ArticleExperimental cell research2011
ATRA-induced HL-60 myeloid leukemia cell differentiation depends on the CD38 cytosolic tail needed for membrane localization, but CD38 enzymatic activity is unnecessary.
Article in Experimental cell research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
- Understanding the Role of All-Trans Retinoic Acid in Acute Myeloid Leukemia Cells.World journal of oncology · 2025Article
- Cell deformability enhances adhesion of ATRA-differentiated HL-60 cells to P-selectin.European journal of medical research · 2025Article
- Phosphatidylglucoside regulates apoptosis of human neutrophilic lineage cells.Frontiers in immunology · 2025Article
- Skewing cPLAScience signaling · 2023Article
- Omics Technologies to Decipher Regulatory Networks in Granulocytic Cell Differentiation.Biomolecules · 2021Article
- Dissecting the novel partners of nuclear c-Raf and its role in all-trans retinoic acid (ATRA)-induced myeloblastic leukemia cells differentiation.Experimental cell research · 2020Article
- Depleting interferon regulatory factor-1(IRF-1) with CRISPR/Cas9 attenuates inducible oxidative metabolism without affecting RA-induced differentiation in HL-60 human AML cells.FASEB bioAdvances · 2020Article
- CD38 is methylated in prostate cancer and regulates extracellular NADCancer & metabolism · 2018Article
- Probing the requirement for CD38 in retinoic acid-induced HL-60 cell differentiation with a small molecule dimerizer and genetic knockout.Scientific reports · 2017Article
- An Effective Model of the Retinoic Acid Induced HL-60 Differentiation Program.Scientific reports · 2017Article
- Mechanical regulation of calcium signaling of HL-60 on P-selectin under flow.Biomedical engineering online · 2016Article
- Phosphorylation of c-Cbl and p85 PI3K driven by all-trans retinoic acid and CD38 depends on Lyn kinase activity.Cellular signalling · 2014Article
- Molecular mechanism of inhibitory effects of C-phycocyanin combined with all-trans-retinoic acid on the growth of HeLa cells in vitro.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- Identification of ADP-ribosylation sites of CD38 mutants by precursor ion scanning mass spectrometry.Analytical biochemistry · 2013Article
- The CD49d/CD29 complex is physically and functionally associated with CD38 in B-cell chronic lymphocytic leukemia cells.Leukemia · 2012Article
- Article
- Argonaute 2 complexes selectively protect the circulating microRNAs in cell-secreted microvesicles.PloS one · 2012Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Leukocyte antigen CD38 expression is an early marker of all-trans retinoic acid (ATRA) stimulated differentiation in the leukemic cell line HL-60. It promotes induced myeloid maturation when overexpressed, whereas knocking it down is inhibitory. It is a type II membrane protein with an extracellular C-terminal enzymatic domain with NADase/NADPase and ADPR cyclase activity and a short cytoplasmic N-terminal tail. Here we determined whether CD38 enzymatic activity or the cytoplasmic tail is required for ATRA-induced differentiation. Neither a specific CD38 ectoenzyme inhibitor nor a point mutation that cripples enzymatic activity (CD38 E226Q) diminishes ATRA-induced differentiation or G1/0 arrest. In contrast a cytosolic deletion mutation (CD38 Δ11-20) prevents membrane expression and inhibits differentiation and G1/0 arrest. These results may be consistent with disrupting the function of critical molecules necessary for membrane-expressed CD38 signal transduction. One candidate molecule is the Src family kinase Fgr, which failed to undergo ATRA-induced upregulation in CD38 Δ11-20 expressing cells. Another is Vav1, which also showed only basal expression after ATRA treatment in CD38 Δ11-20 expressing cells. Therefore, the ability of CD38 to propel ATRA-induced myeloid differentiation and G1/0 arrest is unimpaired by loss of its ectoenzyme activity. However a cytosolic tail deletion mutation disrupted membrane localization and inhibited differentiation. ATRA-induced differentiation thus does not require the CD38 ectoenzyme function, but is dependent on a membrane receptor function.
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