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Editorial
. 2019 Sep;104(9):1694-1696.
doi: 10.3324/haematol.2019.224162.

Ubiquitination is not omnipresent in myeloid leukemia

Ramesh C Nayak  1 , Jose A Cancelas  2   3
Affiliations
Editorial

Ubiquitination is not omnipresent in myeloid leukemia

Ramesh C Nayak et al. Haematologica. 2019 Sep.
No abstract available

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Figures

Figure 1.
Figure 1.
Schematic representation of possible UBE2A-mediated mechanisms controlling myeloid blastic transformation in BCR-ABL leukemias. Possible targets of UBE2A relevant to leukemic myeloid transformation. (A and B) Cytosolic functions. UBE2A is an E2 ubiquitin ligase important in emergency myelopoiesis induced by inflammatory cytokines, abundant in the leukemic microenvironment, through the TRAF/TRIF E3 ligases, regulators of the transcriptional factor NFkB. Loss-of-function of UBE2A may associate with impaired myeloid differentiation. (B) UBE2A regulates the activity of E3 ligases c-CBL and FBW7, which are tumor suppressors with known activity to induce degradation of BCR-ABL and MYC, whose expression in turn is required for leukemic acceleration. Question marks denote that these pathways of activity of UBE2A are speculative and not supported by direct experimental designs. (C and D) Nuclear functions. (C) UBE2A is a well known regulator of DNA repair through its cognate E3 ligase RAD18, which monoubiquitinates the proliferating cell nuclear antigen (PCNA), a modification that recruits translesion DNA polymerases to stalled replication forks. (D) Active UBE2A (phosphorylated by CDK9) regulates H2Bmonoubiquitination through recruitment of the E3 ligase RNF20/40, a major step in regulation of RNA polymerase II and gene transcription.
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Comment on

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