Publications by authors named "Yunwei Qu"

Fluorescence nanoscopy of living cells employs contrast agents to reveal intrinsic correlations between mitochondrial dynamics and functions at the molecular level. However, regular mitochondrial fluorophores usually present poor photostability, low brightness, non-specific inhibitory effects, high phototoxicity, and rapid photobleaching, which have hindered the use of these tools to capture the intricate dynamic features of mitochondria. Herein, we engineered a fluorogen-activating protein (FAP), AmpHecy@HSA, a non-covalent self-assembly of HSA and amphiphilic hemicyanine (AmpHecy) fluorophore, with exceptional cell permeability, long-lasting photostability, high brightness/fluorogenicity, and minimal phototoxicity.

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Fluorophores are considered powerful tools for not only enabling the visualization of cell structures, substructures, and biological processes, but also making for the quantitative and qualitative measurement of various analytes in living systems. However, most fluorophores do not meet the diverse requirements for biological applications in terms of their photophysical and biological properties. Hybridization is an important strategy in molecular engineering that provides fluorophores with complementarity and multifunctionality.

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Article Synopsis
  • Abnormal copper metabolism is linked to several diseases, including Alzheimer's and Wilson's disease, and a new type of cell death called cuproptosis has been identified as significant in understanding these conditions.
  • Current research is hindered by a lack of effective imaging tools to study copper within complex biological systems, but fluorescence turn-on probes show promise in improving imaging resolution and accuracy.
  • This review discusses the development of these probes over the last decade, proposes ideas for future probe designs to advance cuproptosis research, and examines the potential of targeting cuproptosis for disease treatment.
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Abnormal expression of monoamine oxidase A (MAO-A) has been implicated in the development of human glioma, making MAO-A a promising target for therapy. Therefore, a rapid determination of MAO-A is critical for diagnosis. Through in silico screening of two-photon fluorophores, we discovered that a derivative of N,N-dimethyl-naphthalenamine (pre-mito) can effectively fit into the entrance of the MAO-A cavity.

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Article Synopsis
  • Mitochondria are vital for energy regulation and cell death, and damaged ones are eliminated through mitophagy, which is influenced by pH changes and linked to various diseases.
  • Recent advancements have led to the development of small-molecule fluorescent pH probes that help monitor mitophagy with high selectivity and sensitivity.
  • The review highlights different sensing mechanisms of these probes, explores disease models for mitophagy research, and discusses design requirements and future challenges in the field.
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MAO-A promotes the proliferation of human glioma cells. Herein, we report a series of MAO-A specific two-photon small molecular fluorescent probes (A1-5) based on an intramolecular charge transfer enhancing strategy. The activity of endogenous MAO-A can be selectively imaged using A3 as a representative probe in different biological samples including human glioma cells/tissues two-photon fluorescence microscopy.

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Tyrosinase is an important enzyme in controlling the formation of melanin in melanosome, and plays a key role in the pigmentation of hair and skin. The abnormal expression or activation of tyrosinase is associated with several diseases such as albinism, vitiligo, melanoma and Parkinson disease. Excessive deposition of melanin could cause diseases such as freckles and brown spots in the human body, and it is also closely related to browning of fruits and vegetables and insect molting.

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Alzheimer's disease (AD) is currently an incurable neurodegenerative disorder that affects millions of people around the world. The aggregation of amyloid-β peptides (Aβ), one of the primary pathological hallmarks of AD, plays a key role in the AD pathogenesis. In this regard, Aβ aggregates have been considered as both biomarkers and drug targets for the diagnosis and therapy of AD.

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