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The crucial role of KMT2B (show MLL2 ELISA Kits) in the physiological control of voluntary movement.
MLL4 mutation along with BRCA1 mutation confers chemoresistance in breast cancer.
Results show that KMT2B (show MLL2 ELISA Kits) interacts with ERalpha (show ESR1 ELISA Kits) to bind the ERalpha (show ESR1 ELISA Kits)-binding sites of IL-20 (show IL20 ELISA Kits) and other ERalpha (show ESR1 ELISA Kits) target genes with H3K4 modifications suggesting an important role for KMT2B (show MLL2 ELISA Kits) in the epigenetic transcriptional regulation of cytokine IL-20 (show IL20 ELISA Kits), and other ERalpha (show ESR1 ELISA Kits)-responsive genes, in breast cancer cells.
findings thus establish generalized dystonia as the human phenotype associated with haploinsufficiency of KMT2B (show MLL2 ELISA Kits); 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 (show MLL ELISA Kits) SET domains of MLL1 and MLL4 (show MLL2 ELISA Kits) are able to add multiple methyl groups to the target histone H3 (show HIST3H3 ELISA Kits) lysine.
The Aven (show AVEN ELISA Kits) RGG/RG motif bound G4 structures within the coding regions of the MLL1 and MLL4 (show MLL2 ELISA Kits) mRNAs increasing their polysomal association and translation, resulting in the induction of transcription of leukemic genes.
We propose that MLL3 and MLL4 (show MLL2 ELISA Kits) are broadly required for controlling MAFA (show KLRG1 ELISA Kits) and MAFB (show MAFB ELISA Kits) transactivation during development and postnatally.
HBV-MLL4 (show MLL2 ELISA Kits) integration occurred frequently in Chinese HCC (show FAM126A ELISA Kits) patients, representing a unique molecular segment for HCC (show FAM126A ELISA Kits) with HBV infection
Chromosomal translocation in a pediatric undifferentiated spindle cell sarcoma have characterized this alteration to show rearrangement of the MLL4 (show MLL2 ELISA Kits) and GPS2 (show GPS2 ELISA Kits) genes, resulting in fusion gene MLL4 (show MLL2 ELISA Kits)-GPS2 (show GPS2 ELISA Kits), the expression of which promotes independent growth.
KMT2B (show MLL2 ELISA Kits) transgene mediates hippocampal histone 3 lysine 4 di- and trimethylation and is a critical player for memory formation.
Histone H3K4 monomethylation catalyzed by Trr (show TXNRD1 ELISA Kits) and mammalian MLL3/MLL4 proteins at enhancers is dispensable for development and viability.
UTX (show KDM6A ELISA Kits)-MLL4-p300 (show NOTCH1 ELISA Kits) 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 (show RPL38 ELISA Kits) 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 (show MLL2 ELISA Kits) enzyme-dead knockin ES cells and mice indicate that the enzymatic activity of H3K4 methyltransferase MLL4 is required for its protein stability.
Although enhancer priming by H3K4me1/2 methyltransferase MLL4/KMT2D (show MLL2 ELISA Kits) is dispensable for cell-identity maintenance, it controls cell fate transition by orchestrating p300 (show NOTCH1 ELISA Kits)-mediated enhancer activation
KMT2D (show MLL2 ELISA Kits) 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.
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
, mixed lineage leukemia 2
, myeloid/lymphoid or mixed-lineage leukemia protein 4 homolog
, 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