The DOI matches its Crossref record; 21 of the 21 references it cites were found in a registry or an index.
Targeted Disruption of the β2 Adrenergic Receptor Gene
Open accessAbstract
beta-Adrenergic receptors (beta-ARs) are members of the superfamily of G-protein-coupled receptors that mediate the effects of catecholamines in the sympathetic nervous system. Three distinct beta-AR subtypes have been identified (beta1-AR, beta2-AR, and beta3-AR). In order to define further the role of the different beta-AR subtypes, we have used gene targeting to inactivate selectively the beta2-AR gene in mice. Based on intercrosses of heterozygous knockout (beta2-AR +/-) mice, there is no prenatal lethality associated with this mutation. Adult knockout mice (beta2-AR -/-) appear grossly normal and are fertile. Their resting heart rate and blood pressure are normal, and they have a normal chronotropic response to the beta-AR agonist isoproterenol. The hypotensive response to isoproterenol, however, is significantly blunted compared with wild type mice. Despite this defect in vasodilation, beta2-AR -/- mice can still exercise normally and actually have a greater total exercise capacity than wild type mice. At comparable workloads, beta2-AR -/- mice had a lower respiratory exchange ratio than wild type mice suggesting a difference in energy metabolism. beta2-AR -/- mice become hypertensive during exercise and exhibit a greater hypertensive response to epinephrine compared with wild type mice. In summary, the primary physiologic consequences of the beta2-AR gene disruption are observed only during the stress of exercise and are the result of alterations in both vascular tone and energy metabolism.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Derivation of completely cell culture-derived mice from early-passage embryonic stem cells.
Nagy, A., Rossant, J., Nagy, R., Abramow-Newerly, W., & Roder, J. C. (1993) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.90.18.8424 · Cited by 2,329
Differentiation of Receptor Systems activated by Sympathomimetic Amines
LANDS, A. M., ARNOLD, A., MCAULIFF, J. P., LUDUENA, F. P., & BROWN, T. G. (1967) · Nature · doi:10.1038/214597a0 · Cited by 2,065
Targeted disruption of the c-src proto-oncogene leads to osteopetrosis in mice
Soriano, P., Montgomery, C., Geske, R., & Bradley, A. (1991) · Cell · doi:10.1016/0092-8674(91)90499-o · Cited by 2,016
Cloning of the gene and cDNA for mammalian β-adrenergic receptor and homology with rhodopsin
Dixon, R. A. F., Kobilka, B. K., Strader, D. J., Benovic, J. L., Dohlman, H. G., Frielle, T., Bolanowski, M. A., Bennett, C. D., Rands, E., Diehl, R. E., et al. (1986) · Nature · doi:10.1038/321075a0 · Cited by 1,276
Self-citationMolecular Characterization of the Human β 3 -Adrenergic Receptor
Emorine, L. J., Marullo, S., Briend-Sutren, M.-M., Patey, G., Tate, K., Delavier-Klutchko, C., & Strosberg, A. D. (1989) · Science · doi:10.1126/science.2570461 · Cited by 1,088
Plasma catecholamines and essential hypertension. An analytical review.
Goldstein, D. S. (1983) · Hypertension · doi:10.1161/01.hyp.5.1.86 · Cited by 600
Cloning of the cDNA for the human beta 1-adrenergic receptor.
Frielle, T., Collins, S., Daniel, K. W., Caron, M. G., Lefkowitz, R. J., & Kobilka, B. K. (1987) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.84.22.7920 · Cited by 575
Self-citationBrodde, O. E. (1991) · Pharmacological Reviews · doi:10.1016/s0031-6997(25)06662-1 · Cited by 572
Differentiation of receptors responsive to isoproterenol
Lands, A. M., Luduena, F. P., & Buzzo, H. J. (1967) · Life Sciences · doi:10.1016/0024-3205(67)90031-8 · Cited by 480
Rohrer, D. K., Desai, K. H., Jasper, J. R., Stevens, M. E., Regula, D. P., Barsh, G. S., Bernstein, D., & Kobilka, B. K. (1996) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.93.14.7375 · Cited by 310
Self-citation
Cited by
Leptin regulation of bone resorption by the sympathetic nervous system and CART
Elefteriou, F., Ahn, J. D., Takeda, S., Starbuck, M., Yang, X., Liu, X., Kondo, H., Richards, W. G., Bannon, T. W., Noda, M., et al. (2005) · Nature · doi:10.1038/nature03398 · Cited by 1,311
Seven-transmembrane-spanning receptors and heart function
Rockman, H. A., Koch, W. J., & Lefkowitz, R. J. (2002) · Nature · doi:10.1038/415206a · Cited by 938
β2 Adrenergic-Neurotrophin Feedforward Loop Promotes Pancreatic Cancer
Renz, B. W., Takahashi, R., Tanaka, T., Macchini, M., Hayakawa, Y., Dantes, Z., Maurer, H. C., Chen, X., Jiang, Z., Westphalen, C. B., et al. (2018) · Cancer Cell · doi:10.1016/j.ccell.2017.11.007 · Cited by 543
A stress response pathway regulates DNA damage through β2-adrenoreceptors and β-arrestin-1
Hara, M. R., Kovacs, J. J., Whalen, E. J., Rajagopal, S., Strachan, R. T., Grant, W., Towers, A. J., Williams, B., Lam, C. M., Xiao, K., et al. (2011) · Nature · doi:10.1038/nature10368 · Cited by 420
Mutant G-protein-coupled receptors as a cause of human diseases
Schöneberg, T., Schulz, A., Biebermann, H., Hermsdorf, T., Römpler, H., & Sangkuhl, K. (2004) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2004.08.008 · Cited by 337
Metadata
- Authors
- Chruscinski, A. J., Rohrer, D. K., Schauble, E., Desai, K. H., Bernstein, D., & Kobilka, B. K.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 1999-06
- Volume
- 274
- Issue
- 24
- Pages
- 16694-16700
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W1607247437
- Cited by
- 332
- References
- 21
- FWCI
- 5.33
- Type
- journal article
- Language
- en
- Open access
- hybrid
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Targeted Disruption of the β2 Adrenergic Receptor Gene. https://app.cochat.ai/papers/10.1074/jbc.274.24.16694
- The paper
- Chruscinski, A. J., Rohrer, D. K., Schauble, E., Desai, K. H., Bernstein, D., & Kobilka, B. K. (1999). Targeted Disruption of the β2 Adrenergic Receptor Gene. Journal of Biological Chemistry. https://doi.org/10.1074/jbc.274.24.16694
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
