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Xiao-Min Liu
Researcher at Cornell University
Publications - 9
Citations - 776
Xiao-Min Liu is an academic researcher from Cornell University. The author has contributed to research in topics: MRNA methylation & RNA. The author has an hindex of 5, co-authored 9 publications receiving 446 citations. Previous affiliations of Xiao-Min Liu include China Pharmaceutical University.
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Journal ArticleDOI
m 6 A in mRNA coding regions promotes translation via the RNA helicase-containing YTHDC2
TL;DR: It is demonstrated that the m6A reader YTHDC2 — which contains an RNA helicase domain — acts on the coding region to promotes mRNA translation by resolving secondary structures, and established the physiological significance of CDS methylation and uncovered non-overlapping function of m 6A reader proteins.
Journal ArticleDOI
m6A Facilitates eIF4F-Independent mRNA Translation
Ryan Alex Coots,Xiao-Min Liu,Yuanhui Mao,Leiming Dong,Jun Zhou,Ji Wan,Xingqian Zhang,Shu-Bing Qian +7 more
TL;DR: It is reported that N6-methyladenosine (m6A) facilitates mRNA translation that is resistant to eIF4F inactivation, and ABCF1 is identified as a critical mediator of m6A-promoted translation under both stress and physiological conditions.
Journal ArticleDOI
N6-Methyladenosine Guides mRNA Alternative Translation during Integrated Stress Response.
Jun Zhou,Ji Wan,Xin Erica Shu,Yuanhui Mao,Xiao-Min Liu,Xin Yuan,Xingqian Zhang,Martin E. Hess,Jens C. Brüning,Shu-Bing Qian +9 more
TL;DR: It is reported that, in response to amino acid starvation, the reinitiation of ATF4 is not only governed by the eIF2α signaling pathway, but is also subjected to regulation by mRNA methylation in the form of N6-methyladenosine (m6A).
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Programmable RNA N 6 -methyladenosine editing by CRISPR-Cas9 conjugates
TL;DR: ‘m6A editing’ is reported, a powerful approach that enables m6A installation and erasure from cellular RNAs without changing the primary sequence and facilitates mechanistic understanding of epitranscriptome.
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Differential roles of YTHDF1 and YTHDF3 in embryonic stem cell-derived cardiomyocyte differentiation.
TL;DR: Phenotypic and transcriptomic analyses revealed that loss of YTHDF1 led to dramatic impairment of cardiomyocytes (CMs) differentiation, accompanied by downregulated CM-specific genes, and knockdown of Y THDF3 accelerated differentiation through facilitating the expressions ofCM-specific gene.