Receptors, Adrenergic, beta-3

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  Subject Areas on Research

  • Adipocyte β-arrestin-2 is essential for maintaining whole body glucose and energy homeostasis. 
  • 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. 
  • 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.