · 2005Article
- dELL is an essential RNA polymerase II elongation factor with a general role in development.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ELL gene encodes an RNA polymerase II transcription factor that frequently undergoes translocation with the MLL gene in acute human myeloid leukemia. Here, we report that ELL can regulate cell proliferation and survival. In order to better understand the physiological role of the ELL protein, we have developed an ELL-inducible cell line. Cells expressing ELL were uniformly inhibited for growth by a loss of the G(1) population and an increase in the G(2)/M population. This decrease in cell growth is followed by the condensation of chromosomal DNA, activation of caspase 3, poly(ADP ribose) polymerase cleavage, and an increase in sub-G(1) population, which are all indicators of the process of programmed cell death. In support of the role of ELL in induction of cell death, expression of an ELL antisense RNA or addition of the caspase inhibitor ZVAD-fmk results in a reversal of ELL-mediated death. We have also demonstrated that the C-terminal domain of ELL, which is conserved among the ELL family of proteins that we have cloned (ELL, ELL2, and ELL3), is required for ELL's activity in the regulation of cell growth. These novel results indicate that ELL can regulate cell growth and survival and may explain how ELL translocations result in the development of human malignancies.
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.