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ASH1L encodes a member of the trithorax group of transcriptional activators. Zusätzlich bieten wir Ihnen ASH1L Proteine (2) und viele weitere Produktgruppen zu diesem Protein an.
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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 (zeige MLL Antikörper) 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 (zeige SETD2 Antikörper) are H3K36 specific methyltransferases but only SETD2 (zeige SETD2 Antikörper) can trimethylate this mark.
These data demonstrate that miR (zeige MLXIP Antikörper)-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 (zeige RARA Antikörper) and provide insights into mechanisms underlying the establishment of the transcriptional activation that counteracts Polycomb (zeige CBX2 Antikörper) silencing
all of the H3K36-specific methyltransferases, including ASH1L, HYPB (zeige SETD2 Antikörper), NSD1 (zeige NSD1 Antikörper), and NSD2 (zeige WHSC1 Antikörper) were inhibited by ubH2A, whereas the other histone methyltransferases, including PRC2, G9a (zeige EHMT2 Antikörper), and Pr-Set7 (zeige SETD8 Antikörper) were not affected by ubH2A.
induction of Cdk5 (zeige CDK5 Antikörper) activity is a novel mechanism through which hASH1 (zeige ASCL1 Antikörper) may regulate migration in lung carcinogenesis
Long Non-coding RNA, DBE-T recruits the Trithorax (zeige MLLT1 Antikörper) group protein Ash1L to the FSHD locus, driving histone H3 (zeige HIST3H3 Antikörper) lysine 36 dimethylation, chromatin remodeling, and 4q35 gene transcription.
ASH1 (zeige ASCL1 Antikörper) and MLL1 synergize in activation of Hox (zeige MSH2 Antikörper) genes.
Histone Methyltransferase Ash1l Is a Target of miR (zeige MLXIP Antikörper)-291 and Regulates Hox (zeige MSH2 Antikörper) 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 (zeige TNFAIP3 Antikörper) promoter is required for controlling innate IL-6 (zeige IL6 Antikörper) production and suppressing inflammatory autoimmune diseases, providing mechanistic insight into epigenetic modulation of immune responses and inflammation
ASH1 (zeige ASCL1 Antikörper) mono- or di-methylates histone H3 (zeige HIST3H3 Antikörper) K36 (zeige KRT36 Antikörper) but not any other lysine residues of recombinant unmodified mammalian histones
the C-terminal part of ASH1 (zeige ASCL1 Antikörper) interacts with HDAC1 (zeige HDAC1 Antikörper) repression complexes, suggesting that the PHD (zeige PDC Antikörper) finger of ASH1 (zeige ASCL1 Antikörper) 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