ArticleMolecular and cellular biology2000
BCR-ABL prevents c-jun-mediated and proteasome-dependent FUS (TLS) proteolysis through a protein kinase CbetaII-dependent pathway.
Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 61 citations in OpenAlex.
- Regulation of HNRNP family by post-translational modifications in cancer.Cell death discovery · 2024Review
- Nicotinamide riboside, pterostilbene and ibudilast protect motor neurons and extend survival in ALS mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Article
- Abl kinase-mediated FUS Tyr526 phosphorylation alters nucleocytoplasmic FUS localization in FTLD-FUS.Brain : a journal of neurology · 2023Article
- Nuclear RNA transcript levels modulate nucleocytoplasmic distribution of ALS/FTD-associated protein FUS.Scientific reports · 2022Article
- Implications of androgen receptor and FUS expression on tumor progression in urothelial carcinoma.Histology and histopathology · 2021Article
- Post-translational Control of RNA-Binding Proteins and Disease-Related Dysregulation.Frontiers in molecular biosciences · 2021Review
- The signaling axis atypical protein kinase C λ/ι-Satb2 mediates leukemic transformation of B-cell progenitors.Nature communications · 2019Article
- The Role of Post-Translational Modifications on Prion-Like Aggregation and Liquid-Phase Separation of FUS.International journal of molecular sciences · 2018Review
- Oxr1 improves pathogenic cellular features of ALS-associated FUS and TDP-43 mutations.Human molecular genetics · 2015Article
- Biochemical Properties and Biological Functions of FET Proteins.Annual review of biochemistry · 2015Review
- The C-terminal residues of Saccharomyces cerevisiae Mec1 are required for its localization, stability, and function.G3 (Bethesda, Md.) · 2013Article
- Targeting PKC-mediated signal transduction pathways using enzastaurin to promote apoptosis in acute myeloid leukemia-derived cell lines and blast cells.Journal of cellular biochemistry · 2011Article
- Intracellular localization and splicing regulation of FUS/TLS are variably affected by amyotrophic lateral sclerosis-linked mutations.Nucleic acids research · 2011Article
- BCR-ABL1 kinase-dependent alteration of mRNA metabolism: potential alternatives for therapeutic intervention.Leukemia & lymphoma · 2011Review
- Heterogeneous nuclear ribonucleoproteins (hnRNPs) in cellular processes: Focus on hnRNP E1's multifunctional regulatory roles.RNA (New York, N.Y.) · 2010Review
- Small interfering RNA against BCR-ABL transcripts sensitize mutated T315I cells to nilotinib.Haematologica · 2010Article
- Ebp1 sumoylation, regulated by TLS/FUS E3 ligase, is required for its anti-proliferative activity.Oncogene · 2010Article
- The TET family of proteins: functions and roles in disease.Journal of molecular cell biology · 2009Review
- Article
- Preventing the degradation of mps1 at centrosomes is sufficient to cause centrosome reduplication in human cells.Molecular biology of the cell · 2007Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The DNA binding activity of FUS (also known as TLS), a nuclear pro-oncogene involved in multiple translocations, is regulated by BCR-ABL in a protein kinase CbetaII (PKCbetaII)-dependent manner. We show here that in normal myeloid progenitor cells FUS, although not visibly ubiquitinated, undergoes proteasome-dependent degradation, whereas in BCR-ABL-expressing cells, degradation is suppressed by PKCbetaII phosphorylation. Replacement of serine 256 with the phosphomimetic aspartic acid prevents proteasome-dependent proteolysis of FUS, while the serine-256-to-alanine FUS mutant is unstable and susceptible to degradation. Ectopic expression of the phosphomimetic S256D FUS mutant in granulocyte colony-stimulating factor-treated 32Dcl3 cells induces massive apoptosis and inhibits the differentiation of the cells escaping cell death, while the degradation-prone S256A mutant has no effect on either survival or differentiation. FUS proteolysis is induced by c-Jun, is suppressed by BCR-ABL or Jun kinase 1, and does not depend on c-Jun transactivation potential, ubiquitination, or its interaction with Jun kinase 1. In addition, c-Jun-induced FUS proteasome-dependent degradation is enhanced by heterogeneous nuclear ribonucleoprotein (hnRNP) A1 and depends on the formation of a FUS-Jun-hnRNP A1-containing complex and on lack of PKCbetaII phosphorylation at serine 256 but not on FUS ubiquitination. Thus, novel mechanisms appear to be involved in the degradation of FUS in normal myeloid cells; moreover, the ability of the BCR-ABL oncoprotein to suppress FUS degradation by the induction of posttranslational modifications might contribute to the phenotype of BCR-ABL-expressing hematopoietic cells.
Indexed as
Identifiers
What OpenQuestion holds
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.