A DNA Damage and Stress Inducible G Protein-Coupled Receptor Blocks Cells in G2/M

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 G2accumulation), which is predominantly expressed in...

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Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 1998-10, Vol.95 (21), p.12334-12339
Main Authors: Weng, Zhigang, Fluckiger, Anne-Catherine, Nisitani, Sazuku, Wahl, Matthew I., Le, Lu Q., Hunter, Charity A., Fernal, Anthony A., Le Beau, Michelle M., Witte, Owen N.
Format: Article
Language:English
Subjects:
3T3 Cells
Amino Acid Sequence
Animals
B lymphocytes
Base Sequence
Biological Sciences
Bone marrow cells
Cell cycle
Cell Cycle Proteins - chemistry
Cell Cycle Proteins - genetics
Cell Cycle Proteins - metabolism
Cell lines
Cells
Cellular biology
Cloning, Molecular
Deoxyribonucleic acid
DNA
DNA Damage
DNA Primers
DNA Replication
G2 Phase
GTP-Binding Proteins - metabolism
Lymphocytes
Mice
Mitosis
Molecular Sequence Data
Oxidative Stress
Proteins
Rats
Receptors, G-Protein-Coupled
Signal Transduction
Stem cells
T lymphocytes
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Summary: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 G2accumulation), 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.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.95.21.12334