The sequence of the 2391 bp murine CDC10 cDNA is reported. The gene transcription unit, composed of 13 exons, encodes a potential 417/446 amino acid GTP-binding protein, highly similar to human CDC10. The ubiquitous expression of the gene, as judged by Northern analysis, is consistent with its putative promoter structure.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/s0167-4781(98)00183-3 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Registered report protocol: Quantitative analysis of septin Cdc10-associated proteome in Cryptococcus neoformans.
PLoS One
January 2021
Department of Genetics and Biochemistry, Eukaryotic Pathogens Innovation Center, Clemson University, Clemson, SC, United States of America.
Cryptococcus neoformans is a pathogenic basidiomycetous yeast that primarily infects immunocompromised individuals. C. neoformans can thrive during infections due to its three main virulence-related characteristics: the ability to grow at host temperature (37°C), formation of carbohydrate capsule, and its ability to produce melanin.
View Article and Find Full Text PDFTGFβ1 Cell Cycle Arrest Is Mediated by Inhibition of MCM Assembly in Rb-Deficient Conditions.
Mol Cancer Res
January 2019
Department of Molecular Oncology, Moffitt Cancer Center and Research Institute, Tampa, Florida.
Transforming growth factor β1 (TGFβ1) is a potent inhibitor of cell growth that targets gene-regulatory events, but also inhibits the function of CDC45-MCM-GINS helicases (CMG; MCM, Mini-Chromosome Maintenance; GINS, Go-Ichi-Ni-San) through multiple mechanisms to achieve cell-cycle arrest. Early in G, TGFβ1 blocks MCM subunit expression and suppresses Myc and Cyclin E/Cdk2 activity required for CMG assembly, should MCMs be expressed. Once CMGs are assembled in late-G, TGFβ1 blocks CMG activation using a direct mechanism involving the retinoblastoma (Rb) tumor suppressor.
View Article and Find Full Text PDFThe ANK repeats of Notch-4/Int3 activate NF-κB canonical pathway in the absence of Rbpj and causes mammary tumorigenesis.
Sci Rep
October 2017
Basic Research Laboratory, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20814, USA.
Transgenic mice expressing the Notch-4 intracellular domain (designated Int3) in the mammary gland have two phenotypes exhibited with 100% penetrance: arrest of mammary alveolar/lobular development and mammary tumorigenesis. Notch-4 signaling is mediated primarily through the interaction of Int3 with the transcription repressor/activator Rbpj. Interestingly, WAP-Int3/Rbpj knockout mice have normal mammary gland development but still developed mammary tumors with a slightly longer latency than the WAP-Int3 mice.
View Article and Find Full Text PDFThe bZIP transcription factor, C/EBPα is highly inducible by UVB and other DNA damaging agents in keratinocytes. C/EBPα-deficient keratinocytes fail to undergo cell cycle arrest in G1 in response to UVB-induced DNA damage and mice lacking epidermal C/EBPα are highly susceptible to UVB-induced skin cancer. The mechanism through which C/EBPα regulates the cell cycle checkpoint in response to DNA damage is unknown.
View Article and Find Full Text PDFIdentification of the cell targets important for propolis-induced cell death in Candida albicans.
Fungal Genet Biol
November 2013
Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Universidade de São Paulo, São Paulo, Brazil.
Candida albicans is the most common fungal pathogen of humans, forming both commensal and opportunistic pathogenic interactions, causing a variety of skin and soft tissue infections in healthy people. In immunocompromised patients C. albicans can result in invasive, systemic infections that are associated with a high incidence of mortality.
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!