ArticleBiochemical and biophysical research communications2013
Inhibition of GATE-16 attenuates ATRA-induced neutrophil differentiation of APL cells and interferes with autophagosome formation.
Article in Biochemical and biophysical research communications, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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
21 citing papers in PubMed, 31 citations in OpenAlex.
- A new perspective on the autophagic and non-autophagic functions of the GABARAP protein family: a potential therapeutic target for human diseases.Molecular and cellular biochemistry · 2024Review
- Population dynamics of potentially harmful haplotypes: a pedigree analysis.BMC genomics · 2024Article
- The Crosstalk between Autophagy and Nrf2 Signaling in Cancer: from Biology to Clinical Applications.International journal of biological sciences · 2024Review
- A New Potential Therapeutic Target for Cancer in Ubiquitin-Like Proteins-UBL3.International journal of molecular sciences · 2023Review
- Unlocking the gate to GABARAPL2.Biologia futura · 2022Review
- Reducing FASN expression sensitizes acute myeloid leukemia cells to differentiation therapy.Cell death and differentiation · 2021Article
- Review
- A Bioinformatics Model of Human Diseases on the Basis of Differentially Expressed Genes (of Domestic Versus Wild Animals) That Are Orthologs of Human Genes Associated with Reproductive-Potential Changes.International journal of molecular sciences · 2021Article
- Triggering a switch from basal- to luminal-like breast cancer subtype by the small-molecule diptoindonesin G via induction of GABARAPL1.Cell death & disease · 2020Article
- Review
- Low Autophagy (ATG) Gene Expression Is Associated with an Immature AML Blast Cell Phenotype and Can Be Restored during AML Differentiation Therapy.Oxidative medicine and cellular longevity · 2018Article
- The Ins and Outs of Autophagy and Metabolism in Hematopoietic and Leukemic Stem Cells: Food for Thought.Frontiers in cell and developmental biology · 2018Review
- The autophagy scaffold protein ALFY is critical for the granulocytic differentiation of AML cells.Scientific reports · 2017Article
- PU.1 supports TRAIL-induced cell death by inhibiting NF-κB-mediated cell survival and inducing DR5 expression.Cell death and differentiation · 2017Article
- Autophagy-Regulating microRNAs and Cancer.Frontiers in oncology · 2017Review
- ATG7 regulates energy metabolism, differentiation and survival of Philadelphia-chromosome-positive cells.Autophagy · 2016Article
- Induction of autophagy is a key component of all-trans-retinoic acid-induced differentiation in leukemia cells and a potential target for pharmacologic modulation.Experimental hematology · 2015Article
- Activation of RARα induces autophagy in SKBR3 breast cancer cells and depletion of key autophagy genes enhances ATRA toxicity.Cell death & disease · 2015Article
- Autophagy limits proliferation and glycolytic metabolism in acute myeloid leukemia.Cell death discovery · 2015Article
- WIPI-dependent autophagy during neutrophil differentiation of NB4 acute promyelocytic leukemia cells.Cell death & disease · 2014Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Autophagy is an intracellular bulk degradation process involved in cell survival upon stress induction, but also with a newly identified function in myeloid differentiation. The autophagy-related (ATG)8 protein family, including the GABARAP and LC3 subfamilies, is crucial for autophagosome biogenesis. In order to evaluate the significance of the GABARAPs in the pathogenesis of acute myeloid leukemia (AML), we compared their expression in primary AML patient samples, CD34(+) progenitor cells and in granulocytes from healthy donors. GABARAPL1 and GABARAPL2/GATE-16, but not GABARAP, were significantly downregulated in particular AML subtypes compared to normal granulocytes. Moreover, the expression of GABARAPL1 and GATE-16 was significantly induced during ATRA-induced neutrophil differentiation of acute promyelocytic leukemia cells (APL). Lastly, knocking down GABARAPL2/GATE-16 in APL cells attenuated neutrophil differentiation and decreased autophagic flux. In conclusion, low GABARAPL2/GATE-16 expression is associated with an immature myeloid leukemic phenotype and these proteins are necessary for neutrophil differentiation of APL cells.
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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 OpenQuestion graph.