Qingfei Zheng

Prof. Dr. Qingfei Zheng

BMCMP, Purdue University West Lafayette, West Lafayette, Indiana, USA

Research Focus & Metrics

Academic Career Length

14Years (2013-Present)

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

Representative Publications

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20 March 2019 in Nature Communications
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Journal Article
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Qingfei ZhengQingfei Zheng
Qingfei Zheng
NONathaniel D. Omans
Nathaniel D. Omans
RLRachel Leicher
Rachel Leicher
AOAdewola Osunsade
Adewola Osunsade
AAAlbert S. Agustinus
Albert S. Agustinus
YDYael David
Yael David
Cellular proteins continuously undergo non-enzymatic covalent modifications (NECMs) that accumulate under normal physiological conditions and are stimulated by changes in the cellular microenvironment. Glycation, the hallmark of diabetes, is a prevalent NECM associated with an array of pathologies. Histone proteins are particularly susceptible to NECMs due to their long half-lives and nucleophilic disordered tails that undergo extensive regulatory modifications; however, histone NECMs remain poorly understood. Here we perform a detailed analysis of histone glycation in vitro and in vivo and find it has global ramifications on histone enzymatic PTMs, the assembly and stability of nucleosomes, and chromatin architecture. Importantly, we identify a physiologic regulation mechanism, the enzyme DJ-1, which functions as a potent histone deglycase. Finally, we detect intense histone glycation and DJ-1 overexpression in breast cancer tumors. Collectively, our results suggest an additional mechanism for cellular metabolic damage through epigenetic perturbation, with implications in pathogenesis.

2 March 2015 in Nature Chemical Biology
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Journal Article
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ZTZhenhua Tian
Zhenhua Tian
PSPeng Sun
Peng Sun
YYYan Yan
Yan Yan
ZWZhuhua Wu
Zhuhua Wu
Qingfei ZhengQingfei Zheng
Qingfei Zheng
WLWen Liu
Wen Liu

27 July 2023 in Cancer Biology & Therapy
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Journal Article
Open access
SKShruthi Kandalai
Shruthi Kandalai
HLHuapeng Li
Huapeng Li
NZNan Zhang
Nan Zhang
HPHaidong Peng
Haidong Peng
Qingfei ZhengQingfei Zheng
Qingfei Zheng
Recent evidence has shown that the human microbiome is associated with various diseases, including cancer. The salivary microbiome, fecal microbiome, and circulating microbial DNA in blood plasma have all been used experimentally as diagnostic biomarkers for many types of cancer. The microbiomes present within local tissue, other regions, and tumors themselves have been shown to promote and restrict the development and progression of cancer, most often by affecting cancer cells or the host immune system. These microbes have also been shown to impact the efficacy of various cancer therapies, including radiation, chemotherapy, and immunotherapy. Here, we review the research advances focused on how microbes impact these different facets and why they are important to the clinical care of cancer. It is only by better understanding the roles these microbes play in the diagnosis, development, progression, and treatment of cancer, that we will be able to catch and treat cancer early.

30 April 2020 in Protein & Cell
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Journal Article
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Qingfei ZhengQingfei Zheng
Qingfei Zheng
IMIgor Maksimovic
Igor Maksimovic
AUAkhil Upad
Akhil Upad
YDYael David
Yael David
Epigenetic modifications, including those on DNA and histones, have been shown to regulate cellular metabolism by controlling expression of enzymes involved in the corresponding metabolic pathways. In turn, metabolic flux influences epigenetic regulation by affecting the biosynthetic balance of enzyme cofactors or donors for certain chromatin modifications. Recently, non-enzymatic covalent modifications (NECMs) by chemically reactive metabolites have been reported to manipulate chromatin architecture and gene transcription through multiple mechanisms. Here, we summarize these recent advances in the identification and characterization of NECMs on nucleic acids, histones, and transcription factors, providing an additional mechanistic link between metabolism and epigenetics.

2 October 2013 in Angewandte Chemie International Edition
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YYYan Yan
Yan Yan
JCJing Chen
Jing Chen
LZLihan Zhang
Lihan Zhang
Qingfei ZhengQingfei Zheng
Qingfei Zheng
YHYing Han
Ying Han
WLWen Liu
Wen Liu

8 January 2025 in Nature
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Journal Article
Open access
PDF file
Qingfei ZhengQingfei Zheng
Qingfei Zheng
BWBen Weekley
Ben Weekley
DVDavid A. Vinson
David A. Vinson
SZShuai Zhao
Shuai Zhao
RBRyan M. Bastle
Ryan M. Bastle
IMIan Maze
Ian Maze
Histone H3 monoaminylations at Gln5 represent an important family of epigenetic marks in brain that have critical roles in permissive gene expression1–3. We previously demonstrated that serotonylation4–10 and dopaminylation9,11–13 of Gln5 of histone H3 (H3Q5ser and H3Q5dop, respectively) are catalysed by transglutaminase 2 (TG2), and alter both local and global chromatin states. Here we found that TG2 additionally functions as an eraser and exchanger of H3 monoaminylations, including H3Q5 histaminylation (H3Q5his), which displays diurnally rhythmic expression in brain and contributes to circadian gene expression and behaviour. We found that H3Q5his, in contrast to H3Q5ser, inhibits the binding of WDR5, a core member of histone H3 Lys4 (H3K4) methyltransferase complexes, thereby antagonizing methyltransferase activities on H3K4. Taken together, these data elucidate a mechanism through which a single chromatin regulatory enzyme has the ability to sense chemical microenvironments to affect the epigenetic states of cells, the dynamics of which have critical roles in the regulation of neural rhythmicity.