Results 81 to 90 of about 175,165 (326)

Defending the genome from the enemy within:mechanisms of retrotransposon suppression in the mouse germline [PDF]

open access: yes, 2013
The viability of any species requires that the genome is kept stable as it is transmitted from generation to generation by the germ cells. One of the challenges to transgenerational genome stability is the potential mutagenic activity of transposable ...
A Aravin   +241 more
core   +2 more sources

Domain associated with zinc fingers‐containing NF90‐NF45 complex inhibits m6A modification of primary microRNA by suppressing METTL3/14 activity

open access: yesFEBS Open Bio, EarlyView.
NF90–NF45 functions as a negative regulator of methyltransferase‐like 3/14 (METTL3/14)‐mediated N6‐methyladenosine (m6A) modification on primary microRNAs (pri‐miRNAs). NF90–NF45 binds to anti‐oncogenic pri‐miRNAs and inhibits their m6A modification, thereby suppressing the biogenesis of anti‐oncogenic miRNAs.
Takuma Higuchi   +6 more
wiley   +1 more source

Systematic expression analysis of m6A RNA methyltransferases in clear cell renal cell carcinoma

open access: yesBJUI Compass, 2021
Objectives To investigate the regulation of the N‐6‐methyladenosine (m6A) methyltransferases METTL3, METTL14, WTAP, KIAA1429, and METTL4, referred to as “m6A writers,” in clear cell renal cell carcinoma (ccRCC), and other RCC subtypes in respect of the ...
Larissa Gundert   +9 more
doaj   +1 more source

DNMT3B in vitro knocking-down is able to reverse embryonal rhabdomyosarcoma cell phenotype through inhibition of proliferation and induction of myogenic differentiation [PDF]

open access: yes, 2016
Aberrant DNA methylation has been frequently observed in many human cancers, including rhabdomyosarcoma (RMS), the most common soft tissue sarcoma in children.
Camero, Simona   +11 more
core   +1 more source

Targeting histone methyltransferases and demethylases in clinical trials for cancer therapy

open access: yesClinical Epigenetics, 2016
The term epigenetics is defined as heritable changes in gene expression that are not due to alterations of the DNA sequence. In the last years, it has become more and more evident that dysregulated epigenetic regulatory processes have a central role in ...
Ludovica Morera, M. Lübbert, M. Jung
semanticscholar   +1 more source

Aging Is a Key Driver for Adult Acute Myeloid Leukemia

open access: yesAging and Cancer, EarlyView.
Acute myeloid leukemia (AML) is a classical age‐related hematologic malignancy, and a key driver of AML is aging, which profoundly regulates intrinsic factors such as genomic instability, epigenetic reprogramming, and metabolic dysregulation, and alters bone marrow microenvironment.
Rong Yin, Haojian Zhang
wiley   +1 more source

Correction: Dietary Flavones as Dual Inhibitors of DNA Methyltransferases and Histone Methyltransferases. [PDF]

open access: yesPLoS ONE, 2016
[This corrects the article DOI: 10.1371/journal.pone.0162956.].
Rajnee Kanwal   +3 more
doaj   +1 more source

DNA methylation dynamics in aging: How far are we from understanding the mechanisms? [PDF]

open access: yes, 2018
DNA methylation is currently the most promising molecular marker for monitoring aging and predicting life expectancy. However, the mechanisms underlying age-related DNA methylation changes remain mostly undiscovered.Here we discuss the current knowledge ...
Caiafa, Paola   +3 more
core   +1 more source

The interactome of a family of potential methyltransferases in HeLa cells

open access: yesScientific Reports, 2019
Human methytransferase like proteins (METTL) are part of a large protein family characterized by the presence of binding domains for S-adenosyl methionine, a co-substrate for methylation reactions.
V. Ignatova   +4 more
semanticscholar   +1 more source

Mutant NPM1 in Acute Myeloid Leukemia Initiation and Maintenance

open access: yesAging and Cancer, EarlyView.
NPM1 mutations drive acute myeloid leukemia by acting as neomorphic transcriptional regulators that cooperate with Menin–MLL and XPO1 to sustain HOX/MEIS1 expression and block differentiation. Targeting these mutant‐specific transcriptional dependencies provides a rational therapeutic strategy for NPM1‐mutated AML.
Yanan Jiang   +3 more
wiley   +1 more source

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