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The protein encoded by DOT1L is a histone methyltransferase that methylates lysine-79 of histone H3. Additionally we are shipping DOT1-Like, Histone H3 Methyltransferase (S. Cerevisiae) Antibodies (78) and DOT1-Like, Histone H3 Methyltransferase (S. Cerevisiae) Proteins (4) and many more products for this protein.
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this study shows that Dot1l expression predicts adverse postoperative prognosis of patients with clear-cell renal cell carcinoma
facilitates DNA damage repair; plays a protective role in ultraviolet radiation-induced melanomagenesis
DOT1L cooperates with transcription factor ETS-1 (show ETS1 ELISA Kits) to stimulate the expression of VEGFR2 (show KDR ELISA Kits), thereby activating ERK1/2 (show MAPK1/3 ELISA Kits) and AKT (show AKT1 ELISA Kits) signaling pathways and promoting angiogenesis.
findings demonstrate that DOT1L over-expression has important clinical significance in ovarian cancer and also clarify that it drives cell cycle progression through transcriptional regulation of CDK6 (show CDK6 ELISA Kits) and CCND3 (show CCND3 ELISA Kits) through H3K79 methylation
MLL-AF4 spreading gene expression is downregulated by inhibitors of the H3K79 methyltransferase DOT1L.
our results identify DOT1L as a novel cofactor in N-Myc-mediated transcriptional activation of target genes and neuroblastoma oncogenesis. Furthermore, they characterize DOT1L inhibitors as novel anticancer agents against MYCN-amplified neuroblastoma.
These results reveal a cooperative transcriptional activation mechanism of AEP and DOT1L and suggest a molecular rationale for the simultaneous inhibition of the MLL fusion-AF4 complex and DOT1L for more effective treatment of MLL-rearranged leukemia.
this indicates that DOT1L function, like MLL, does not completely rely on its methyltransferase activity. Nevertheless, the small molecule DOT1L inhibition is sufficient to block the proliferation of MLL fusion-induced leukemia cells of murine and human origin
DOT1L may play a critical role in DNMT3A (show DNMT3A ELISA Kits)-mutant leukemia.
DOT1L, via dimethylated histone H3 (show HIST3H3 ELISA Kits) K79, facilitates histone H4 acetylation, which in turn regulates the binding of BRD4 (show BRD4 ELISA Kits) to chromatin in acute lymphoblastic leukemia.
In the absence of DOT1L, ultraviolet radiation (UVR)-induced DNA damage is inefficiently repaired, so that DOT1L loss promotes melanoma development after exposure to UVR.
We will highlight the structural basis of chromatin targeting of DOT1L through its cofactors and the role of DOT1L in repelling transcription repressive complexes during leukemia development.
Dot1l is a new epigenetic regulator of principal cells and intercalated cell differentiation and Atp6v1b1 is a new transcriptional target of Dot1l.
results demonstrate that histone methylation, and in particular DOT1L-mediated H3K79me2 modification, drives cardiomyogenesis through the definition of a specific transcriptional landscape
Interference with DOT1L activity resulted in transcriptional activation of Atf4 (show ATF4 ELISA Kits) and Ddit3 (show DDIT3 ELISA Kits) accompanied by decreased levels of H3K79 dimethylation.
MLL1 and DOT1L cooperate with meningioma-1 to induce acute myeloid leukemia (show BCL11A ELISA Kits).
DOT1L has a role in inhibiting SIRT1-mediated epigenetic silencing to maintain leukemic gene expression in MLL-rearranged leukemia
The protein encoded by this gene is a histone methyltransferase that methylates lysine-79 of histone H3. It is inactive against free core histones, but shows significant histone methyltransferase activity against nucleosomes.
histone-lysine N-methyltransferase, H3 lysine-79 specific
, DOT1-like, histone H3 methyltransferase (S. cerevisiae)
, histone-lysine N-methyltransferase, H3 lysine-79 specific-like
, possible nucleosomal histone methylase
, DOT1-like protein
, DOT1-like, histone H3 methyltransferase
, histone H3-K79 methyltransferase
, histone methyltransferase DOT1L
, lysine N-methyltransferase 4
, DOT1-like histone H3 methyltransferase
, histone H3 methyltransferase DOT1