A gene cassette, p35S-CNO, was designed to express three gene products driven by a single constitutive CaMV 35S promoter. The individual coding regions were linked in frame to produce a single polyprotein, using spacer sequences encoding a specific heptapeptide cleavage recognition site (ENLYFQS) for the nuclear-inclusion-a (NIa) proteinase of tobacco etch virus (TEV). The protein coding sequences used were: a Trichoderma harzinum endochitinase, a truncated NIa proteinase of TEV, and a wheat oxalate oxidase. When p35S-CNO construct was tested in Arabidopsis thaliana, the polyprotein was properly cleaved after translation and the products exhibited functional enzymatic activity in vivo.
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http://dx.doi.org/10.1007/s10529-005-1884-9 | DOI Listing |
Acta Neuropathol
December 2024
Department of Neurology, Mitchell Center for Neurodegenerative Diseases, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX, 77555, USA.
In Alzheimer's disease (AD), the propagation and spreading of CNS tau pathology closely correlates with cognitive decline, positioning tau as an attractive therapeutic target. Amyloid beta (Aβ) has been strongly implicated in driving tau spread, whereas primary tauopathies such as primary age-related tauopathy (PART)-which lack Aβ pathology-exhibit limited tau spread and minimal-to-no cognitive decline. Emerging evidence converges on a trans-synaptic mechanism of tau spread, facilitated by the transfer of misfolded tau aggregates (e.
View Article and Find Full Text PDFPLoS One
December 2024
Yunnan Key Laboratory for Basic Research on Bone and Joint Diseases, Kunming University, Kunming, China.
Renal interstitial fibrosis, a condition prevalent in aging humans and animals, is closely linked to the eventual development of renal failure. Establishing an animal model that exactly replicates the pathogenesis of renal interstitial fibrosis induced by natural aging in humans is crucial for advancing mechanistic studies and testing antifibrotic therapies. Implanted allogeneic or xenogeneic cells are cleared by the immune system when stem cell therapy is applied in nonimmunodeficient animal fibrosis models, affecting the effect of the intervention and making it difficult to demonstrate the survival, proliferation, differentiation, or secretion of the delivered autologous human-derived cells.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
December 2024
Department of Cell Biology, Harvard Medical School, Boston MA 02115.
A hallmark of neurodegenerative diseases (NDs) is the progressive loss of proteostasis, leading to the accumulation of misfolded proteins or protein aggregates, with subsequent cytotoxicity. To combat this toxicity, cells have evolved degradation pathways (ubiquitin-proteasome system and autophagy) that detect and degrade misfolded proteins. However, studying the underlying cellular pathways and mechanisms has remained a challenge, as formation of many types of protein aggregates is asynchronous, with individual cells displaying distinct kinetics, thereby hindering rigorous time-course studies.
View Article and Find Full Text PDFVirology
January 2025
Summerland Research and Development Centre, Agriculture and Agri-Food Canada, 4200 Highway 97, V0H 1Z0, Summerland, BC, Canada. Electronic address:
Plant viruses of the families Potyviridae and Secoviridae encode 3C-like proteases (3CL) that are related to picornavirus 3C proteases. This review discusses recent advances in deciphering the multifunctional activities of plant virus 3CL. These proteases regulate viral polyprotein processing and facilitate virus replication.
View Article and Find Full Text PDFMol Neurodegener
November 2024
Department of Neuroscience, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT, 06030-3401, USA.
Background: The accumulation of β-amyloid (Aβ) peptides into insoluble plaques is an early pathological feature of Alzheimer's disease (AD). BACE1 is the sole β-secretase for Aβ generation, making it an attractive therapeutic target for AD therapy. While BACE1 inhibitors have been shown to reduce Aβ levels in people with AD, clinical trials targeting BACE1 have failed due to unwanted synaptic deficits.
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