Characterizing the binding mechanism of Bt (Bacillus thuringiensis) Cry toxin to the cadherin receptor is indispensable to understanding the specific insecticidal activity of this toxin. To this end, we constructed 30 loop mutants by randomly inserting four serial amino acids covering all four receptor binding loops (loops α8, 1, 2 and 3) and analysed their binding affinities for Bombyx mori cadherin receptors via Biacore. High binding affinities were confirmed for all 30 mutants containing loop sequences that differed from those of wild-type. Insecticidal activities were confirmed in at least one mutant from loops 1, 2 and 3, suggesting that there is no critical amino acid sequence for the binding of the four loops to BtR175. When two mutations at different loops were integrated into one molecule, no reduction in binding affinity was observed compared with wild-type sequences. Based on these results, we discussed the binding mechanism of Cry toxin to cadherin protein.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3546355 | PMC |
| http://dx.doi.org/10.1042/BSR20120113 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Exosomal miR-552-5p Regulates the Role of NK Cells in EMT of Gastric Cancer via the PD-1/PD-L1 Axis.
J Cancer
January 2025
Department of Gastroenterology and Respiratory Internal Medicine & Endoscopy Center, Guangxi Medical University Cancer Hospital, Nanning, Guangxi 530021, P.R. China.
While previous studies have established the role of exosomal miR-552-5p in promoting gastric cancer (GC) progression, the exact mechanisms through which it modulates the PD-1/PD-L1 axis to affect NK cell function and subsequently influence GC epithelial-mesenchymal transition (EMT) remain to be elucidated. Western blot, transmission electron microscopy (TEM), and nanoparticle tracking analysis were used to characterize exosomes that were isolated from GC cell supernatants. Subcutaneous AGS cell injections expressing either Lv-miR-552-5p or Lv-NC were administered to nude BALB/C mice.
View Article and Find Full Text PDFALCAM is an entry factor for severe community acquired Pneumonia-associated Human adenovirus species B.
Nat Commun
December 2024
Department of Pulmonary and Critical Care Medicine, Ruijin Hospital, Institutes of Respiratory Diseases, School of Medicine, Shanghai Jiao Tong University and Shanghai Key Laboratory of Emergency Prevention, Diagnosis and Treatment of Respiratory Infectious Diseases, Shanghai, China.
Human adenovirus (HAdV) is a widely spread respiratory pathogen that can cause infections in multiple tissues and organs. Previous studies have established an association between HAdV species B (HAdV-B) infection and severe community-acquired pneumonia (SCAP). However, the connection between SCAP-associated HAdV-B infection and host factor expression profile in patients has not been systematically investigated.
View Article and Find Full Text PDFInvestigating the anti-cancer potential of sulfatase 1 and its underlying mechanism in non-small cell lung cancer.
Cytojournal
November 2024
Medical College, Ningbo University Health Science Center, Ningbo, China.
Objective: Patients with non-small cell lung cancer (NSCLC) have poor prognoses. Sulfatase 1 (SULF1) is an extracellular neutral sulfatase and is involved in multiple physiological processes. Hence, this study investigated the function and possible mechanisms of SULF1 in NSCLC.
View Article and Find Full Text PDFMicroRNA-668 alleviates renal fibrosis through PPARα/PGC-1α pathway.
Eur J Med Res
December 2024
Department of Nephrology, The Third Xiangya Hospital, Central South University, Changsha, China.
Background: The involvement of microRNA-668 (miR-668) in the onset and progression of renal fibrosis remains unclear. To this end, we aimed to explore the relevant mechanism of miR-668 in renal fibrosis.
Methods: C57BL/6 J male mice were randomly divided into sham-operated, unilateral ureteral obstruction (UUO), and UUO-fenofibrate groups.
SIRT1 Activation Suppresses Corneal Endothelial-Mesenchymal Transition via the TGF-β/Smad2/3 Pathway.
Curr Issues Mol Biol
December 2024
State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Guangzhou 510060, China.
Endothelial-mesenchymal transition (EnMT) is the transversion of endothelial cells to mesenchymal cells under certain physiological or pathological conditions. When EnMT occurs in the corneal endothelium, corneal endothelial cells (CECs) lose their normal function and thus cannot maintain corneal clarity. Studies have shown that the mechanism of EnMT in CECs involves the transforming growth factor-β (TGF-β) signaling pathway, and one of the important inhibitors of the TGF-β/Smad2/3 pathway is sirtuin-1 (SIRT1).
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!