ArticleThe Journal of biological chemistry2009
c-Cbl tyrosine kinase-binding domain mutant G306E abolishes the interaction of c-Cbl with CD38 and fails to promote retinoic acid-induced cell differentiation and G0 arrest.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 26 citations in OpenAlex.
- Evidence of off-target effects of bosutinib that promote retinoic acid-induced differentiation of non-APL AML cells.Cell cycle (Georgetown, Tex.) · 2021Article
- Role for Fgr and Numb in retinoic acid-induced differentiation and G0 arrest of non-APL AML cells.Oncotarget · 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
- Roscovitine enhances all-Oncotarget · 2020Article
- Retinoic acid and 6-formylindolo(3,2-b)carbazole (FICZ) combination therapy reveals putative targets for enhancing response in non-APL AML.Leukemia & lymphoma · 2019Article
- Potential for subsets of wt-NPM1 primary AML blasts to respond to retinoic acid treatment.Oncotarget · 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
- MicroRNA-155 regulates the proliferation, cell cycle, apoptosis and migration of colon cancer cells and targets CBL.Experimental and therapeutic medicine · 2017Article
- An Effective Model of the Retinoic Acid Induced HL-60 Differentiation Program.Scientific reports · 2017Article
- Article
- The AhR agonist VAF347 augments retinoic acid-induced differentiation in leukemia cells.FEBS open bio · 2015Article
- Phosphorylation of c-Cbl and p85 PI3K driven by all-trans retinoic acid and CD38 depends on Lyn kinase activity.Cellular signalling · 2014Article
- Nuclear Raf-1 kinase regulates the CXCR5 promoter by associating with NFATc3 to drive retinoic acid-induced leukemic cell differentiation.The FEBS journal · 2014Article
- Retinoic acid therapy resistance progresses from unilineage to bilineage in HL-60 leukemic blasts.PloS one · 2014Article
- 6-Formylindolo (3,2-b)carbazole (FICZ) enhances retinoic acid (RA)-induced differentiation of HL-60 myeloblastic leukemia cells.Molecular cancer · 2013Article
- Article
- Interferon regulatory factor-1 binds c-Cbl, enhances mitogen activated protein kinase signaling and promotes retinoic acid-induced differentiation of HL-60 human myelo-monoblastic leukemia cells.Leukemia & lymphoma · 2011Article
- ATRA-induced HL-60 myeloid leukemia cell differentiation depends on the CD38 cytosolic tail needed for membrane localization, but CD38 enzymatic activity is unnecessary.Experimental cell research · 2011Article
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2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Retinoic acid (RA) causes HL-60 human myeloblastic leukemia cell myeloid differentiation that is dependent on MAPK signaling. The process is propelled by c-Cbl, which binds the CD38 receptor as part of a signaling complex generating MAPK signaling. Here we report that the capability of c-Cbl to do this is lost in the G306E tyrosine kinase-binding domain mutant. Unlike wild-type (WT) c-Cbl, the G306E mutant c-Cbl fails to propel RA-induced differentiation, and disrupts the normal association with CD38. The G306E mutant does, like WT c-Cbl, co-immunoprecipitate with Vav, Slp-76, and p38. But unlike WT c-Cbl, does not cause MAPK signaling. In contrast, the C381A Ring finger domain mutant functions like WT c-Cbl. It binds CD38 and is part of the same apparent c-Cbl/Slp-76/Vav/p38 signaling complex. The C381A mutant causes MAPK signaling and propels RA-induced differentiation. In addition to HL-60 cells and their WT or mutant c-Cbl stable transfectants, the c-Cbl/Vav/Slp-76 complex is also found in NB4 cells where c-Cbl was previously also found to bind CD38. The data are consistent with a model in which the G306E mutant c-Cbl forms a signaling complex that includes Slp-76, Vav, and p38; but does not drive MAPK signaling because it fails to bind the CD38 receptor. Without the G306E mutation the c-Cbl unites CD38 with the signaling complex and delivers a MAPK signal that drives RA-induced differentiation. The results demonstrate the importance of the Gly306 residue in the ability of c-Cbl to propel RA-induced differentiation.
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