Multiple Interactions Recruit MLL1 and MLL1 Fusion Proteins to the HOXA9 Locus in Leukemogenesis

Multiple Interactions Recruit MLL1 and MLL1 Fusion Proteins to the HOXA9 Locus in Leukemogenesis

Veure altres versions (1)

Dades bibliogràfiques
Autors principals:	Milne, T, Kim, J, Wang, G, Stadler, S, Basrur, V, Whitcomb, S, Wang, Z, Ruthenburg, A, Elenitoba-Johnson, K, Roeder, R, Allis, C
Format:	Journal article
Publicat:	2010

Ítems similars

Multiple interactions recruit MLL1 and MLL1 fusion proteins to the HOXA9 locus in leukemogenesis.
per: Milne, T, et al.
Publicat: (2010)

Function of leukemogenic mixed lineage leukemia 1 (MLL) fusion proteins through distinct partner protein complexes.
per: Biswas, D, et al.
Publicat: (2011)

Molecular and Epigenetic Mechanisms of MLL in Human Leukemogenesis.
per: Ballabio, E, et al.
Publicat: (2012)

PAF1 and FACT cooperate with MLL-AF4 to drive enhancer activity in leukemia
per: Milne, T, et al.
Publicat: (2022)

Regulation of MLL1 H3K4 methyltransferase activity by its core components.
per: Dou, Y, et al.
Publicat: (2006)

The Histone Methyltransferase Activity of MLL1 Is Dispensable for Hematopoiesis and Leukemogenesis
per: Bibhu P. Mishra, et al.
Publicat: (2014-05-01)

Hoxa9 and Meis1 are key targets for MLL-ENL-mediated cellular immortalization.
per: Zeisig, B, et al.
Publicat: (2004)

Extending the repertoire of the mixed-lineage leukemia gene MLL in leukemogenesis.
per: Daser, A, et al.
Publicat: (2004)

MLL-AF4 cooperates with PAF1 and FACT to drive high-density enhancer interactions in leukemia
per: Crump, NT, et al.
Publicat: (2023)

FBXO22 promotes leukemogenesis by targeting BACH1 in MLL-rearranged acute myeloid leukemia
per: Xiao-Na Zhu, et al.
Publicat: (2023-02-01)

HBO1-MLL interaction promotes AF4/ENL/P-TEFb-mediated leukemogenesis
per: Satoshi Takahashi, et al.
Publicat: (2021-08-01)

MLL-AF4 cooperates with PAF1 and FACT to drive high-density enhancer interactions in leukemia
per: Nicholas T. Crump, et al.
Publicat: (2023-08-01)

Loss of MBD2 attenuates MLL-AF9-driven leukemogenesis by suppressing the leukemic cell cycle via CDKN1C
per: Kuangguo Zhou, et al.
Publicat: (2021-11-01)

Development of a multi-step leukemogenesis model of MLL-rearranged leukemia using humanized mice.
per: Kunihiko Moriya, et al.
Publicat: (2012-01-01)

An Ash2L/RbBP5 heterodimer stimulates the MLL1 methyltransferase activity through coordinated substrate interactions with the MLL1 SET domain.
per: Fang Cao, et al.
Publicat: (2010-11-01)

TIFAB accelerates MLL-AF9−Induced acute myeloid leukemia through upregulation of HOXA9
per: Jinming Zhao, et al.
Publicat: (2021-12-01)

Systematic characterization of the HOXA9 downstream targets in MLL-r leukemia by noncoding CRISPR screens
per: Shaela Wright, et al.
Publicat: (2023-11-01)

Dimerization of MLL fusion proteins immortalizes hematopoietic cells.
per: Martin, M, et al.
Publicat: (2003)

Cdx4 is dispensable for murine adult hematopoietic stem cells but promotes MLL-AF9-mediated leukemogenesis
per: Sumin Koo, et al.
Publicat: (2010-10-01)

Identification of genes transcriptionally responsive to the loss of MLL fusions in MLL-rearranged acute lymphoblastic leukemia.
per: Marieke H van der Linden, et al.
Publicat: (2015-01-01)

Essential Functions of MLL1 and MLL2 in Retinal Development and Cone Cell Maintenance
per: Chi Sun, et al.
Publicat: (2022-02-01)

MLL targets SET domain methyltransferase activity to Hox gene promoters.
per: Milne, T, et al.
Publicat: (2002)

The MLL family of proteins in normal development and disease
per: Milne, TA
Publicat: (2020)

MLL associates specifically with a subset of transcriptionally active target genes.
per: Milne, T, et al.
Publicat: (2005)

Genome-wide analyses reveal new insights into MLL fusion protein recruitment mechanisms
per: Kerry, J
Publicat: (2015)

Registered report: Inhibition of BET recruitment to chromatin as an effective treatment for MLL-fusion leukemia
per: Juan José Fung, et al.
Publicat: (2015-09-01)

Replication Study: Inhibition of BET recruitment to chromatin as an effective treatment for MLL-fusion leukaemia
per: Xiaochuan Shan, et al.
Publicat: (2017-06-01)

Research progress in Menin-MLL interaction and its inhibitors in MLL-rearranged leukemia
per: FANG Xinyue, et al.
Publicat: (2024-10-01)

Histone H3K36me2-Specific Methyltransferase ASH1L Promotes MLL-AF9-Induced Leukemogenesis
per: Mohammad B. Aljazi, et al.
Publicat: (2021-10-01)

Molecular characterization of an MLL1 fusion and its role in chromosomal instability
per: Sreejit Parameswaran, et al.
Publicat: (2019-02-01)

Physical association and coordinate function of the H3 K4 methyltransferase MLL1 and the H4 K16 acetyltransferase MOF.
per: Dou, Y, et al.
Publicat: (2005)

Leukemogenic MLL fusion proteins bind across a broad region of the Hox a9 locus, promoting transcription and multiple histone modifications.
per: Milne, T, et al.
Publicat: (2005)

Correction: Replication Study: Inhibition of BET recruitment to chromatin as an effective treatment for MLL-fusion leukaemia
per: Xiaochuan Shan, et al.
Publicat: (2018-01-01)

MLL3 regulates the CDKN2A tumor suppressor locus in liver cancer
per: Changyu Zhu, et al.
Publicat: (2023-06-01)

Trithorax and polycomb cooperation in MLL fusion acute leukemia
per: Helene Méreau, et al.
Publicat: (2013-06-01)

FOXQ1 recruits the MLL complex to activate transcription of EMT and promote breast cancer metastasis
per: Allison V. Mitchell, et al.
Publicat: (2022-11-01)

RUNX1 is a key target in t(4;11) leukemias that contributes to gene activation through an AF4-MLL complex interaction.
per: Wilkinson, A, et al.
Publicat: (2013)

Unlike its Paralog LEDGF/p75, HRP-2 Is Dispensable for MLL-R Leukemogenesis but Important for Leukemic Cell Survival
per: Siska Van Belle, et al.
Publicat: (2021-01-01)

The deficiency of tumor suppressor prep1 accelerates the onset of meis1- hoxa9 leukemogenesis.
per: Leila Dardaei, et al.
Publicat: (2014-01-01)

MLL rearrangements in pediatric acute lymphoblastic and myeloblastic leukemias: MLL specific and lineage specific signatures
per: te Kronnie Geertruy, et al.
Publicat: (2009-06-01)