Yunjiao Zhang
Tuning Autophagy-Inducing Activity and Toxicity for Lanthanide Nanocrystals
Tuning Autophagy-Inducing Activity and Toxicity for Lanthanide Nanocrystals
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- More about Tuning Autophagy-Inducing Activity and Toxicity for Lanthanide Nanocrystals
This thesis presents a novel surface engineering approach using non-covalent binding peptides to control the autophagy-inducing activity of nanomaterials and nanodevices. RE-1, a short synthetic peptide, effectively binds to lanthanide oxide and upconversion nanocrystals, inhibiting their autophagy-inducing activity and toxicity. This provides a versatile tool for tuning cell interactions and applications in diagnostics and therapeutics.
Format: Paperback / softback
Length: 156 pages
Publication date: 10 January 2023
Publisher: Springer Verlag, Singapore
This thesis presents a groundbreaking surface engineering solution that harnesses the power of non-covalent binding peptides to regulate the autophagy-inducing activity of nanomaterials and nanodevices. The author unveils RE-1, a short synthetic peptide that exhibits sequence-specific binding affinity towards lanthanide (LN) oxide and upconversion nanocrystals, which was discovered through an innovative phage display approach. RE-1 effectively suppresses the autophagy-inducing activity and toxicity of these nanocrystals by forming a stable coating layer on their surface, thereby reducing their sedimentation and cell interaction. Moreover, RE-1 and its variants offer a versatile tool for fine-tuning cell interactions, enabling the attainment of desired autophagic responses and making them invaluable for a wide range of diagnostic and therapeutic applications involving LN-based nanomaterials and nanodevices.
The author's innovative approach involves the utilization of phage display, a technique that allows for the screening of large libraries of peptides to identify those with specific binding properties towards target molecules. In this case, the author identified RE-1, a peptide that exhibits high affinity for lanthanide oxide and upconversion nanocrystals. The binding of RE-1 to these nanocrystals is sequence-specific, as it targets specific regions within the peptide sequence that are responsible for the interaction with the nanocrystal surface.
Once RE-1 is bound to the nanocrystals, it forms a stable coating layer on their surface. This coating layer acts as a barrier, preventing the nanocrystals from interacting with cells and promoting their sedimentation. Additionally, the coating layer reduces the toxicity of the nanocrystals by preventing their entry into cells and disrupting cellular processes.
The significance of RE-1 and its variants lies in their ability to tune cell interactions. By controlling the autophagy-inducing activity and toxicity of nanocrystals, RE-1 and its variants can be used to achieve the desired level of autophagic response in cells. This can be beneficial in various diagnostic and therapeutic applications, such as cancer therapy, where autophagy plays a crucial role in the degradation of cancer cells.
Furthermore, RE-1 and its variants offer potential applications in other fields, such as drug delivery and tissue engineering. By controlling the interactions between nanocrystals and cells, RE-1 and its variants can be used to enhance the efficacy of drugs and promote tissue regeneration.
In conclusion, this thesis presents a simple yet highly effective surface engineering solution that uses non-covalent binding peptides to control the autophagy-inducing activity of nanomaterials and nanodevices. The discovery of RE-1, a short synthetic peptide that sequence-specifically binds to lanthanide oxide and upconversion nanocrystals, provides a versatile tool for tuning cell interactions and achieving desired autophagic responses. The potential applications of RE-1 and its variants in various fields, including cancer therapy, drug delivery, and tissue engineering, make it a promising area of research for future development.
Weight: 273g
Dimension: 235 x 155 (mm)
ISBN-13: 9789811681684
Edition number: 1st ed. 2022
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