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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
Two patients' presentation of Kabuki syndrome has been described caused by different KMT2D mutations, both including an interrupted/bipartite clavicle.
data support akey role forKMT2D in modulating the chromatin competence necessary for the assembly of the ER-FOXA1 (show FOXA1 Antibodies)-PBX1 (show PBX1 Antibodies) transcriptional regulatory network in breast cancer.
A possible correlation between the position of the KMT2D premature termination codon caused by the mutation and height SDS (show SDS Antibodies) was assessed, but a significant difference could not be observed for the Kabuki syndrome patients
KMT2D p.Gln3575His segregated with disease status in the family, and is associated with a unique and conserved phenotype in the affected family members, with features overlapping with Kabuki and CHARGE syndromes. Our findings further support the potential etiological link between these two classically distinct conditions.
Three of four cases of histiocytic sarcoma had alterations in the KMT2D gene.
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 Antibodies) elements, it regulates transcription at a limited number of genes including those required for primordial germ cell specification.
KMT2D Mutation is associated with esophageal squamous cell carcinoma.
The crucial role of KMT2B in the physiological control of voluntary movement.
MLL1 and MLL2 collaborate to regulate gene expression and leukemia maintenance not through redundancy, but through distinct pathways.
Our findings provide evidence that CHARGE and Kabuki syndromes result from dysregulatrion of CHD7 (show CHD7 Antibodies) and KMT2D genes involved embryonal development that are expressed in a tissue-specific manner.
Histone H3K4 monomethylation catalyzed by Trr (show TXNRD1 Antibodies) and mammalian MLL3/MLL4 (show MLL4 Antibodies) proteins at enhancers is dispensable for development and viability.
UTX (show KDM6A Antibodies)-MLL4 (show MLL4 Antibodies)-p300 (show NOTCH1 Antibodies) transcriptional regulatory network establishing an "active enhancer landscape" and defines a detailed mechanism for the joint deposition of H3K4me1 and H3K27ac.
MLL4 (show MLL4 Antibodies) 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 (show MLL4 Antibodies) but were enhancers that interacted with MLL4 (show MLL4 Antibodies)-bound sites.
Study shows the contribution of MLL2 (show MLL4 Antibodies)'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 Antibodies) 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 (show MLL4 Antibodies) is required for its protein stability.
Although enhancer priming by H3K4me1/2 methyltransferase MLL4/KMT2D is dispensable for cell-identity maintenance, it controls cell fate transition by orchestrating p300 (show NOTCH1 Antibodies)-mediated enhancer activation
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.
MLL2 is essential for porcine embryo development by the regulation of methylation of H3K4 in vitro.
The protein encoded by this gene is a histone methyltransferase that methylates the Lys-4 position of histone H3. The encoded protein is part of a large protein complex called ASCOM, which has been shown to be a transcriptional regulator of the beta-globin and estrogen receptor genes. Mutations in this gene have been shown to be a cause of Kabuki syndrome.
myeloid/lymphoid or mixed-lineage leukemia 2
, glutathione S-transferase omega 1
, FAD-linked sulfhydryl oxidase ALR
, augmenter of liver regeneration
, growth factor, erv1 homolog
, growth factor, erv1-like (augmenter of liver regeneration)
, 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 protein 2
, Kabuki make-up syndrome
, Kabuki mental retardation syndrome
, trinucleotide repeat containing 21