binding peptide
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Langmuir ◽  
2022 ◽  
Author(s):  
Tal Duanis-Assaf ◽  
Tan Hu ◽  
Maayan Lavie ◽  
Zhuo Zhang ◽  
Meital Reches

2021 ◽  
Vol 23 (1) ◽  
pp. 447
Author(s):  
Helena Crijns ◽  
Lowie Adyns ◽  
Eva Ganseman ◽  
Seppe Cambier ◽  
Eline Vandekerckhove ◽  
...  

Although glycosaminoglycan (GAG)–protein interactions are important in many physiological and pathological processes, the structural requirements for binding are poorly defined. Starting with GAG-binding peptide CXCL9(74-103), peptides were designed to elucidate the contribution to the GAG-binding affinity of different: (1) GAG-binding motifs (i.e., BBXB and BBBXXB); (2) amino acids in GAG-binding motifs and linker sequences; and (3) numbers of GAG-binding motifs. The affinity of eight chemically synthesized peptides for various GAGs was determined by isothermal fluorescence titration (IFT). Moreover, the binding of peptides to cellular GAGs on Chinese hamster ovary (CHO) cells was assessed using flow cytometry with and without soluble GAGs. The repetition of GAG-binding motifs in the peptides contributed to a higher affinity for heparan sulfate (HS) in the IFT measurements. Furthermore, the presence of Gln residues in both GAG-binding motifs and linker sequences increased the affinity of trimer peptides for low-molecular-weight heparin (LMWH), partially desulfated (ds)LMWH and HS, but not for hyaluronic acid. In addition, the peptides bound to cellular GAGs with differential affinity, and the addition of soluble HS or heparin reduced the binding of CXCL9(74-103) to cellular GAGs. These results indicate that the affinity and specificity of peptides for GAGs can be tuned by adapting their amino acid sequence and their number of GAG-binding motifs.


2021 ◽  
Vol 29 ◽  
Author(s):  
Lingyan Zuo ◽  
Weiqian Li ◽  
Jifang Shi ◽  
Yingzhen Su ◽  
Hongyan Shuai ◽  
...  

Background: Polyglutamine diseases are degenerative diseases in the central nervous system caused by CAG trinucleotide repeat expansion which encodes polyglutamine tracts, leading to the misfolding of pathological proteins. Small peptides can be designed to prevent polyglutamine diseases by inhibiting the polyglutamine protein aggregation, for example, polyglutamine binding peptide 1(QBP1). However, the transportation capability of polyglutamine binding peptide 1 across the blood-brain barrier is less efficient. We hypothesized whether its therapeutic effect could be improved by increasing the rate of membrane penetration. Objectives: The objective of the study was to explore whether polyglutamine binding peptide 1 conjugated cell-penetrating peptides could pass through the blood-brain barrier and inhibit the aggregation of polyglutamine proteins. Methods: n order to investigate the toxic effects, we constructed a novel stable inducible PC12 cells to express Huntington protein that either has 11 glutamine repeats or 63 glutamine repeats to mimic wild type and polyglutamine expand Huntington protein, respectively. Both SynB3 and TAT conjugated polyglutamine binding peptide 1 was synthesized, respectively, and we tested their capabilities to pass through a Trans-well system and subsequently studied the counteractive effects on polyglutamine protein aggregation. Results: The conjugation of cell-penetrating peptides to SynB3 and TAT enhanced the transportation of polyglutamine binding peptide 1 across the mono-cell layer and ameliorated polyglutamine-expanded Huntington protein aggregation; moreover, SynB3 showed better delivery efficiency than TAT. Interestingly, it has been observed that polyglutamine binding peptide 1 specifically inhibited polyglutamine-expanded protein aggregation rather than affected other amyloidosis proteins, for example, β-Amyloid. Conclusion: Our study indicated that SynB3 could be an effective carrier for polyglutamine binding peptide 1 distribution through the blood-brain barrier model and ameliorate the formation of polyglutamine inclusions, thus SynB3 conjugated polyglutamine binding peptide 1 could be considered as a therapeutic candidate for polyglutamine diseases.


2021 ◽  
Vol 22 (22) ◽  
pp. 12544
Author(s):  
Wan Yang ◽  
Vijay Singh Gondil ◽  
Dehua Luo ◽  
Jin He ◽  
Hongping Wei ◽  
...  

Staphylococcal-associated device-related infections (DRIs) represent a significant clinical challenge causing major medical and economic sequelae. Bacterial colonization, proliferation, and biofilm formation after adherence to surfaces of the indwelling device are probably the primary cause of DRIs. To address this issue, we incorporated constructs of silica-binding peptide (SiBP) with ClyF, an anti-staphylococcal lysin, into functionalized coatings to impart bactericidal activity against planktonic and sessile Staphylococcus aureus. An optimized construct, SiBP1-ClyF, exhibited improved thermostability and staphylolytic activity compared to its parental lysin ClyF. SiBP1-ClyF-functionalized coatings were efficient in killing MRSA strain N315 (>99.999% within 1 h) and preventing the growth of static and dynamic S. aureus biofilms on various surfaces, including siliconized glass, silicone-coated latex catheter, and silicone catheter. Additionally, SiBP1-ClyF-immobilized surfaces supported normal attachment and growth of mammalian cells. Although the recycling potential and long-term stability of lysin-immobilized surfaces are still affected by the fragility of biological protein molecules, the present study provides a generic strategy for efficient delivery of bactericidal lysin to solid surfaces, which serves as a new approach to prevent the growth of antibiotic-resistant microorganisms on surfaces in hospital settings and could be adapted for other target pathogens as well.


ACS Nano ◽  
2021 ◽  
Author(s):  
Zak E. Hughes ◽  
Michelle A. Nguyen ◽  
Jialei Wang ◽  
Yang Liu ◽  
Mark T. Swihart ◽  
...  

Author(s):  
Anja Ziegler ◽  
Judith Olzhausen ◽  
Eman Hamza ◽  
Ana Stojiljkovic ◽  
Michael H. Stoffel ◽  
...  

2021 ◽  
Vol 65 (22) ◽  
pp. 2170058
Author(s):  
Gary Ro‐Lin Chang ◽  
Min‐Yu Tu ◽  
Yu‐Hsuan Chen ◽  
Ku‐Yi Chang ◽  
Chien‐Fu Chen ◽  
...  

2021 ◽  
Vol 580 ◽  
pp. 93-99
Author(s):  
Moon Hwa Kwak ◽  
Seung Mok Yang ◽  
Seul Ki Yun ◽  
Sol Kim ◽  
Myung-Gyu Choi ◽  
...  

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