Publications by authors named "Zetao Hu"
Article Synopsis
- METTL4 is a methyltransferase in Arabidopsis that mediates the methylation of RNA and DNA, specifically functioning as a U2 snRNA MTase for N-2'-O-dimethyladenosine (mAm) which affects flowering time.
- The study reveals that METTL4 catalyzes the N-methylation of 2'-O-methyladenosine (Am) in vitro, using structural insights that show its unique binding cavity and catalytic center crucial for substrate interaction.
- Comparisons with other methyltransferases suggest that METTL4 shares a similar catalytic mechanism with the mRNA m6A enzyme complex (METTL3/METTL14), highlighting a potential commonality among
Structural basis of the bHLH domains of MyoD-E47 heterodimer.
Biochem Biophys Res Commun
September 2022
The basic helix-loop-helix (bHLH) family is one of the most conserved transcription factor families that plays an important role in regulating cell growth, differentiation and tissue development. Typically, members of this family form homo- or heterodimers to recognize specific motifs and activate transcription. MyoD is a vital transcription factor that regulates muscle cell differentiation.
View Article and Find Full Text PDFAsp50Glu mutation in MurA results in fosfomycin resistance in Enterococcus faecium.
J Glob Antimicrob Resist
September 2022
Objectives: Enterococcus faecium is one of the important pathogens causing nosocomial infection, which can be resistant to fosfomycin by obtaining the plasmid-encoded fosfomycin resistance genes, and the mutation of MurA protein encoded by chromosome is a newly discovered fosfomycin resistance mechanism in recent years.
Methods: In this study, we found a fosfomycin-resistant clinical isolate of E. faecium Efm_1415 with fosfomycin MIC of 512 mg/L, carrying Asp50Glu mutant of MurA protein, which was never reported before.
Background & Aims: Despite remarkable advances in treatment, most patients with hepatocellular carcinoma (HCC) respond poorly to anti-programmed cell death 1 (anti-PD1) therapy. A deeper insight into the tolerance mechanism of HCC against this therapy is urgently needed.
Methods: We performed next-generation sequencing, multiplex immunofluorescence, and dual-color immunohistochemistry and constructed an orthotopic HCC xenograft tumor model to identify the key gene associated with anti-PD1 tolerance.