α-Synuclein is involved in many important molecular processes in neuronal cells and their synapses, and its malfunction has been linked to the development of Parkinson's and certain other neurodegenerative diseases. Animal models allowing tightly monitored conditional inactivation of the encoding gene, Snca, are indispensible for studies aimed at understanding normal function of α-synuclein in various neuronal populations and its role in pathogenesis of neurodegenerative diseases. We have recently reported the production of several novel mouse lines for manipulating expression of the endogenous Snca gene, including a line for Cre-recombinase-driven conditional inactivation of the gene (mice with floxed Snca) and a new line with a constitutive knockout of α-synuclein. Rosa26-stop-lacZ reporter cassette is commonly used for monitoring efficiency of Cre-recombination but in mouse genome Snca and Rosa26 loci are located on the same chromosome. Here we describe production of lines with a modified Snca locus, either floxed or constitutively inactivated and the Rosa26-stop-lacZ reporter cassette located in cis on the mouse chromosome 6. These new mouse lines are invaluable for fast identification of cells with inactivation of Snca by Cre-recombination and represent useful tools for in vivo studies of α-synuclein function and dysfunction.
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http://dx.doi.org/10.1007/s11248-016-9995-8 | DOI Listing |
Bull Exp Biol Med
January 2025
Center for Digital and Translational Biomedicine, Center for Molecular Health LLC, Moscow, Russia.
Changes in the lipid and carbohydrate metabolism, adipokines, and growth factors during the development of metabolic disorders were studied in three mouse models: C57BL/6 (alimentary obesity), db/db (leptin-resistant obesity), and NOD (diabetes mellitus) lines. In the group of alimentary obesity, moderate fatty infiltration of the liver and hypertrophy of the adipose tissue, hyperglycemia, and increased concentrations of adiponectin, transforming growth factor β1 (TGF-β1), leptin, and cholesterol were detected. In the group of leptin-resistant obesity, multiple pathological changes in tissues, severe hyperglycemia and hyperleptinemia, hyperinsulinemia, and reduced concentrations of triglycerides, adiponectin, myostatin, and TGF-β1 were detected.
View Article and Find Full Text PDFClin Cancer Res
January 2025
University of Nebraska Medical Center, OMAHA, NE, United States.
Purpose: Breast cancer (BC) brain metastasis (BrM) remains a significant clinical problem. Mucins have been implicated in metastasis; however, if they are also involved in BCBrM remains unknown. We queried BrM patient databases and found Mucin 5AC (MUC5AC) to be upregulated and therefore sought to define the role of MUC5AC in BCBrM.
View Article and Find Full Text PDFFASEB J
January 2025
Department of Molecular Medicine, Scripps Research Institute, La Jolla, California, USA.
Tumors require ample protein synthesis to grow, and aminoacyl-tRNA synthetases, as critical translation factors, are expected to support cancer progression. Unexpectedly, overexpression of seryl-tRNA synthetase (SerRS) suppresses primary tumor growth of breast cancer. However, the effects of SerRS on metastasis have not been studied.
View Article and Find Full Text PDFJ Investig Med
January 2025
Department of Oncology, The First Hospital of Hebei Medical University, Shijiazhuang, Hebei province, China.
Pancreatic cancer is characterized by occult onset, low early diagnosis rate, rapid progress, and poor prognosis. Due to the low response rate and low PD-L1 expression in pancreatic cancer, the therapeutic application of PL-L1 inhibitors in pancreatic cancer is greatly limited. In vitro studies showed that the expression of PD-L1 increased in pancreatic cancer cells stimulated by fluorouracil (5-FU).
View Article and Find Full Text PDFMol Ther Oncol
December 2024
Department of Gene Therapy, Ulm University, 89081 Ulm, Germany.
Human adenovirus type 5 (HAdV-5)-based oncolytic viruses hold significant promise for anti-cancer therapy. However, poor tumor-targeting and off-target organ transduction after systemic administration limit their therapeutic efficacy. In addition, the strong liver tropism of HAdV-5-based vectors poses the risk of hepatotoxicity.
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