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Human Monoclonal MLL2 Primary Antibody für 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
In the univariate analyses, TP53 (zeige TP53 Antikörper), PPP1R3A (zeige PPP1R3A Antikörper), 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 (zeige CDK2 Antikörper) 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 (zeige ESR1 Antikörper) to bind the ERalpha (zeige ESR1 Antikörper)-binding sites of IL-20 (zeige IL20 Antikörper) and other ERalpha (zeige ESR1 Antikörper) target genes with H3K4 modifications suggesting an important role for KMT2B in the epigenetic transcriptional regulation of cytokine IL-20 (zeige IL20 Antikörper), and other ERalpha (zeige ESR1 Antikörper)-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 (zeige MLL Antikörper) SET domains of MLL1 and MLL4 are able to add multiple methyl groups to the target histone H3 (zeige HIST3H3 Antikörper) lysine.
The Aven (zeige AVEN Antikörper) 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 (zeige KLRG1 Antikörper) and MAFB (zeige MAFB Antikörper) transactivation during development and postnatally.
HBV-MLL4 integration occurred frequently in Chinese HCC (zeige FAM126A Antikörper) patients, representing a unique molecular segment for HCC (zeige FAM126A Antikörper) with HBV infection
Although enhancer priming by H3K4me1/2 methyltransferase MLL4/KMT2D is dispensable for cell-identity maintenance, it controls cell fate transition by orchestrating p300 (zeige NOTCH1 Antikörper)-mediated enhancer activation
results indicated a coordinated role of the activating H3K4 methyltransferases Mll2 (zeige MLL4 Antikörper) and the suppressing Zfp281 (zeige ZNF281 Antikörper)-Tet1 (zeige TET1 Antikörper)-Sin3A (zeige SIN3A Antikörper) pathway in the regulation of subsets of young L1 expression
Enhancer-priming by MLL3/MLL4 (zeige MLL4 Antikörper) followed by enhancer-activation by CBP/p300 (zeige CREBBP Antikörper) sequentially shape dynamic enhancer landscapes during cell differentiation
These results uncover a murine hepatic steatosis regulatory axis consisting of ABL1 (zeige ABL1 Antikörper)-PPARgamma2 (zeige PPARG Antikörper)-MLL4 (zeige MLL4 Antikörper), which may serve as a target of anti-steatosis drug development.
Histone H3K4 monomethylation catalyzed by Trr (zeige TXNRD1 Antikörper) and mammalian MLL3/MLL4 (zeige MLL4 Antikörper) proteins at enhancers is dispensable for development and viability.
UTX (zeige KDM6A Antikörper)-MLL4 (zeige MLL4 Antikörper)-p300 (zeige NOTCH1 Antikörper) transcriptional regulatory network establishing an "active enhancer landscape" and defines a detailed mechanism for the joint deposition of H3K4me1 and H3K27ac.
MLL4 (zeige MLL4 Antikörper) 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 (zeige MLL4 Antikörper) but were enhancers that interacted with MLL4 (zeige MLL4 Antikörper)-bound sites.
Study shows the contribution of MLL2 (zeige MLL4 Antikörper)'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 (zeige RPL38 Antikörper) 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 (zeige 0 Antikörper) 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 (zeige MLL4 Antikörper) is required for its protein stability.
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