ArticleBMC molecular biology2010
Essential role for ALCAM gene silencing in megakaryocytic differentiation of K562 cells.
Article in BMC molecular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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.
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Who cites it
6 citing papers in PubMed, 18 citations in OpenAlex.
- Human thrombopoiesis depends on Protein kinase Cδ/protein kinase Cε functional couple.Haematologica · 2016Article
- Article
- Megakaryocytic differentiation of K562 cells induced by PMA reduced the activity of respiratory chain complex IV.PloS one · 2014Article
- Alcam regulates long-term hematopoietic stem cell engraftment and self-renewal.Stem cells (Dayton, Ohio) · 2013Article
- Cloning of the human activated leukocyte cell adhesion molecule promoter and identification of its tissue-independent transcriptional activation by Sp1.Cellular & molecular biology letters · 2012Article
- A regulatory role for CHD2 in myelopoiesis.EpigeneticsArticle
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundActivated leukocyte cell adhesion molecule (ALCAM/CD166) is expressed by hematopoietic stem cells. However, its role in hematopoietic differentiation has not previously been defined.
resultsIn this study, we show that ALCAM expression is silenced in erythromegakaryocytic progenitor cell lines. In agreement with this finding, the ALCAM promoter is occupied by GATA-1 in vivo, and a cognate motif at -850 inhibited promoter activity in K562 and MEG-01 cells. Gain-of-function studies showed that ALCAM clusters K562 cells in a process that requires PKC. Induction of megakaryocytic differentiation in K562 clones expressing ALCAM activated PKC-δ and triggered apoptosis.
conclusionsThere is a lineage-specific silencing of ALCAM in bi-potential erythromegakaryocytic progenitor cell lines. Marked apoptosis of ALCAM-expressing K562 clones treated with PMA suggests that aberrant ALCAM expression in erythromegakaryocytic progenitors may contribute to megakaryocytopenia.
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