A hybrid plasmid, pKY159, carrying the promoter and the proximal region of the gene cluster for proton-translocating ATPase caused growth inhibition of Escherichia coli cells (K. Yamaguchi and M. Yamaguchi, J. Bacteriol. 153:550-554, 1983). The mechanism of this growth inhibition was studied, especially in terms of the responsible gene(s). Insertion of IS1, IS5, or gamma delta between the promoter and the gene for a possible component of the ATPase of 14,000 daltons (14K protein) released the inhibitory effect by pKY159. Deletion of the gene for subunit a also released the effect. However, deletion in the gene for the 14K protein released the effect only with an additional insertion within the gene. These results suggested that overproduction of subunit a is closely related to growth inhibition, whereas the 14K protein is not.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC215412 | PMC |
http://dx.doi.org/10.1128/jb.158.1.300-306.1984 | DOI Listing |
Mol Cancer Res
January 2025
Fox Chase Cancer Center, Philadelphia, PA, United States.
Breast cancers of the IntClust-2 type, characterized by amplification of a small portion of chromosome 11, have a median survival of only five years. Several cancer-relevant genes occupy this portion of chromosome 11, and it is thought that overexpression of a combination of driver genes in this region is responsible for the poor outcome of women in this group. In this study we used a gene editing method to knock out, one by one, each of 198 genes that are located within the amplified region of chromosome 11 and determined how much each of these genes contributed to the survival of breast cancer cells.
View Article and Find Full Text PDFInvest Ophthalmol Vis Sci
January 2025
John F. Hardesty, MD, Department of Ophthalmology and Visual Sciences, Washington University School of Medicine in St. Louis, St. Louis, Missouri, United States.
Ever since the US Food and Drug Administration (FDA) approved the first vascular endothelial growth factor (VEGF) antagonist 2 decades ago, inhibitors of VEGF have revolutionized the treatment of a variety of ocular disorders involving pathologic neovascularization and retinal exudation. In this perspective, we evaluate the current status of anti-VEGF therapies and the real-world challenges encountered with maintaining therapeutic outcomes. Finally, we describe novel VEGF-based and combinatorial approaches that are in clinical development.
View Article and Find Full Text PDFJ Exp Med
March 2025
Department of Hematology, The Second Affiliated Hospital of Chongqing Medical University, School of Basic Medical Sciences, Chongqing Medical University, Chongqing, China.
Hematopoietic stem cells (HSCs) are susceptible to replication stress, which is a major contributor to HSC defects in Fanconi anemia (FA). Here, we report that HSCs relax the global chromatin by downregulating the expression of a chromatin architectural protein, DEK, in response to replication stress. DEK is abnormally accumulated in bone marrow (BM) CD34+ cells from patients with FA and in Fancd2-deficient HSCs.
View Article and Find Full Text PDFBiomater Sci
January 2025
Department of Urology, The Third Xiangya Hospital of Central South University, No. 138, Tongzipo Road, Changsha, 410013, Hunan, China.
Gemcitabine (GEM) is a first line chemotherapy drug for bladder cancer (BCa). GEM's lack of specificity has led to disadvantages, resulting in low efficiency, especially when combined with the targeted treatment of BCa stem cells (CSCs), which is considered the cause of BCa recurrence and progression. To enhance the anti-cancer effect and reduce the side effects of GEM targeting of BCa cells/CSCs, an aptamer drug conjugate (ApDC) targeted delivery system was used to improve the efficiency of GEM in BCa therapy using EpCAM aptamer-GEM conjugates based on the epithelial cell adhesion molecule (EpCAM), which is highly expressed on the cell membrane of BCa cells/CSCs.
View Article and Find Full Text PDFElife
January 2025
Department of Neurology, Weill Institute for Neuroscience, University of California San Francisco, San Francisco, United States.
Mutations in Sonic Hedgehog (SHH) signaling pathway genes, for example, (SUFU), drive granule neuron precursors (GNP) to form medulloblastomas (MB). However, how different molecular lesions in the Shh pathway drive transformation is frequently unclear, and mutations in the cerebellum seem distinct. In this study, we show that fibroblast growth factor 5 (FGF5) signaling is integral for many infantile MB cases and that expression is uniquely upregulated in infantile MB tumors.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!