Muscarinic Acetylcholine Receptor Subtypes as Agonist-Dependent Oncogenes

We have evaluated the muscarinic acetylcholine family of G protein-coupled receptors (mAChRs) for their oncogenic potential. These receptors are preferentially expressed in postmitotic cells, transducing signals specified by their endogenous agonist, the neurotransmitter acetylcholine. Cells transfe...

Ausführliche Beschreibung

Bibliographische Detailangaben
Veröffentlicht in:	Proceedings of the National Academy of Sciences of the United States of America. - National Academy of Sciences of the United States of America. - 88(1991), 11, Seite 4703-4707
1. Verfasser:	Gutkind, J. Silvio (VerfasserIn)
Weitere Verfasser:	Novotny, Elizabeth A., Brann, Mark R., Robbins, Keith C.
Format:	Online-Aufsatz
Sprache:	English
Veröffentlicht:	1991
Zugriff auf das übergeordnete Werk:	Proceedings of the National Academy of Sciences of the United States of America
Schlagworte:	Cell Biology Malignant Transformation Second Messengers G Proteins Neurotransmitter Physical sciences Biological sciences Health sciences


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100	1		\|a Gutkind, J. Silvio \|e verfasserin \|4 aut
245	1	0	\|a Muscarinic Acetylcholine Receptor Subtypes as Agonist-Dependent Oncogenes
264		1	\|c 1991
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520			\|a We have evaluated the muscarinic acetylcholine family of G protein-coupled receptors (mAChRs) for their oncogenic potential. These receptors are preferentially expressed in postmitotic cells, transducing signals specified by their endogenous agonist, the neurotransmitter acetylcholine. Cells transfected with individual human mAChR genes were morphologically indistinguishable from parental NIH 3T3 cells in the absence of agonist. In contrast, when cultures were supplemented with carbachol, a stable analog of acetylcholine, foci of transformation readily appeared in m1, m3, or m5 but not in m2 or m4 mAChRs transfectants. Receptor expression was verified by ligand binding and was similar for each transfected culture. Transformation was dose-dependent and required only low levels of receptor expression. In transformation-competent cells, agonist induced phosphatidylinositol hydrolysis, whereas in m2 or m4 transfectants, receptors were coupled to the inhibition of adenylyl cyclase. These findings demonstrate that mAChRs linked to phosphatidylinositol hydrolysis can act as conditional oncogenes when expressed in cells capable of proliferation.
540			\|a Copyright 1991 The National Academy of Sciences of the United States of America
650		4	\|a Cell Biology
650		4	\|a Malignant
650		4	\|a Transformation
650		4	\|a Second Messengers
650		4	\|a G Proteins
650		4	\|a Neurotransmitter
650		4	\|a Physical sciences \|x Chemistry \|x Chemical compounds \|x Chemicals \|x Polymers \|x Biopolymers \|x Proteins \|x Receptors
650		4	\|a Biological sciences \|x Biology \|x Genetics \|x Genetic research \|x Genetic engineering \|x Gene transfer techniques \|x Transfection
650		4	\|a Biological sciences \|x Biology \|x Cytology \|x Cell biology \|x Cells \|x Cultured cells \|x Cell lines \|x 3T3 cells \|x NIH 3T3 cells
650		4	\|a Physical sciences \|x Chemistry \|x Chemical reactions \|x Chemical processes \|x Chemical decomposition \|x Hydrolysis
650		4	\|a Physical sciences \|x Chemistry \|x Chemical compounds \|x Agonists
650		4	\|a Biological sciences \|x Biology \|x Cytology \|x Cell biology \|x Cells \|x Cultured cells \|x Cell lines \|x 3T3 cells
650		4	\|a Physical sciences \|x Chemistry \|x Chemical compounds \|x Chemicals \|x Acids \|x Nucleic acids \|x DNA
650		4	\|a Health sciences \|x Medical sciences \|x Pharmaceutics \|x Pharmaceutical preparations \|x Medications \|x Central nervous system agents \|x Psychotropics \|x Stimulants \|x Atropine
650		4	\|a Physical sciences \|x Chemistry \|x Chemical compounds \|x Chemicals \|x Ligands
650		4	\|a Biological sciences \|x Biochemistry \|x Biomolecules \|x Macromolecules \|x Lipids \|x Membrane lipids \|x Phospholipids \|x Glycerophosphates \|x Phosphatidic acids \|x Glycerophospholipids \|x Phosphatidylinositols
655		4	\|a research-article
700	1		\|a Novotny, Elizabeth A. \|e verfasserin \|4 aut
700	1		\|a Brann, Mark R. \|e verfasserin \|4 aut
700	1		\|a Robbins, Keith C. \|e verfasserin \|4 aut
773	0	8	\|i Enthalten in \|t Proceedings of the National Academy of Sciences of the United States of America \|d National Academy of Sciences of the United States of America \|g 88(1991), 11, Seite 4703-4707 \|w (DE-627)254235379 \|w (DE-600)1461794-8 \|x 10916490 \|7 nnns
773	1	8	\|g volume:88 \|g year:1991 \|g number:11 \|g pages:4703-4707
856	4	0	\|u https://www.jstor.org/stable/2357121 \|3 Volltext
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912			\|a GBV_ILN_110
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912			\|a GBV_ILN_151
912			\|a GBV_ILN_161
912			\|a GBV_ILN_168
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912			\|a GBV_ILN_171
912			\|a GBV_ILN_213
912			\|a GBV_ILN_230
912			\|a GBV_ILN_252
912			\|a GBV_ILN_285
912			\|a GBV_ILN_293
912			\|a GBV_ILN_370
912			\|a GBV_ILN_374
912			\|a GBV_ILN_381
912			\|a GBV_ILN_602
912			\|a GBV_ILN_702
912			\|a GBV_ILN_2001
912			\|a GBV_ILN_2003
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912			\|a GBV_ILN_2018
912			\|a GBV_ILN_2020
912			\|a GBV_ILN_2021
912			\|a GBV_ILN_2026
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912			\|a GBV_ILN_2050
912			\|a GBV_ILN_2057
912			\|a GBV_ILN_2061
912			\|a GBV_ILN_2088
912			\|a GBV_ILN_2107
912			\|a GBV_ILN_2110
912			\|a GBV_ILN_2190
912			\|a GBV_ILN_2360
912			\|a GBV_ILN_2943
912			\|a GBV_ILN_2946
912			\|a GBV_ILN_2949
912			\|a GBV_ILN_2951
912			\|a GBV_ILN_4012
912			\|a GBV_ILN_4035
912			\|a GBV_ILN_4037
912			\|a GBV_ILN_4046
912			\|a GBV_ILN_4112
912			\|a GBV_ILN_4125
912			\|a GBV_ILN_4126
912			\|a GBV_ILN_4242
912			\|a GBV_ILN_4249
912			\|a GBV_ILN_4251
912			\|a GBV_ILN_4305
912			\|a GBV_ILN_4306
912			\|a GBV_ILN_4307
912			\|a GBV_ILN_4313
912			\|a GBV_ILN_4322
912			\|a GBV_ILN_4323
912			\|a GBV_ILN_4324
912			\|a GBV_ILN_4325
912			\|a GBV_ILN_4335
912			\|a GBV_ILN_4338
912			\|a GBV_ILN_4346
912			\|a GBV_ILN_4367
912			\|a GBV_ILN_4393
912			\|a GBV_ILN_4700
951			\|a AR
952			\|d 88 \|j 1991 \|e 11 \|h 4703-4707