Expression of growth arrest-specific (gas) genes in senescent murine cells.

Exp Cell Res

European Molecular Biology Laboratory, Heidelberg, Germany.

Published: April 1994

The growth arrest-specific (gas) genes were initially identified on the basis of their preferential expression in mouse fibroblasts during quiescence, followed by down-regulation upon reentry into the cell cycle. We here report studies on the expression of these genes in murine fibroblasts undergoing replicative senescence in vitro. Our results indicate a different behavior between senescent and GO-arrested quiescent fibroblasts. Expression of the gas1 and 6 genes was dramatically reduced in senescent cells. Only basal levels of gas2, 3, and 5 genes were detected in senescent fibroblasts, and they were independent of the growing conditions of the cultures. Down-regulation of the gas1 gene expression in senescent cells was apparently due to reduced transcription of the gas1 gene. This correlates with an altered pattern of factors that bind to the promoter region of the gas1 gene, as measured by band shift assay with nuclear extracts of senescent fibroblasts.

Download full-text PDF

Source
http://dx.doi.org/10.1006/excr.1994.1078DOI Listing

Publication Analysis

Top Keywords

gas1 gene
12
growth arrest-specific
8
arrest-specific gas
8
gas genes
8
senescent cells
8
senescent fibroblasts
8
senescent
6
expression
5
genes
5
fibroblasts
5

Similar Publications

Background: Microsatellite instability (MSI) significantly impacts treatment response and outcomes in colon cancer; however, its underlying molecular mechanisms remain unclear. This study aimed to identify prognostic biomarkers by comparing MSI and microsatellite stability (MSS).

Methods: Data from the GSE39582 dataset downloaded from the Gene Expression Omnibus database were analyzed for differentially expressed genes (DEGs) and immune cell infiltration between MSI and MSS.

View Article and Find Full Text PDF

Growth arrest specific 1 (GAS1) is a key regulator of mammalian embryogenesis, best known for its role in hedgehog (HH) signaling, but with additional described roles in the FGF, RET, and NOTCH pathways. Previous work indicated a later role for GAS1 in kidney development through FGF pathway modulation. Here, we demonstrate that GAS1 is essential for both mesonephrogenesis and metanephrogenesis - most notably, Gas1 deletion in mice results in renal agenesis in a genetic background-dependent fashion.

View Article and Find Full Text PDF
Article Synopsis
  • Ovarian cancer (OC) is a serious health issue for women, characterized by a poor prognosis and limited treatment options, requiring further study on its underlying mechanisms and immune interactions.
  • The research focused on identifying cuproptosis-related genes (CRGs) to categorize OC into distinct subtypes and create a risk score (RS) model for predicting patient outcomes using data from various databases.
  • The findings established three clinical subtypes of OC based on CRG expression, highlighted six key hub genes with oncogenic properties, and emphasized the potential of the RS model to improve survival predictions and therapeutic strategies.
View Article and Find Full Text PDF

You Don't Always Get What You Want!

Anesthesiology

October 2024

Department of Anesthesiology and Pain Medicine, University of Washington and Seattle Children's Research Institute, Seattle, Washington.

Background: Mutations in several genes of Caenorhabditis elegans confer altered sensitivities to volatile anesthetics. A mutation in one gene, gas-1(fc21), causes animals to be immobilized at lower concentrations of all volatile anesthetics than in the wild type, and it does not depend on mutations in other genes to control anesthetic sensitivity. gas-1 confers different sensitivities to stereoisomers of isoflurane, and thus may be a direct target for volatile anesthetics.

View Article and Find Full Text PDF
Article Synopsis
  • * These p16-sn fibroblasts accumulate with age, act as inflammatory cancer-associated fibroblasts (CAFs), and significantly contribute to bladder tumor growth by expressing the CXCL12 gene.
  • * Targeting p16-sn cells or blocking CXCL12 signaling can reduce bladder tumor growth, indicating that these cells create an environment that supports cancer development in older individuals.
View Article and Find Full Text PDF

Want 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!