ArticleMolecular and cellular biology1994
Muscarinic receptors transform NIH 3T3 cells through a Ras-dependent signalling pathway inhibited by the Ras-GTPase-activating protein SH3 domain.
Article in Molecular and cellular biology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 87 citations in OpenAlex.
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- The role of Lutheran/basal cell adhesion molecule in human bladder carcinogenesis.Journal of biomedical science · 2017Article
- Denervation suppresses gastric tumorigenesis.Science translational medicine · 2014Article
- Identification of Signaling Protein Complexes by Parallel Affinity Precipitation Coupled with Mass Spectrometry.Cell communication insights · 2013Article
- The serine/threonine kinase Par1b regulates epithelial lumen polarity via IRSp53-mediated cell-ECM signaling.The Journal of cell biology · 2011Article
- Walleye dermal sarcoma virus Orf B functions through receptor for activated C kinase (RACK1) and protein kinase C.Virology · 2008Article
- The Ras-GRF1 exchange factor coordinates activation of H-Ras and Rac1 to control neuronal morphology.Molecular biology of the cell · 2006Article
- Attenuation of estrogen receptor alpha-mediated transcription through estrogen-stimulated recruitment of a negative elongation factor.Genes & development · 2004Article
- Motoneurons express heteromeric TWIK-related acid-sensitive K+ (TASK) channels containing TASK-1 (KCNK3) and TASK-3 (KCNK9) subunits.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004Article
- Coordination of DNA damage responses via the Smc5/Smc6 complex.Molecular and cellular biology · 2004Article
- Walleye dermal sarcoma virus cyclin interacts with components of the mediator complex and the RNA polymerase II holoenzyme.Journal of virology · 2002Article
- Dissection of the cytoplasmic domains of cytokine receptors involved in STAT and Ras dependent proliferation.Oncogene · 2002Article
- High RhoA activity maintains the undifferentiated mesenchymal cell phenotype, whereas RhoA down-regulation by laminin-2 induces smooth muscle myogenesis.The Journal of cell biology · 2002Article
- Insulin-stimulated phosphorylation of lipin mediated by the mammalian target of rapamycin.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Characterization of regulatory events associated with membrane targeting of p90 ribosomal S6 kinase 1.Molecular and cellular biology · 2001Article
- Rit, a non-lipid-modified Ras-related protein, transforms NIH3T3 cells without activating the ERK, JNK, p38 MAPK or PI3K/Akt pathways.Oncogene · 2000Article
- Facilitated nucleocytoplasmic shuttling of the Ran binding protein RanBP1.Molecular and cellular biology · 2000Article
- Platelet-derived growth factor-dependent association of the GTPase-activating protein of Ras and Src.The Biochemical journal · 1999Article
- RanBP3 contains an unusual nuclear localization signal that is imported preferentially by importin-alpha3.Molecular and cellular biology · 1999Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Expression of certain subtypes of human muscarinic receptors in NIH 3T3 cells provides an agonist-dependent model of cellular transformation by formation of foci in response to carbachol. Although focus formation correlates with the ability of the muscarinic receptors to activate phospholipase C, the actual mitogenic signal transduction pathway is unknown. Through cotransfection experiments and measurement of the activation state of native and epitope-tagged Ras proteins, the contributions of Ras and Ras GTPase-activating protein (Ras-GAP) to muscarinic receptor-dependent transformation were defined. Transforming muscarinic receptors were able to activate Ras, and such activation was required for transformation because focus formation was inhibited by coexpression of either Ras with a dominant-negative mutation or constructs of Ras-GAP that include the catalytic domain. Coexpression of the N-terminal region of GAP or of its isolated SH3 (Src homology 3) domain, but not its SH2 domain, was also sufficient to suppress muscarinic receptor-dependent focus formation. Point mutations at conserved residues in the Ras-GAP SH3 domain reversed its action, leading to an increase in carbachol-dependent transformation. The inhibitory effect of expression of the Ras-GAP SH3 domain occurs proximal to Ras activation and is selective for the mitogenic pathway activated by carbachol, as cellular transformation by either v-Ras or trkA/nerve growth factor is unaffected.
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