![Loading...](https://link.springer.com/static/c4a417b97a76cc2980e3c25e2271af3129e08bbe/images/pdf-preview/spacer.gif)
-
Chapter
N6-Methyladenosine RNA Modification in Normal and Malignant Hematopoiesis
Over 170 nucleotide variants have been discovered in messenger RNAs (mRNAs) and non-coding RNAs so far. However, only a few of them, including N6-methyladenosine (m6A), 5-methylcytidine (m5C), and N1-methyladenos...
-
Article
Publisher Correction: Recognition of RNA N6-methyladenosine by IGF2BP proteins enhances mRNA stability and translation
An amendment to this paper has been published and can be accessed via a link at the top of the paper.
-
Article
Open AccessRoles of METTL3 in cancer: mechanisms and therapeutic targeting
N6-methyladenosine (m6A) is the most abundant mRNA modification and is catalyzed by the methyltransferase complex, in which methyltransferase-like 3 (METTL3) is the sole catalytic subunit. Accumulating evidence i...
-
Article
Histone H3 trimethylation at lysine 36 guides m6A RNA modification co-transcriptionally
DNA and histone modifications have notable effects on gene expression1. Being the most prevalent internal modification in mRNA, the N6-methyladenosine (m6A) mRNA modification is as an important post-transcription...
-
Chapter
RNA N 6-Methyladenosine Modification in Normal and Malignant Hematopoiesis
As the most abundant internal modification in eukaryotic messenger RNAs (mRNAs), N 6-methyladenosine (m6A) modification has been shown recently to posttranscriptionally regulate expression of thousands of messeng...
-
Article
Author Correction: Recognition of RNA N6-methyladenosine by IGF2BP proteins enhances mRNA stability and translation
In the version of this Article originally published, the authors incorrectly listed an accession code as GES90642. The correct code is GSE90642. This has now...
-
Article
Open AccessRNA N6-methyladenosine modification in cancers: current status and perspectives
N6-methyladenosine (m6A), the most abundant internal modification in eukaryotic messenger RNAs (mRNAs), has been shown to play critical roles in various normal bioprocesses such as tissue development, stem cell s...
-
Article
Recognition of RNA N6-methyladenosine by IGF2BP proteins enhances mRNA stability and translation
N6-methyladenosine (m6A) is the most prevalent modification in eukaryotic messenger RNAs (mRNAs) and is interpreted by its readers, such as YTH domain-containing proteins, to regulate mRNA fate. Here, we report t...
-
Article
Open AccessAuthor Correction: Targeted inhibition of STAT/TET1 axis as a therapeutic strategy for acute myeloid leukemia
The original version of this Article contained an error in the spelling of the author James C. Mulloy, which was incorrectly given as James Mulloy. This has now been corrected in both the PDF and HTML versions...
-
Article
Open AccessTargeted inhibition of STAT/TET1 axis as a therapeutic strategy for acute myeloid leukemia
Effective therapy of acute myeloid leukemia (AML) remains an unmet need. DNA methylcytosine dioxygenase Ten-eleven translocation 1 (TET1) is a critical oncoprotein in AML. Through a series of data analysis and...
-
Article
Open AccessALOX5 exhibits anti-tumor and drug-sensitizing effects in MLL-rearranged leukemia
MLL-rearranged acute myeloid leukemia (AML) remains a fatal disease with a high rate of relapse and therapeutic failure due to chemotherapy resistance. In analysis of our Affymetrix micro...
-
Article
Open AccessOridonin Triggers Chaperon-mediated Proteasomal Degradation of BCR-ABL in Leukemia
Inducing degradation of oncoproteins by small molecule compounds has the potential to avoid drug resistance and therefore deserves to be exploited for new therapies. Oridonin is a natural compound with promisi...
-
Article
Open AccessmiR-22 has a potent anti-tumour role with therapeutic potential in acute myeloid leukaemia
MicroRNAs are subject to precise regulation and have key roles in tumorigenesis. In contrast to the oncogenic role of miR-22 reported in myelodysplastic syndrome (MDS) and breast cancer, here we show that miR-...