Article: A DNA damage and stress inducible G protein-coupled receptor blocks cells in G2/M.
Proceedings of the National Academy of Sciences of the United States of America
1998 Volume 95, Issue 21, Page(s) 12334–12339
Abstract: ... T and B lymphocyte progenitors and is a member of the seven membrane-spanning G protein-coupled ... and leads to accumulation of cells at G2/M independently of p53 and c-Abl. G2A can be induced ...
Abstract | Cell cycle progression is monitored by highly coordinated checkpoint machinery, which is activated to induce cell cycle arrest until defects like DNA damage are corrected. We have isolated an anti-proliferative cell cycle regulator named G2A (for G2 accumulation), which is predominantly expressed in immature T and B lymphocyte progenitors and is a member of the seven membrane-spanning G protein-coupled receptor family. G2A overexpression attenuates the transformation potential of BCR-ABL and other oncogenes, and leads to accumulation of cells at G2/M independently of p53 and c-Abl. G2A can be induced in lymphocytes and to a lesser extent in nonlymphocyte cell lines or tissues by multiple stimuli including different classes of DNA-damaging agents and serves as a response to damage and cellular stimulation which functions to slow cell cycle progression. |
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MeSH term(s) | 3T3 Cells ; Amino Acid Sequence ; Animals ; Base Sequence ; Cell Cycle Proteins/chemistry ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Cloning, Molecular ; DNA Damage ; DNA Primers ; DNA Replication ; G2 Phase ; GTP-Binding Proteins/metabolism ; Mice ; Mitosis ; Molecular Sequence Data ; Oxidative Stress ; Rats ; Receptors, G-Protein-Coupled ; Signal Transduction |
Chemical Substances | Cell Cycle Proteins ; DNA Primers ; G2A receptor ; Receptors, G-Protein-Coupled ; GTP-Binding Proteins (EC 3.6.1.-) |
Language | English |
Publishing date | 1998-10-13 |
Publishing country | United States |
Document type | Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S. |
ZDB-ID | 209104-5 |
ISSN | 1091-6490 ; 0027-8424 |
ISSN (online) | 1091-6490 |
ISSN | 0027-8424 |
DOI | 10.1073/pnas.95.21.12334 |
Database | MEDical Literature Analysis and Retrieval System OnLINE |
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