Receptors, Adrenergic, beta-3
-
Subject Areas on Research
- Augmentation of cardiac contractility mediated by the human beta(3)-adrenergic receptor overexpressed in the hearts of transgenic mice.
- CCAAT/enhancer-binding protein alpha is required for transcription of the beta 3-adrenergic receptor gene during adipogenesis.
- Cardiac function in genetically engineered mice with altered adrenergic receptor signaling.
- Catechol-O-methyltransferase inhibition increases pain sensitivity through activation of both beta2- and beta3-adrenergic receptors.
- Depressed expression of adipocyte beta-adrenergic receptors is a common feature of congenital and diet-induced obesity in rodents.
- Direct binding of activated c-Src to the beta 3-adrenergic receptor is required for MAP kinase activation.
- Maximal beta3-adrenergic regulation of lipolysis involves Src and epidermal growth factor receptor-dependent ERK1/2 activation.
- Role of β-3 adrenergic receptor polymorphism in overactive bladder.
- Signaling pathways mediating beta3-adrenergic receptor-induced production of interleukin-6 in adipocytes.
- Strain-specific response to beta 3-adrenergic receptor agonist treatment of diet-induced obesity in mice.
- Sustained Adrenergic Signaling Promotes Intratumoral Innervation through BDNF Induction.
- Sustained stimulation of β2- and β3-adrenergic receptors leads to persistent functional pain and neuroinflammation.
- The beta-adrenergic receptors and the control of adipose tissue metabolism and thermogenesis.
- The beta3-adrenergic receptor activates mitogen-activated protein kinase in adipocytes through a Gi-dependent mechanism.
- The third beta is not the charm.
- Zfp423 Maintains White Adipocyte Identity through Suppression of the Beige Cell Thermogenic Gene Program.
- beta(3)-adrenoceptor deficiency blocks nitric oxide-dependent inhibition of myocardial contractility.
- beta-Adrenergic activation of p38 MAP kinase in adipocytes: cAMP induction of the uncoupling protein 1 (UCP1) gene requires p38 MAP kinase.
- β2- and β3-adrenergic receptors drive COMT-dependent pain by increasing production of nitric oxide and cytokines.