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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Myeloid/lymphoid or mixed-lineage leukemia 5

This gene is a member of the myeloid/lymphoid or mixed-lineage leukemia (MLL) family and encodes a protein with an N-terminal PHD zinc finger and a central SET domain. Overexpression of the protein inhibits cell cycle progression. Alternate transcriptional splice variants have been characterized. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Histone, SET, MLL, V1a, CAN
Papers on MLL5
MLL5 Promotes Self-Renewing Glioblastoma Growth via H3.3 Suppression.
In Cancer Discov, Jan 2016
In adult GBM, MLL5 reduces H3.3 occupancy, globally reorganizes chromatin, and promotes self-renewal.
MLL5 Orchestrates a Cancer Self-Renewal State by Repressing the Histone Variant H3.3 and Globally Reorganizing Chromatin.
Dirks et al., Toronto, Canada. In Cancer Cell, Jan 2016
H3.3 is repressed by mixed lineage leukemia 5 (MLL5) in self-renewing GBM cells.
Functional proteomics of the epigenetic regulators ASXL1, ASXL2 and ASXL3: a convergence of proteomics and epigenetics for translational medicine.
Katoh, Tokyo, Japan. In Expert Rev Proteomics, Jun 2015
Phylogenetic analyses of 139 human PHD fingers revealed that ASXL PHD fingers cluster with those of BPTF, DIDO, ING1, KDM5A (JARID1A), KMT2E (MLL5), PHF2, PHF8 and PHF23.
Mouse BRWD1 is critical for spermatid postmeiotic transcription and female meiotic chromosome stability.
De La Fuente et al., Athens, United States. In J Cell Biol, Feb 2015
In females, Brwd1 ablation caused severe chromosome condensation and structural defects associated with abnormal telomere structure but only minor changes in gene expression at the germinal vesicle stage, including more than twofold overexpression of the histone methyltransferase MLL5 and LINE-1 elements transposons.
[Significance of chromosome 7 abnormalities in myeloid malignancies].
Chang et al., Shanghai, China. In Zhongguo Shi Yan Xue Ye Xue Za Zhi, 2014
Genes (EZH2, MLL5, DOCK4, SAMD9L/SAMD9) located in commonly deleted segments of 7q have been cloned and characterized along with the advance of molecular biology.This review summaries the current advancement about myeloid malignancies associated with monosomy7/del(7q).
Common Viral Integration Sites Identified in Avian Leukosis Virus-Induced B-Cell Lymphomas.
Beemon et al., Baltimore, United States. In Mbio, 2014
In addition to the four genes implicated previously, we identify other genes as common integration sites, including TNFRSF1A, MEF2C, CTDSPL, TAB2, RUNX1, MLL5, CXorf57, and BACH2.
Association of the histone-lysine N-methyltransferase MLL5 gene with coronary artery disease in Chinese Han people.
Ma et al., Ürümqi, China. In Meta Gene, 2014
The aim of this study was to explore the relationship between the interaction of histone-lysine N-methyltransferase MLL5 gene polymorphism and CAD in a Chinese Han population.
Mixed Lineage Leukemia 5 (MLL5) Protein Stability Is Cooperatively Regulated by O-GlcNac Transferase (OGT) and Ubiquitin Specific Protease 7 (USP7).
Zhang et al., Nanjing, China. In Plos One, 2014
Mixed lineage leukemia 5 (MLL5) protein is a trithorax family histone 3 lysine 4 (H3K4) methyltransferase that regulates diverse biological processes, including cell cycle progression, hematopoiesis and cancer.
Targeted silencing of MLL5β inhibits tumor growth and promotes gamma-irradiation sensitization in HPV16/18-associated cervical cancers.
Deng et al., Singapore, Singapore. In Mol Cancer Ther, 2014
We previously identified a novel MLL5 isoform, MLL5β, which was essential for E6 and E7 transcriptional activation in HPV16/18-associated cervical cancers.
De novo insertions and deletions of predominantly paternal origin are associated with autism spectrum disorder.
Sanders et al., Beijing, China. In Cell Rep, 2014
Finally, by observing clustering of mutations in unrelated probands, we uncover two ASD-associated genes: KMT2E (MLL5), a chromatin regulator, and RIMS1, a regulator of synaptic vesicle release.
Regulation of histone H3K4 methylation in brain development and disease.
Akbarian et al., New York City, United States. In Philos Trans R Soc Lond B Biol Sci, 2014
Importantly, the reported alterations for some of the diseased brain specimens included a widespread broadening of H3K4 methylation profiles at gene promoters, a process that could be regulated by the UpSET(KMT2E/MLL5)-histone deacetylase complex.
A novel MLL5 isoform that is essential to activate E6 and E7 transcription in HPV16/18-associated cervical cancers.
Deng et al., Singapore, Singapore. In Cancer Res, 2011
A new isoform, MLL5beta, truncated in exon 14, regulates E6 & E7 transcription in cervical carcinoma cells. Interaction of MLL5beta with the AP-1-binding site at the distal region of the HPV18 long control region activated E6/E7 transcription.
Incidence and prognostic influence of DNMT3A mutations in acute myeloid leukemia.
Heuser et al., Hannover, Germany. In J Clin Oncol, 2011
The prognostic impact of DNMT3A mutations was evaluated in the context of other clinical prognostic markers and genetic risk factors (cytogenetic risk group; mutations in NPM1, FLT3, CEBPA, IDH1, IDH2, MLL1, NRAS, WT1, and WT1 SNPrs16754; expression levels of BAALC, ERG, EVI1, MLL5, MN1, and WT1).
Prognostic importance of histone methyltransferase MLL5 expression in acute myeloid leukemia.
Heuser et al., Hannover, Germany. In J Clin Oncol, 2011
High MLL5 expression levels are associated with a favorable outcome and may improve risk and treatment stratification in acute myeloid leukemia
Phosphorylation of mixed lineage leukemia 5 by CDC2 affects its cellular distribution and is required for mitotic entry.
Deng et al., Singapore, Singapore. In J Biol Chem, 2010
Phosphorylation of MLL5 may have an indispensable role in the mitotic progression in mixed lineage leukemia cells.
Mixed lineage leukemia: roles in gene expression, hormone signaling and mRNA processing.
Mandal et al., Arlington, United States. In Febs J, 2010
There are several MLL family proteins such as MLL1, MLL2, MLL3, MLL4, MLL5, Set1A and Set1B, and each possesses histone H3 lysine 4 (H3K4)-specific methyltransferase activity and has critical roles in gene activation and epigenetics.
GlcNAcylation of a histone methyltransferase in retinoic-acid-induced granulopoiesis.
Kato et al., Tokyo, Japan. In Nature, 2009
nuclear MLL5 GlcNAcylation triggers cell lineage determination of HL60 through activation of its histone lysine methyltransferase activity
MLL5, a trithorax homolog, indirectly regulates H3K4 methylation, represses cyclin A2 expression, and promotes myogenic differentiation.
Dhawan et al., Hyderābād, India. In Proc Natl Acad Sci U S A, 2009
MLL5 plays an integral role in novel chromatin regulatory mechanisms that suppress inappropriate expression of S-phase-promoting genes and maintain expression of determination genes in quiescent cells.
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