Objective: Palladin is a ubiquitous phosphoprotein expressed in vertebrate cells that works as a scaffolding protein. Several isoforms deriving from alternative splicing are originated from the palladin gene and involved in mesenchymal and muscle cells formation, maturation, migration, and contraction. Recent studies have linked palladin to the invasive spread of cancer and myogenesis. However, since its discovery, the promoter region of the palladin gene has never been studied. The objective of this study was to predict, identify, and measure the activity of the promoter regions of palladin gene.
Results: By using promoter prediction programs, we successfully identified the transcription start sites for the Palld isoforms and revealed the presence of a variety of transcriptional regulatory elements including TATA box, GATA, MyoD, myogenin, MEF, Nkx2-5, and Tcf3 upstream promoter regions. The transcriptome profiling approach confirmed the active role of predicted transcription factors in the mouse genome. This study complements the missing piece in the characterization of palladin gene and certainly contributes to understanding the complexity and enrollment of palladin regulatory factors in gene transcription.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7333403 | PMC |
http://dx.doi.org/10.1186/s13104-020-05152-9 | DOI Listing |
Endocr Regul
January 2024
1Department of Molecular Biology, Palladin Institute of Biochemistry, National Academy of Sciences of Ukraine, Kyiv 01054, Ukraine.
Nanographene oxide (nGO) nanoparticles (NPs) have unique properties and are widely used in various fields, including biomedicine. These NPs, however, also exhibit toxic ef-fects and therefore, the understanding of the molecular mechanism of nGO toxicity is very im-portant mainly for the nanomedicine, especially the cancer therapy. This study aimed to examine the impact of nGO NPs on the expression of genes associated with endoplasmic reticulum (ER) stress, proliferation, and cancerogenesis in both normal human astrocytes and U87MG glioblas-toma cells.
View Article and Find Full Text PDFEndocr Regul
January 2024
Department of Molecular Biology, Palladin Institute of Biochemistry, National Academy of Sciences of Ukraine, Kyiv, Ukraine.
Carboxypeptidase E (CPE) plays an important role in the biosynthesis of neurotransmitters and peptide hormones including insulin. It also promotes cell proliferation, survival, and invasion of tumor cells. The endoplasmic reticulum stress, hypoxia, and nutrient supply are significant factors of malignant tumor growth including glioblastoma.
View Article and Find Full Text PDFFront Immunol
September 2024
Department of Research Support Utilizing Bioresource Bank, Graduate School of Medicine, Juntendo University, Tokyo, Japan.
Fitoterapia
December 2024
Laboratory of Cell and Molecular Biology, Department of Botany, Centre of Advanced Study, University of Calcutta, Kolkata 700 019, West Bengal, India. Electronic address:
The non-specificity of contemporary cancer therapeutics has enticed us to develop safer, anticancer alternatives from natural resources. Lichens are unique natural entities which have long been neglected for explorations in cancer therapy, despite their vast potential. Our present study aims to investigate the anti-cancer potential of a wild lichen Parmelinella wallichiana.
View Article and Find Full Text PDFArch Biochem Biophys
September 2024
Department of Molecular Biology, Palladin Institute of Biochemistry National Academy of Sciences of Ukraine, Kyiv, Ukraine.
Background: Endoplasmic reticulum stress and synthesis of serine are essential for tumor growth, but the mechanism of their interaction is not clarified yet. The overarching goal of this work was to investigate the impact of ERN1 (endoplasmic reticulum to nucleus signaling 1) inhibition on the expression of serine synthesis genes in U87MG glioblastoma cells concerning the suppression of cell proliferation.
Methods: Wild type U87MG glioblastoma cells and their clones with overexpression of transgenes dnERN1 (without cytoplasmic domain of ERN1) and dnrERN1 (with mutation in endoribonuclease of ERN1), and empty vector (as control) were used.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!