ArticleProceedings of the National Academy of Sciences of the United States of America2013
GABP transcription factor is required for development of chronic myelogenous leukemia via its control of PRKD2.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 28 citations in OpenAlex.
- PRKD2 as a novel target for targeting the diabetes-osteoporosis nexus.Scientific reports · 2025Article
- GABPα inhibits tumor progression and angiogenesis via a novel 18-bp indel withinCancer biomarkers : section A of Disease markers · 2024Article
- GABPA inhibits tumorigenesis in clear cell renal cell carcinoma by regulating ferroptosis through ACSL4.Scientific reports · 2024Article
- Random walk with restart on multilayer networks: from node prioritisation to supervised link prediction and beyond.BMC bioinformatics · 2024Article
- HAX1-dependent control of mitochondrial proteostasis governs neutrophil granulocyte differentiation.The Journal of clinical investigation · 2022Article
- Advances in molecular characterization of myeloid proliferations associated with Down syndrome.Frontiers in genetics · 2022Review
- A mitochondria-targeted caffeic acid derivative reverts cellular and mitochondrial defects in human skin fibroblasts from male sporadic Parkinson's disease patients.Redox biology · 2021Article
- GABPA Expression in Endometrial Carcinoma: A Prognostic Marker.Disease markers · 2021Article
- GABPA is a master regulator of luminal identity and restrains aggressive diseases in bladder cancer.Cell death and differentiation · 2020Article
- Loss of Kat2a enhances transcriptional noise and depletes acute myeloid leukemia stem-like cells.eLife · 2020Article
- Hematopoietic Stem Cell Transcription Factors in Cardiovascular Pathology.Frontiers in genetics · 2020Review
- Identifying clusters ofGenome research · 2019Article
- Metabolic, Anti-apoptotic and Immune Evasion Strategies of Primary Human Myeloma Cells Indicate Adaptations to Hypoxia.Molecular & cellular proteomics : MCP · 2019Article
- GABPA inhibits invasion/metastasis in papillary thyroid carcinoma by regulating DICER1 expression.Oncogene · 2019Article
- Ets transcription factor GABP controls T cell homeostasis and immunity.Nature communications · 2017Article
- Article
- Cooperative Activity of GABP with PU.1 or C/EBPε Regulates Lamin B Receptor Gene Expression, Implicating Their Roles in Granulocyte Nuclear Maturation.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Functional and therapeutic significance of protein kinase D enzymes in invasive breast cancer.Cellular and molecular life sciences : CMLS · 2015Review
- MiR-320e is a novel prognostic biomarker in colorectal cancer.British journal of cancer · 2015Article
- Leukemia stem cells: the root of chronic myeloid leukemia.Protein & cell · 2015Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Hematopoietic stem cells (HSCs) are the source of all blood lineages, and HSCs must balance quiescence, self-renewal, and differentiation to meet lifelong needs for blood cell development. Transformation of HSCs by the breakpoint cluster region-ABL tyrosine kinase (BCR-ABL) oncogene causes chronic myelogenous leukemia (CML). The E-twenty six (ets) transcription factor GA binding protein (GABP) is a tetrameric transcription factor complex that contains GABPα and GABPβ proteins. Deletion in bone marrow of Gabpa, the gene that encodes the DNA-binding component, caused cell cycle arrest in HSCs and profound loss of hematopoietic progenitor cells. Loss of Gabpα prevented development of CML, although mice continued to generate BCR-ABL-expressing Gabpα-null cells for months that were serially transplantable and contributed to all lineages in secondary recipients. A bioinformatic screen identified the serine-threonine kinase protein kinase D2 (PRKD2) as a potential effector of GABP in HSCs. Prkd2 expression was markedly reduced in Gabpα-null HSCs and progenitor cells. Reduced expression of PRKD2 or pharmacologic inhibition decreased cell cycling, and PRKD2 rescued growth of Gabpα-null BCR-ABL-expressing cells. Thus, GABP is required for HSC cell cycle entry and CML development through its control of PRKD2. This offers a potential therapeutic target in leukemia.
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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 Socratic graph.