ArticleCell cycle (Georgetown, Tex.)2016
TBP loading by AF4 through SL1 is the major rate-limiting step in MLL fusion-dependent transcription.
Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- The MLLT3 YEATS domain binds histone marks (H3K9/18/27ac/cr) and ncRNA (7SK), linking transcription and RNA signaling to regulate hematopoiesis.Cell reports · 2026Article
- KMT2A-rearranged leukemia: from mechanism to drug development.Experimental hematology · 2025Review
- The MLLT3 YEATS domain is a dual reader of histone marks (H3K9/18/27ac/cr) and ncRNA (7SK), linking epigenetic and RNA signaling to regulate hematopoiesis.bioRxiv : the preprint server for biology · 2025Article
- RNA-binding proteins of KHDRBS and IGF2BP families control the oncogenic activity of MLL-AF4.Nature communications · 2022Article
- The 3' Pol II pausing at replication-dependent histone genes is regulated by Mediator through Cajal bodies' association with histone locus bodies.Nature communications · 2022Article
- Article
- Modeling by disruption and a selected-for partner for the nude locus.EMBO reports · 2021Article
- Crosstalk between 14-3-3θ and AF4 enhances MLL-AF4 activity and promotes leukemia cell proliferation.Cellular oncology (Dordrecht, Netherlands) · 2019Article
- Another piece of the puzzle added to understand t(4;11) leukemia better.Haematologica · 2019Article
- Pharmacological perturbation of CDK9 using selective CDK9 inhibition or degradation.Nature chemical biology · 2018Article
- Molecular processes involved in B cell acute lymphoblastic leukaemia.Cellular and molecular life sciences : CMLS · 2018Review
- RNA Polymerase II-Dependent Transcription Initiated by Selectivity Factor 1: A Central Mechanism Used by MLL Fusion Proteins in Leukemic Transformation.Frontiers in genetics · 2018Review
- Article
- Myeloid Progenitor Transformation Assay.Bio-protocol · 2017Article
- Cooperative gene activation by AF4 and DOT1L drives MLL-rearranged leukemia.The Journal of clinical investigation · 2017Article
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4 authors at 1 institution in 1 country.
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Abstract
Gene rearrangement of the mixed lineage leukemia (MLL) gene causes leukemia by inducing the constitutive expression of a gene subset normally expressed only in the immature haematopoietic progenitor cells. MLL gene rearrangements often generate fusion products of MLL and a component of the AF4 family/ENL family/P-TEFb (AEP) complex. MLL-AEP fusion proteins have the potential of constitutively recruiting the P-TEFb elongation complex. Thus, it is hypothesized that relieving the promoter proximal pausing of RNA polymerase II is the rate-limiting step of MLL fusion-dependent transcription. AEP also has the potential to recruit the mediator complex via MED26. We recently showed that AEP activates transcription initiation by facilitating TBP loading to the TATA element through the SL1 complex. In the present study, we show that the key activity responsible for the oncogenic property of MLL-AEP fusion proteins is the TBP loading activity, and not the mediator recruitment or transcriptional elongation activities. Thus, we propose that TBP loading by AF4 through SL1 is the major rate-limiting step in MLL fusion-dependent transcription.
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