The transport and localization of env-proteins of ts1 virus (a paralytogenic temperature-sensitive mutant of Moloney murine leukemia virus) in infected cells of the TB cell line have been studied at the ultrastructural level. It was found that the envelope precursor polyprotein gPr80-env of ts1 was inefficiently transported out of the endoplasmic reticulum at the restrictive temperature. It was speculated that inefficient transport correlates with inefficient processing of gPr80env into gp70 and Prp15E and leads to paralytic disease.
Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
Pro-viral Insertion site for the Moloney Murine Leukemia virus 1 (PIM-1) is widely involved in various biological processes and diseases, which is based on its structure and functional sites. However, the relationship between active sites and function of PIM-1 kinase remains unclear due to the lack of effective study approaches in live cells. Herein, to visualize the effect of different active sites in PIM-1 protein on its function activity and relation with PI3K/Akt/mTOR pathway, three mutant probes of EPHY which was developed previously based on fluorescence resonance energy transfer (FRET) technology to detect PIM-1 kinase activity in living cells were further constructed and transfected into cells followed by treating with PIM-1 inhibitors, ATP and PI3K inhibitor, respectively.
View Article and Find Full Text PDFPIM1 kinase promotes EMT-associated osimertinib resistance via regulating GSK3β signaling pathway in EGFR-mutant non-small cell lung cancer.
Cell Death Dis
September 2024
Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin, China.
Acquired resistance is inevitable in the treatment of non-small cell lung cancer (NSCLC) with osimertinib, and one of the primary mechanisms responsible for this resistance is the epithelial-mesenchymal transition (EMT). We identify upregulation of the proviral integration site for Moloney murine leukemia virus 1 (PIM1) and functional inactivation of glycogen synthase kinase 3β (GSK3β) as drivers of EMT-associated osimertinib resistance. Upregulation of PIM1 promotes the growth, invasion, and resistance of osimertinib-resistant cells and is significantly correlated with EMT molecules expression.
View Article and Find Full Text PDFTumor Microenvironment Landscapes Supporting EGFR-mutant NSCLC Are Modulated at the Single-cell Interaction Level by Unesbulin Treatment.
Cancer Res Commun
March 2024
Harvard Medical School, Boston, Massachusetts.
Article Synopsis
- Lung cancer, particularly lethal pulmonary adenocarcinomas, often shows mutations in the EGFR gene, making understanding tumor behavior and treatment important.
- Researchers utilized genetically engineered mice to study how tumors evolve and interact with their surrounding environment, identifying specific vulnerable cells and their communication with other cells in the tumor microenvironment.
- The drug Unesbulin, a tubulin binding agent, was found to decrease tumor growth and alter the interactions within the tumor environment, suggesting it could be a promising therapeutic strategy for treating EGFR-mutant lung cancers.
Generation of an Avian Myeloblastosis Virus (AMV) Reverse Transcriptase Prime Editor.
Adv Exp Med Biol
July 2023
Edward S. Harkness Eye Institute, Department of Ophthalmology, Columbia University Irving Medical Center/New York-Presbyterian Hospital, New York, NY, USA.
Prime editing (PE) is a novel, double-strand break (DSB)-independent gene editing technology that represents an exciting avenue for the treatment of inherited retinal diseases (IRDs). Given the extensive and heterogenous nature of the 280 genes associated with IRDs, genome editing has presented countless complications. However, recent advances in genome editing technologies have identified PE to have tremendous potential, with the capability to ameliorate small deletions and insertions in addition to all twelve possible transition and transversion mutations.
View Article and Find Full Text PDFSpecific overexpression of SIRT1 in mesenchymal stem cells rescues hematopoiesis niche in BMI1 knockout mice through promoting CXCL12 expression.
Int J Biol Sci
April 2022
State Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing, Jiangsu 210029, China.
Osteoblastic lineage cells (OBCs) are bone-building cells and essential component of hematopoietic niche, but mechanisms whereby bone-building and hematopoiesis-supportive activities of OBCs could be regulated simultaneously remain largely unknown. Here we found that B cell-specific Moloney murine leukemia virus integration site 1 (Bmi1) was involved in such a co-regulatory mechanism. In this study, we first found that, accompanied with marked decline of osteogenic activity, the hematopoietic niche in Bmi1 knockout (KO) mice was severely impaired and manifested as CXCL12 expression falls and LSK homing failure; however, intratibial injection with CXCL12 effectively facilitated LSK accumulation in bone marrow of Bmi1 KO mice.
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!