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ASH1L encodes a member of the trithorax group of transcriptional activators. Additionally we are shipping ASH1L Antibodies (40) and many more products for this protein.
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suppresses matrix metalloproteinase through mitogen-activated protein kinase (show MAPK1 Proteins) signaling pathway in pulpitis
There has been increasing evidence that heterozygous mutation of ASH1L is associated with ID and autism spectrum disorders. We suggest that ASH1L abnormalities may cause a novel MCA (show RSPH1 Proteins)/ID syndrome.
Epigenetic regulators play vital roles in cancer pathogenesis and represent a new frontier in therapeutic targeting. Our studies provide basic mechanistic insight into the role of H3K36me2 in transcription activation and MLL (show MLL Proteins) leukemia pathogenesis and implicate ASH1L histone methyltransferase as a promising target for novel molecular therapy.
Our data suggest a role for ASH1L, a methyl transferase protein and member of the trithorax (Trx) family, in regulation of the HBB gene and as a potential modifier of beta-thalassaemia severity.
Structural features were identified in ASH1L related to its' function and enzymatic activity.
Both ASH1L and SETD2 are H3K36 specific methyltransferases but only SETD2 can trimethylate this mark.
These data demonstrate that miR (show MLXIP Proteins)-142-3p downregulation has a role in thyroid tumorigenesis, by regulating ASH1L and MLL1.
Our results uncover a novel regulatory cascade orchestrated by Ash1l with RAR (show RARA Proteins) and provide insights into mechanisms underlying the establishment of the transcriptional activation that counteracts Polycomb (show CBX2 Proteins) silencing
all of the H3K36-specific methyltransferases, including ASH1L, HYPB, NSD1, and NSD2 (show WHSC1 Proteins) were inhibited by ubH2A, whereas the other histone methyltransferases, including PRC2, G9a (show EHMT2 Proteins), and Pr-Set7 (show SETD8 Proteins) were not affected by ubH2A.
induction of Cdk5 (show CDK5 Proteins) activity is a novel mechanism through which hASH1 (show ASCL1 Proteins) may regulate migration in lung carcinogenesis
Histone Methyltransferase Ash1l Is a Target of miR (show MLXIP Proteins)-291 and Regulates Hox (show MSH2 Proteins) Gene Expression.
Ash1l is a novel key regulator of changes associated with the adaptation of HSCs to the BM niche at the fetal to adult transition or upon transplantation of HSCs into an adult recipient.
Ash1l-mediated H3K4 methylation at the Tnfaip3 (show TNFAIP3 Proteins) promoter is required for controlling innate IL-6 (show IL6 Proteins) production and suppressing inflammatory autoimmune diseases, providing mechanistic insight into epigenetic modulation of immune responses and inflammation
ASH1 (show ASCL1 Proteins) mono- or di-methylates histone H3 (show HIST3H3 Proteins) K36 (show KRT36 Proteins) but not any other lysine residues of recombinant unmodified mammalian histones
the C-terminal part of ASH1 (show ASCL1 Proteins) interacts with HDAC1 (show HDAC1 Proteins) repression complexes, suggesting that the PHD (show PDC Proteins) finger of ASH1 (show ASCL1 Proteins) may be involved in down-regulation of genes for normal development of alphabeta T cells.
This gene encodes a member of the trithorax group of transcriptional activators. The protein contains four AT hooks, a SET domain, a PHD-finger motif, and a bromodomain. It is localized to many small speckles in the nucleus, and also to cell-cell tight junctions.
probable histone-lysine N-methyltransferase ASH1L
, ash1 (absent, small, or homeotic)-like (Drosophila)
, zinc finger (PHD)-13
, Ash1l protein
, absent, small, or homeotic 1-like
, ASH1-like protein
, absent small and homeotic disks protein 1 homolog
, histone-lysine N-methyltransferase ASH1L
, lysine N-methyltransferase 2H
, absent, small, or homeotic discs 1
, chromatin remodeling factor