The modified Cry1Ac was expressed in transgenic tobacco plants. To allow secretion of the Cry1Ac protein into the intercellular space, the signal peptide sequence of potato proteinase inhibitor II (pinII) was N-terminally fused to the Cry1Ac encoding region. Expression of Cry1Ac in transgenic tobacco plants was assayed with ELISA. The results showed that pinII signal peptide sequence enhanced the expression of Cry1Ac protein and led to the secretion of the Cry1Ac protein in transgenic tobacco plants. GFP gene was also fused to the signal peptide sequence and transformed to tobacco. The results of fluorescent detection showed that GFP had localized in the apoplast of transgenic plants.
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http://dx.doi.org/10.1093/abbs/36.8.553 | DOI Listing |
ACS Appl Mater Interfaces
January 2025
Department of Nuclear Medicine, The Third Affiliated Hospital of Sun Yat-sen University, 600 Tianhe Road, Guangzhou 510630, China.
Epstein-Barr nuclear antigen 1 (EBNA1), a sequence-specific DNA binding protein of Epstein-Barr virus (EBV), is essential for viral genome replication and maintenance and is therefore an attractive target for the therapeutic intervention of EBV-associated cancers. Several EBNA1-specific inhibitors have demonstrated the ability to block EBNA1 function in vitro, but practical delivery strategies for these inhibitors in vivo are still lacking. Here, we report an intelligent hierarchical targeting theranostic nanosystem (denoted as mZGOCS@MnO-P5) that integrates an azide (N3) terminal dual-targeting peptide (N3-P5), a tumor microenvironment-responsive degradable MnO nanosheet, and a mesoporous ZnGaO:Cr, Sn near-infrared persistent luminescence (NIR-PL) nanosphere (mZGOCS).
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Background: Clinicopathological studies of Alzheimer's disease (AD) have demonstrated that synaptic or neuronal loss and clinical cognitive decline do not reliably correlate with fibrillar amyloid burden. We created a transgenic mouse model overexpressing Dutch (E693Q) mutant human amyloid precursor protein (APP) driven by the pan-neuronal Thy1 promoter. Accumulation of APP carboxyl-terminal fragments was observed in the brains of these mice, which develop an impaired learning phenotype directly proportional to brain oAβ levels.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Karolinska Institutet, Solna, Sweden.
Background: Signal Peptide Peptidase-Like 2b (SPPL2b) is relevant for AD, being a brain-specific intramembrane protein involved in the cleavage of Alzheimer's disease (AD)-related proteins, such as BRI2, inflammatory-related proteins like CD74, TNFalpha, and Clec7a, and synaptic proteins Neuregulin-1 and VAMP 1-4. SPPL2b is specifically expressed in the hippocampus and cortex. The cleavage of TNFalpha by SPPL2b promotes the inflammatory pathway.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Icahn School of Medicine at Mount Sinai Medical Center, New York, NY, USA.
Background: Presenilin1 (PS1)/γ-secretase cleaves within the transmembrane domain of numerous receptor substrates. Mutations in PS1 have implications on the catalytic subunit of γ-secretase decreasing its activity and becoming a potential causative factor for Familial Alzheimer's Disease (FAD). This work studies the role of PS1/γ-secretase on the processing, angiogenic signaling, and functions of VEGFR2 and the effects of PS1 FAD mutants on the γ-secretase-mediated epsilon cleavage of VEGFR2.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Dr. John T. Macdonald Foundation Department of Human Genetics, University of Miami Miller School of Medicine, Miami, FL, USA.
Background: Hispanic/Latino populations are underrepresented in Alzheimer Disease (AD) genetic studies. The Puerto Rican (PR) population, a three-way admixed (European, African, and Amerindian) population is the second-largest Hispanic group in the continental US. We performed a genome-wide association study (GWAS) in the PR population to identify novel AD susceptibility loci and characterize known AD genetic risk loci.
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