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