A DNA damage and stress inducible G protein-coupled receptor blocks cells in G2/M

Zhigang Weng, Anne Catherine Fluckiger, Sazuku Nisitani, Matthew I. Wahl, Lu Q. Le, Charity A. Hunter, Anthony A. Fernal, Michelle M. Le Beau, Owen N. Witte

Research output: Contribution to journalArticle

108 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)12334-12339
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume95
Issue number21
DOIs
StatePublished - Oct 13 1998

Fingerprint

G-Protein-Coupled Receptors
DNA Damage
Cell Cycle
B-Lymphoid Precursor Cells
Cell Cycle Checkpoints
Oncogenes
Lymphocytes
T-Lymphocytes
Cell Line
Membranes
DNA

ASJC Scopus subject areas

  • Genetics
  • General

Cite this

A DNA damage and stress inducible G protein-coupled receptor blocks cells in G2/M. / 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.

In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 95, No. 21, 13.10.1998, p. 12334-12339.

Research output: Contribution to journalArticle

Weng, Z, Fluckiger, AC, Nisitani, S, Wahl, MI, Le, LQ, Hunter, CA, Fernal, AA, Le Beau, MM & Witte, ON 1998, '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, vol. 95, no. 21, pp. 12334-12339. https://doi.org/10.1073/pnas.95.21.12334
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. / A DNA damage and stress inducible G protein-coupled receptor blocks cells in G2/M. In: Proceedings of the National Academy of Sciences of the United States of America. 1998 ; Vol. 95, No. 21. pp. 12334-12339.
@article{2af1583ef0494330abb0cec87ac7cb7f,
title = "A DNA damage and stress inducible G protein-coupled receptor blocks cells in G2/M",
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.",
author = "Zhigang Weng and Fluckiger, {Anne Catherine} and Sazuku Nisitani and Wahl, {Matthew I.} and Le, {Lu Q.} and Hunter, {Charity A.} and Fernal, {Anthony A.} and {Le Beau}, {Michelle M.} and Witte, {Owen N.}",
year = "1998",
month = "10",
day = "13",
doi = "10.1073/pnas.95.21.12334",
language = "English (US)",
volume = "95",
pages = "12334--12339",
journal = "Proceedings of the National Academy of Sciences of the United States of America",
issn = "0027-8424",
number = "21",

}

TY - JOUR

T1 - A DNA damage and stress inducible G protein-coupled receptor blocks cells in G2/M

AU - Weng, Zhigang

AU - Fluckiger, Anne Catherine

AU - Nisitani, Sazuku

AU - Wahl, Matthew I.

AU - Le, Lu Q.

AU - Hunter, Charity A.

AU - Fernal, Anthony A.

AU - Le Beau, Michelle M.

AU - Witte, Owen N.

PY - 1998/10/13

Y1 - 1998/10/13

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=0032514679&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0032514679&partnerID=8YFLogxK

U2 - 10.1073/pnas.95.21.12334

DO - 10.1073/pnas.95.21.12334

M3 - Article

C2 - 9770487

AN - SCOPUS:0032514679

VL - 95

SP - 12334

EP - 12339

JO - Proceedings of the National Academy of Sciences of the United States of America

JF - Proceedings of the National Academy of Sciences of the United States of America

SN - 0027-8424

IS - 21

ER -