Xingyu Zhou

Dr. Xingyu Zhou


Research Focus & Metrics

Academic Career Length

11Years (2016-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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15 November 2016 in Journal of Cell Science
Verified
Journal Article
Open access
PDF file
XZXingyu Zhou
Xingyu Zhou
MLMingsen Li
Mingsen Li
HHHuaxing Huang
Huaxing Huang
KCKeren Chen
Keren Chen
ZYZhuning Yuan
Zhuning Yuan
DMDelin Mo
Delin Mo
Although the mechanism underlying modulation of transcription factors in myogenesis has been well elucidated, the function of the transcription cofactors involved in this process remains poorly understood. Here, we identified HMGB2 as an essential nuclear transcriptional co-regulator in myogenesis. HMGB2 was highly expressed in undifferentiated myoblasts and regenerating muscle. Knockdown of HMGB2 inhibited myoblast proliferation and stimulated its differentiation. HMGB2 depletion downregulated Myf5 and cyclin A2 at the protein but not mRNA level. In contrast, overexpression of HMGB2 promoted Myf5 and cyclin A2 protein upregulation. Furthermore, we found that the RNA-binding protein IGF2BP2 is a downstream target of HMGB2, as previously shown for HMGA2. IGF2BP2 binds to mRNAs of Myf5 or cyclin A2, resulting in translation enhancement or mRNA stabilization, respectively. Notably, overexpression of IGF2BP2 could partially rescue protein levels of Myf5 and cyclin A2, in response to HMGB2 decrease. Moreover, depletion of HMGB2 in vivo severely attenuated muscle repair; this was due to a decrease in satellite cells. Taken together, these results highlight the previously undiscovered and crucial role of the HMGB2–IGF2BP2 axis in myogenesis and muscle regeneration.

1 March 2017 in Biochemical and Biophysical Research Communications
Verified
Journal Article
Closed access
ZYZhuning Yuan
Zhuning Yuan
YCYaosheng Chen
Yaosheng Chen
Xumeng ZhangXumeng Zhang
Xumeng Zhang
XZXingyu Zhou
Xingyu Zhou
MLMingsen Li
Mingsen Li
DMDelin Mo
Delin Mo

2 December 2019 in RSC Advances
Verified
Journal Article
Open access
PDF file
HLHuaguang Liu
Huaguang Liu
XZXingyu Zhou
Xingyu Zhou
CZChaoshen Zhang
Chaoshen Zhang
JZJinsong Zhang
Jinsong Zhang
Resourceful disposal of landfill leachate has always been an intractable worldwide problem. This study was conducted to investigate the feasibility of biologically treating a combined waste stream of landfill leachate and high-concentration nitrate nitrogen (high-nitrate) wastewater. Raw landfill leachate was pretreated using anaerobic fermentation and ammonia stripping to improve biodegradability. The control sequencing batch reactor (SBR, named R0) was fed only with synthetic high-nitrate wastewater with sodium acetate as the carbon source, whereas the other experimental SBR (named R1) was loaded with mixtures containing leachates. Excessive increase in leachate adversely affected the cotreatment, and it was concluded that the landfill leachate volume ratio should never exceed 7.5% of the total wastewater (14% of the initial COD) based on further batch experiments. The maximum specific denitrification rate of 58.05 mg NO3 −-N (gVSS h)−1 was attained in R1, while that of 32.32 mg NO3 −-N (gVSS h)−1 was obtained in R0. Illumina MiSeq sequencing revealed that adding landfill leachate did not change the fact that Pseudomonas, Thauera, and Pannonibacter dominant in the sodium acetate supported the denitrification systems, but led to the adjustment of their relative abundance. Moreover, the narG, nirK, nirS, and norB denitrifying genes exhibited increased abundance by 138–980% in the cotreated system, which was confirmed by q-PCR analyses. These findings reveal that the denitrification efficiency of activated sludge in SBR cotreated with landfill leachate and high-nitrate wastewater significantly improved, and this may contribute toward the understanding of the molecular mechanisms of biological denitrification under the blending treatment of leachate and high-nitrate wastewater.

10 November 2023 in Geobios
Verified
Journal Article
Closed access
JQJiachen Qin
Jiachen Qin
YLYunhuan LIU
Yunhuan LIU
TSTiequan Shao
Tiequan Shao
XZXingyu Zhou
Xingyu Zhou
MLMingjin Liu
Mingjin Liu
QWQi Wang
Qi Wang