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

Myeloid/lymphoid or mixed-lineage leukemia 3

This gene is a member of the myeloid/lymphoid or mixed-lineage leukemia (MLL) family and encodes a nuclear protein with an AT hook DNA-binding domain, a DHHC-type zinc finger, six PHD-type zinc fingers, a SET domain, a post-SET domain and a RING-type zinc finger. This protein is a member of the ASC-2/NCOA6 complex (ASCOM), which possesses histone methylation activity and is involved in transcriptional coactivation. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Histone, p53, MLL, SET, CAN
Papers on MLL3
Frequent BCOR Aberrations in Extranodal NK/T-Cell Lymphoma, Nasal Type.
Takeuchi et al., Tokyo, Japan. In Genes Chromosomes Cancer, Feb 2016
We identified several recurrent somatic mutations involving BCOR (32%), TP53 (16%), DDX3X (12%), FAT4 (8%), NRAS (8%), MLL3 (12%) and MIR17HG (8%).
A PTIP-PA1 subcomplex promotes transcription for IgH class switching independently from the associated MLL3/MLL4 methyltransferase complex.
Daniel et al., Copenhagen, Denmark. In Genes Dev, Feb 2016
Although PTIP is a unique component of the mixed-lineage leukemia 3 (MLL3)/MLL4 chromatin-modifying complex, the mechanisms for how PTIP promotes transcription remain unclear.
Identification of the BRAF V600E mutation in gastroenteropancreatic neuroendocrine tumors.
Kim et al., Seoul, South Korea. In Oncotarget, Jan 2016
Among 12 GEP-NETs, eight showed mutations of more than one cancer-related gene, including TP53, CNBD1, RB1, APC, BCOR, BRAF, CTNNB1, EGFR, EP300, ERBB3, KDM6A, KRAS, MGA, MLL3, PTEN, RASA1, SMARCB1, SPEN, TBC1D12, and VHL.
Genetic landscapes of relapsed and refractory diffuse large B cell lymphomas.
Johnson et al., Vancouver, Canada. In Clin Cancer Res, Jan 2016
RESULTS: Based on the a higher frequency at relapse and evidence for clonal selection, TP53, FOXO1, MLL3, CCND3, NFKBIZ and STAT6 emerged as top candidate genes implicated in therapeutic resistance.
Mutational landscape of MCPyV-positive and MCPyV-negative merkel cell carcinomas with implications for immunotherapy.
Choi et al., New Haven, United States. In Oncotarget, Jan 2016
We show that MCPyV-negative MCCs have a high mutation burden (median of 1121 somatic single nucleotide variants (SSNVs) per-exome with frequent mutations in RB1 and TP53 and additional damaging mutations in genes in the chromatin modification (ASXL1, MLL2, and MLL3), JNK (MAP3K1 and TRAF7), and DNA-damage pathways (ATM, MSH2, and BRCA1).
The mutational landscape of cutaneous T cell lymphoma and Sézary syndrome.
Palomero et al., New York City, United States. In Nat Genet, Dec 2015
Mutation analysis identified a broad spectrum of somatic mutations in key genes involved in epigenetic regulation (TET2, CREBBP, KMT2D (MLL2), KMT2C (MLL3), BRD9, SMARCA4 and CHD3) and signaling, including MAPK1, BRAF, CARD11 and PRKG1 mutations driving increased MAPK, NF-κB and NFAT activity upon T cell receptor stimulation.
The cancer COMPASS: navigating the functions of MLL complexes in cancer.
Dingwall et al., Maywood, United States. In Cancer Genet, May 2015
However, in recent years, a multitude of tumor exome sequencing studies have revealed that orthologues MLL3/KMT2C and MLL2/KMT2D are mutated in a significant percentage of a large variety of malignancies, particularly solid tumors.
Genetics of Opisthorchis viverrini-related cholangiocarcinoma.
Teh et al., Khon Kaen, Thailand. In Curr Opin Gastroenterol, May 2015
MLL3 (13%) and IDH1/2 (2.8%)], WNT signaling [RNF43 (9.3%) and PEG3 (5.6%)] and KRAS/G protein signaling [GNAS (9.3%) and ROBO2 (9.3%)].
Pathogenesis of cholangiocarcinoma: From genetics to signalling pathways.
Teh et al., Singapore, Singapore. In Best Pract Res Clin Gastroenterol, Apr 2015
A series of highly recurrent mutations in genes such as TP53, KRAS, SMAD4, BRAF, MLL3, ARID1A, PBRM1 and BAP1, which are known to be involved in cell cycle control, cell signalling pathways and chromatin dynamics, have led to investigations of their roles, through molecular to mouse modelling studies, in cholangiocarcinogenesis.
Genetic landscape of esophageal squamous cell carcinoma.
He et al., Beijing, China. In Nat Genet, 2014
Histone modifier genes were frequently mutated, including KMT2D (also called MLL2; 19%), KMT2C (MLL3; 6%), KDM6A (7%), EP300 (10%) and CREBBP (6%).
Combinatorial haplo-deficient tumor suppression in 7q-deficient myelodysplastic syndrome and acute myeloid leukemia.
Steidl et al., New York City, United States. In Cancer Cell, 2014
In this issue of Cancer Cell, Chen and colleagues identify MLL3 as a novel haplo-insufficient tumor suppressor on 7q that, in combination with NF1 suppression and TP53 deficiency, mediates MDS and AML phenotypes in mouse and human systems.
MLL3 is a haploinsufficient 7q tumor suppressor in acute myeloid leukemia.
Lowe et al., New York City, United States. In Cancer Cell, 2014
Using RNAi and CRISPR/Cas9 approaches, we show that an ∼50% reduction in gene dosage of the mixed lineage leukemia 3 (MLL3) gene, located on 7q36.1, cooperates with other events occurring in -7/del(7q) AMLs to promote leukemogenesis.
Identification of genomic alterations in oesophageal squamous cell cancer.
Zhan et al., Beijing, China. In Nature, 2014
Moreover, we have found that several important histone regulator genes (MLL2 (also called KMT2D), ASH1L, MLL3 (KMT2C), SETD1B, CREBBP and EP300) are frequently altered in ESCC.
An updated review of gastric cancer in the next-generation sequencing era: insights from bench to bedside and vice versa.
Itoh et al., Kawasaki, Japan. In World J Gastroenterol, 2014
Mutations in chromatin remodeling genes (ARID1A, MLL3 and MLL) have been found in 47% of GCs.
Enhancer malfunction in cancer.
Shilatifard et al., Kansas City, United States. In Mol Cell, 2014
In this Perspective, we will discuss recent findings in the identification of cancer-related enhancer mutations and the role of Drosophila Trr and its human homologs, the MLL3 and MLL4/COMPASS-like complexes, as enhancer histone H3 lysine 4 (H3K4) monomethyltransferases functioning in enhancer-promoter communication.
Mutations of PTCH1, MLL2, and MLL3 are not frequent events in hepatoblastoma.
López-Terrada et al., In Pediatr Blood Cancer, 2012
No somatic mutations were identified in the PTCH1, MLL2, and MLL3 genes in our cohort of hepatoblastoma samples
Requirement for MLL3 in p53 regulation of hepatic expression of small heterodimer partner and bile acid homeostasis.
Lee et al., Portland, United States. In Mol Endocrinol, 2011
p53-dependent histone 3-lysine-4-trimethylation of small heterodimer partner requires MLL3
HOXC6 Is transcriptionally regulated via coordination of MLL histone methylase and estrogen receptor in an estrogen environment.
Mandal et al., Arlington, United States. In J Mol Biol, 2011
These studies demonstrated that HOXC6 is an estrogen-responsive gene, and that histone methylases MLL2 and MLL3, in coordination with ERalpha and ERbeta, transcriptionally regulate HOXC6 in an estrogen-dependent manner.
Four enzymes cooperate to displace histone H1 during the first minute of hormonal gene activation.
Beato et al., Barcelona, Spain. In Genes Dev, 2011
The trimethylation of histone H3 at Lys 4 by the MLL2/MLL3 subunits of ASCOM, enhanced by the hormone-induced displacement of the H3K4 demethylase KDM5B, stabilizes NURF binding.
Frequent alteration of MLL3 frameshift mutations in microsatellite deficient colorectal cancer.
Issa et al., Houston, United States. In Plos One, 2010
Frameshift mutations of MLL3 in both colorectal cancer cells and primary tumor that were more common in cases with microsatellite instability.
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