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Human Polyclonal MLL2 Primary Antibody for ELISA, WB - ABIN6243263
Dhar, Lee, Kan, Voigt, Ma, Shi, Reinberg, Lee: Trans-tail regulation of MLL4-catalyzed H3K4 methylation by H4R3 symmetric dimethylation is mediated by a tandem PHD of MLL4. in Genes & development 2012
Show all 3 Pubmed References
Human Monoclonal MLL2 Primary Antibody for ELISA, WB - ABIN948660
Micale, Augello, Maffeo, Selicorni, Zucchetti, Fusco, De Nittis, Pellico, Mandriani, Fischetto, Boccone, Silengo, Biamino, Perria, Sotgiu, Serra, Lapi, Neri, Ferlini, Cavaliere, Chiurazzi, Monica et al.: Molecular analysis, pathogenic mechanisms, and readthrough therapy on a large cohort of Kabuki syndrome patients. ... in Human mutation 2014
Gene silencing experiments of MLL4 and the subunits PA1 and PTIP confirm TGF-beta-specific genes to be regulated by the MLL4 complex, which links TGF-beta signaling to transcription regulation by the MLL4 methyltransferase complex.
Summary of variants in KMT2B associated with dystonia, as well as the clinical phenotype (review)
Rare missense variation in KMT2B represents an additional cause of generalized dystonia.
In the univariate analyses, TP53, PPP1R3A, and KMT2B were significantly more frequently mutated in interval cancers than in screen-detected cancers.
we describe a method to seamlessly modify a putative CDK2 phosphorylation site on MLL2 to restrict its phosphorylation and activation. Specifically, by utilizing dimeric CRISPR RNA-guided nucleases, RFNs (commercially known as the NextGENtrade mark CRISPR), in combination with an excision-only piggyBactrade mark transposase, we demonstrate how to generate a point mutation of threonine-542, a predicted site to prevent M...
The crucial role of KMT2B in the physiological control of voluntary movement.
MLL4 mutation along with BRCA1 mutation confers chemoresistance in breast cancer.
Results show that KMT2B interacts with ERalpha to bind the ERalpha-binding sites of IL-20 and other ERalpha target genes with H3K4 modifications suggesting an important role for KMT2B in the epigenetic transcriptional regulation of cytokine IL-20, and other ERalpha-responsive genes, in breast cancer cells.
findings thus establish generalized dystonia as the human phenotype associated with haploinsufficiency of KMT2B; moreover, we provide evidence for a causative role of disordered histone modification, chromatin states, and transcriptional deregulation in dystonia pathogenesis
The results explain how the MLL SET domains of MLL1 and MLL4 are able to add multiple methyl groups to the target histone H3 lysine.
The Aven RGG/RG motif bound G4 structures within the coding regions of the MLL1 and MLL4 mRNAs increasing their polysomal association and translation, resulting in the induction of transcription of leukemic genes.
We propose that MLL3 and MLL4 are broadly required for controlling MAFA and MAFB transactivation during development and postnatally.
HBV-MLL4 integration occurred frequently in Chinese HCC patients, representing a unique molecular segment for HCC with HBV infection
Chromosomal translocation in a pediatric undifferentiated spindle cell sarcoma have characterized this alteration to show rearrangement of the MLL4 and GPS2 genes, resulting in fusion gene MLL4-GPS2, the expression of which promotes independent growth.
KMT2B transgene mediates hippocampal histone 3 lysine 4 di- and trimethylation and is a critical player for memory formation.
the second PHD finger (PHD2) of MLL1 is an E3 ubiquitin ligase in the presence of the E2-conjugating enzyme CDC34. This activity is conserved in the second PHD finger of MLL4, the closest homolog to MLL1 but not in MLL2 or MLL3.
knockdown of MLL4 severely affects cell-cycle progression and induces apoptotic cell death in cultured tumour cells.
Alterations of the CxxC domain preclude oncogenic activation of mixed-lineage leukemia 2
data suggest that the translocation breakpoint of MLL4 gene is one of the preferential targets for HBV DNA integration into the MLL4 gene and the HBV DNA integration may be involved in liver oncogenesis
Although enhancer priming by H3K4me1/2 methyltransferase MLL4/KMT2D is dispensable for cell-identity maintenance, it controls cell fate transition by orchestrating p300-mediated enhancer activation
results indicated a coordinated role of the activating H3K4 methyltransferases Mll2 and the suppressing Zfp281-Tet1-Sin3A pathway in the regulation of subsets of young L1 expression
Enhancer-priming by MLL3/MLL4 followed by enhancer-activation by CBP/p300 sequentially shape dynamic enhancer landscapes during cell differentiation
These results uncover a murine hepatic steatosis regulatory axis consisting of ABL1-PPARgamma2-MLL4, which may serve as a target of anti-steatosis drug development.
Histone H3K4 monomethylation catalyzed by Trr and mammalian MLL3/MLL4 proteins at enhancers is dispensable for development and viability.
UTX-MLL4-p300 transcriptional regulatory network establishing an "active enhancer landscape" and defines a detailed mechanism for the joint deposition of H3K4me1 and H3K27ac.
MLL4 deficiency compromised the development of regulatory T cells (Treg cells) and resulted in a substantial decrease in monomethylated H3K4 (H3K4me1) and chromatin interaction at putative gene enhancers, a considerable portion of which were not direct targets of MLL4 but were enhancers that interacted with MLL4-bound sites.
Study shows the contribution of MLL2's methyltransferase and CXXC domain in the trimethylation of H3K4 in embryonic stem cells and find that while it trimethylates H3K4 at both bivalent gene promoters and non-TSS elements, it regulates transcription at a limited number of genes including those required for primordial germ cell specification.
While H3K4me1 partially supports H3K27ac at active enhancers, it is largely dispensable for transcription. By contrast, Mll3/4 proteins themselves are required for enhancer Pol II loading, eRNA synthesis, and gene expression.
Data from MLL4/KMT2D enzyme-dead knockin ES cells and mice indicate that the enzymatic activity of H3K4 methyltransferase MLL4 is required for its protein stability.
KMT2D is essential for regulating cardiac gene expression during heart development primarily via H3K4 di-methylation
MLL2 interacts with RNA polymerase II (RNAPII) and RECQL5, and, although MLL2 mutated cells have normal overall H3K4me levels in genes, nucleosomes in the immediate vicinity of RNAPII are hypomethylated.
MLL4 (KMT2D) is a major H3K4 mono- and di-methyltransferase with partial functional redundancy with MLL3 (KMT2C) in mouse and human cells. MLL4 is enriched on enhancers and is required for enhancer activation, cell-type-specific gene expression and cell differentiation.
Both MLL3 and MLL4 complexes act as major epigenetic regulators of diverse metabolic processes (including circadian control of bile acid homeostasis).
Mll2, one of the six Set1/Trithorax-type H3K4 methyltransferases in mammals, is required for trimethylation of bivalent promoters in mouse embryonic stem cells, whereas Mll1 is redundant.
results demonstrate that histone H3K4 methyltransferase Mll2 is a component of the genetic regulation necessary for glucose homeostasis, resulting in a specific disease pattern linking chromatin modification with causes and progression of type 2 diabetes
Reexpression of KMT2B was sufficient to reinstate an active MagohB promoter.
MLL2 is essential for porcine embryo development by the regulation of methylation of H3K4 in vitro.
This gene encodes a protein which contains multiple domains including a CXXC zinc finger, three PHD zinc fingers, two FY-rich domains, and a SET (suppressor of variegation, enhancer of zeste, and trithorax) domain. The SET domain is a conserved C-terminal domain that characterizes proteins of the MLL (mixed-lineage leukemia) family. This gene is ubiquitously expressed in adult tissues. It is also amplified in solid tumor cell lines, and may be involved in human cancer. Two alternatively spliced transcript variants encoding distinct isoforms have been reported for this gene, however, the full length nature of the shorter transcript is not known.
, WW domain binding protein 7
, WW domain-binding protein 7
, histone-lysine N-methyltransferase 2B
, histone-lysine N-methyltransferase MLL4
, lysine N-methyltransferase 2B
, lysine N-methyltransferase 2D
, mixed lineage leukemia gene homolog 2
, myeloid/lymphoid or mixed-lineage leukemia (trithorax homolog, Drosophila) 4
, myeloid/lymphoid or mixed-lineage leukemia 4
, myeloid/lymphoid or mixed-lineage leukemia protein 4
, trithorax homolog 2
, trithorax homologue 2
, ALL1-related protein
, histone-lysine N-methyltransferase 2D
, histone-lysine N-methyltransferase MLL2
, myeloid/lymphoid or mixed-lineage leukemia 2
, myeloid/lymphoid or mixed-lineage leukemia protein 2
, LOW QUALITY PROTEIN: histone-lysine N-methyltransferase 2D
, lysine (K)-specific methyltransferase 2D