Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Polyomavirus hr-t mutant-specific induction of a G2/M cell-cycle arrest that is not overcome by the expression of middle T and/or small T.

Virology - 15 Mar 2003

Spink Kathryn M, Fluck Michele M

Abstract excerpt

The polyomavirus hr-t class of mutants has served as a major prototype to study the function of middle T + small T in the virus lytic cycle, Biochem. Biophys. Acta 695 (2), 69-95). The properties of these middle T + small T defective mutants were defined by comparisons with "wild-type" strains reconstructed by marker rescue. Similar comparisons in the A2 genetic background have revealed a number of differences,...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to 3T3 Cells
Share to Antigens, Polyomavirus Transforming
Share to DNA Replication

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to DNA, Viral

Share to G2 Phase

Share to Mitosis

Share to Polyomavirus

Share to Trans-Activators

Source

Identifiers

PMID: 12667790
DOI: 10.1016/s0042-6822(02)00030-2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Polyomavirus hr-t mutant-specific induction of a G2/M cell-cycle arrest that is not overcome by the expression of middle T and/or small T.PMID 12667790Read ↗

Separation of immortalization from tumor induction with polyoma large T mutants that fail to bind the retinoblastoma gene product.Semantic proximity Read ↗

Host range and cell cycle activation properties of polyomavirus large T-antigen mutants defective in pRB binding.Semantic proximity Read ↗

Enhancer-mediated role for polyomavirus middle T/small T in DNA replication.Semantic proximity Read ↗

Isolation of temperature-sensitive cell cycle mutants from mouse FM3A cells. Characterization of mutants with special reference to DNA replication.Semantic proximity Read ↗

Signaling from polyomavirus middle T and small T defines different roles for protein phosphatase 2A.Semantic proximity Read ↗

Transformation-defective polyoma middle T antigen mutants defective in PLCgamma, PI-3, or src kinase activation enhance ERK2 activation and promote retinoic acid-induced, cell differentiation like wild-type middle T.Semantic proximity Read ↗

Limits of transforming competence of SV40 nuclear and cytoplasmic large T mutants with altered Rb binding sequences.Semantic proximity Read ↗

Polyoma virus middle T is essential for virus replication and persistence as well as for tumor induction in mice.Semantic proximity Read ↗

Independent contributions of polyomavirus middle T and small T to the regulation of early and late gene expression and DNA replication.Semantic proximity Read ↗

SV40 small T antigen enhances progression to >G2 during lytic infection.Semantic proximity Read ↗

Analysis of mouse polyomavirus mutants with lesions in the minor capsid proteins.Semantic proximity Read ↗

A completely transformation-defective point mutant of polyomavirus middle T antigen which retains full associated phosphatidylinositol kinase activity.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.