Ubiquitylation in normal and malignant hematopoiesis: novel therapeutic targets

Marteijn, Jürgen A.; Jansen, Joop H.; Reijden, Bert A. van der

doi:10.1038/sj.leu.2404319

Cited by 15 publications

(18 citation statements)

References 63 publications

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“…4,[6][7][8] By correlating outlier expression of Ub genes with clinical outcome in 525 AML patients, we identified differentially high expression of EVI1 and BRE as prognostic factors. Previous research has already shown that high EVI1 expression is an independent poor prognostic factor, 13 providing proof-of-principle that outlier analysis is a powerful approach to identify prognostic factors.…”

Section: Discussionmentioning

confidence: 99%

“…[1][2][3] Recently, mutations in genes that are involved in ubiquitination have been identified in AML pathogenesis as well. 4 Ubiquitination is a posttranslational modification of cellular proteins. In this process, the small ubiquitin protein is conjugated to substrate proteins as a single moiety or as ubiquitin chains.…”

Section: Introductionmentioning

confidence: 99%

“…This may mark substrates for degradation by the 26S proteasome or may alter the substrate's functional activity, depending on the type of ubiquitin chain that is attached. 4 Substrate ubiquitination is catalyzed via a 3-step cascade involving E1-activating enzymes, E2-conjugating enzymes, and E3 ligases. Like other posttranslational modifications, ubiquitination is a reversible process, as deubiquitinases (DUBs) remove ubiquitin chains from substrates.…”

Section: Introductionmentioning

confidence: 99%

“…Because of its versatile role in many biologic pathways, it is not surprising that changes in protein ubiquitination contribute to cancer development including malignant hematopoiesis. 4,5 For example, mutations in the E3 ligase C-CBL have been described in AML and other myeloid neoplasms. 6,7 Mutations in this important negative regulator of receptor tyrosine kinases lead to prolonged receptor signaling and hence enhanced proliferation.…”

Section: Introductionmentioning

confidence: 99%

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High BRE expression predicts favorable outcome in adult acute myeloid leukemia, in particular among MLL-AF9–positive patients

Noordermeer

Sanders

Gilissen

et al. 2011

Blood

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Aberrations in protein ubiquitination have recently been identified in the pathogenesis of acute myeloid leukemia (AML). We studied whether expression changes of more than 1600 ubiquitination related genes correlated with clinical outcome in 525 adult AML patients. High expression of one of these genes, BRE, was observed in 3% of the cases and predicted favorable prognosis independently of known prognostic factors (5-year overall survival: 57%). Remarkably, unsupervised expression profiling showed that 86% of high BREexpressing patients were confined to a previously unrecognized cluster. High

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

High BRE expression predicts favorable outcome in adult acute myeloid leukemia, in particular among MLL-AF9–positive patients

Noordermeer

Sanders

Gilissen

et al. 2011

Blood

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“…For example, defects in core components of a complex with E3 ubiquitin ligase activity give rise to Fanconi anemia (52,53). It has been recently proposed that the proteasome machinery is required to maintain the balance of alpha-and betaglobin chains within a maturing erythroid cell and that protein quality control is crucial in the erythropoietic process (54).…”

Section: Discussionmentioning

confidence: 99%

Erythropoietic Defect Associated with Reduced Cell Proliferation in Mice Lacking the 26S Proteasome Shuttling Factor Rad23b

Bergink

Theil

Toussaint

et al. 2013

Molecular and Cellular Biology

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k Rad23a and Rad23b proteins are linked to nucleotide excision DNA repair (NER) via association with the DNA damage recognition protein xeroderma pigmentosum group C (XPC) are and known to be implicated in protein turnover by the 26S proteasome. Rad23b-null mice are NER proficient, likely due to the redundant function of the Rad23b paralogue, Rad23a. However, Rad23b-null midgestation embryos are anemic, and most embryos die before birth. Using an unbiased proteomics approach, we found that the majority of Rad23b-interacting partners are associated with the ubiquitin-proteasome system (UPS). We tested the requirement for Rad23b-dependent UPS activity in cellular proliferation and more specifically in the process of erythropoiesis. In cultured fibroblasts derived from embryos lacking Rad23b, proliferation rates were reduced. In fetal livers of Rad23b-null embryos, we observed reduced proliferation, accumulation of early erythroid progenitors, and a block during erythroid maturation. In primary wild-type (WT) erythroid cells, knockdown of Rad23b or chemical inhibition of the proteasome reduced survival and differentiation capability. Finally, the defects linked to Rad23b loss specifically affected fetal definitive erythropoiesis and stress erythropoiesis in adult mice. Together, these data indicate a previously unappreciated requirement for Rad23b and the UPS in regulation of proliferation in different cell types.

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Differential regulation of PML–RARα stability by the ubiquitin ligases SIAH1/SIAH2 and TRIAD1

Pietschmann¹,

Buchwald²,

Muller³

et al. 2012

The International Journal of Biochemistry & Cell Biology

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Ubiquitylation in normal and malignant hematopoiesis: novel therapeutic targets

Cited by 15 publications

References 63 publications

High BRE expression predicts favorable outcome in adult acute myeloid leukemia, in particular among MLL-AF9–positive patients

High BRE expression predicts favorable outcome in adult acute myeloid leukemia, in particular among MLL-AF9–positive patients

Erythropoietic Defect Associated with Reduced Cell Proliferation in Mice Lacking the 26S Proteasome Shuttling Factor Rad23b

Differential regulation of PML–RARα stability by the ubiquitin ligases SIAH1/SIAH2 and TRIAD1

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