ArticleProceedings of the National Academy of Sciences of the United States of America2013
Deficiency of the RIIβ subunit of PKA affects locomotor activity and energy homeostasis in distinct neuronal populations.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
23 citing papers in PubMed, 31 citations in OpenAlex.
- Knockdown of Esr1 from DRD1-Rich Brain Regions Affects Adipose Tissue Metabolism: Potential Crosstalk between Nucleus Accumbens and Adipose Tissue.International journal of molecular sciences · 2024Article
- Article
- RIIβ-PKA in GABAergic Neurons of Dorsal Median Hypothalamus Governs White Adipose Browning.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- PRKAR2A deficiency protects mice from experimental colitis by increasing IFN-stimulated gene expression and modulating the intestinal microbiota.Mucosal immunology · 2021Article
- The PRKAR1B p.R115K Variant is Associated with Lipoprotein Profile in African American Youth with Metabolic Challenges.Journal of the Endocrine Society · 2021Article
- PKA-RIIβ autophosphorylation modulates PKA activity and seizure phenotypes in mice.Communications biology · 2021Article
- PKA functions in metabolism and resistance to obesity: lessons from mouse and human studies.The Journal of endocrinology · 2020Review
- Article
- Hypothalamic dopamine signaling regulates brown fat thermogenesis.Nature metabolism · 2019Article
- Hepatic PKA inhibition accelerates the lipid accumulation in liver.Nutrition & metabolism · 2019Article
- Locomotion Behavior Is Affected by the GαGenetics · 2017Article
- [Effect of baicalin on ATPase and LDH and its regulatory effect on the AC/cAMP/PKA signaling pathway in rats with attention deficit hyperactivity disorder].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2017Article
- PKA Differentially Regulates Adipose Depots to Control Energy Expenditure.Endocrinology · 2017Article
- α-MSH and Foxc2 promote fatty acid oxidation through C/EBPβ negative transcription in mice adipose tissue.Scientific reports · 2016Article
- A novel thermoregulatory role for PDE10A in mouse and human adipocytes.EMBO molecular medicine · 2016Article
- Protein kinase A induces UCP1 expression in specific adipose depots to increase energy expenditure and improve metabolic health.American journal of physiology. Regulatory, integrative and comparative physiology · 2016Article
- Disruption of type 3 adenylyl cyclase expression in the hypothalamus leads to obesity.Integrative obesity and diabetes · 2016Article
- Hypothalamic PKA regulates leptin sensitivity and adiposity.Nature communications · 2015Article
- Article
- Adolescent and adult rat cortical protein kinase A display divergent responses to acute ethanol exposure.Alcohol (Fayetteville, N.Y.) · 2014Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Targeted disruption of RIIβ-protein kinase A (PKA) in mice leads to a lean phenotype, increased nocturnal locomotor activity, and activation of brown adipose tissue. Because RIIβ is abundantly expressed in both white and brown adipose tissue as well as the brain, the contribution of neuronal vs. peripheral PKA to these phenotypes was investigated. We used a Cre-Lox strategy to reexpress RIIβ in a tissue-specific manner in either adipocytes or neurons. Mice with adipocyte-specific RIIβ reexpression remained hyperactive and lean, but pan-neuronal RIIβ reexpression reversed both phenotypes. Selective RIIβ reexpression in all striatal medium spiny neurons with Darpp32-Cre corrected the hyperlocomotor phenotype, but the mice remained lean. Further analysis revealed that RIIβ reexpression in D2 dopamine receptor-expressing medium spiny neurons corrected the hyperlocomotor phenotype, which demonstrated that the lean phenotype in RIIβ-PKA-deficient mice does not develop because of increased locomotor activity. To identify the neurons responsible for the lean phenotype, we used specific Cre-driver mice to reexpress RIIβ in agouti-related peptide (AgRP)-, proopiomelanocortin (POMC)-, single-minded 1 (Sim1)-, or steroidogenic factor 1 (SF1)-expressing neurons in the hypothalamus, but observed no rescue of the lean phenotype. However, when RIIβ was reexpressed in multiple regions of the hypothalamus and striatum driven by Rip2-Cre, or specifically in GABAergic neurons driven by Vgat-ires-Cre, both the hyperactive and lean phenotypes were completely corrected. Bilateral injection of adeno-associated virus1 (AAV1)-Cre directly into the hypothalamus caused reexpression of RIIβ and partially reversed the lean phenotype. These data demonstrate that RIIβ-PKA deficiency in a subset of hypothalamic GABAergic neurons leads to the lean phenotype.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.