CRF, bovine (TFA) is a potent agonist of CRF receptor, and displaces [125I-Tyr]ovine CRF with a Ki of 3.52 nM[1]. Ki: 3.52 nM (CRF receptor)[1].
CRF, bovine is a potent agonist of CRF receptor, and displaces [125I-Tyr]ovine CRF with a Ki of 3.52 nM[1]. CRF shows pEC50s of 11.16, 8.53 and 8.70 for human CRF1, human CRF2 and rat CRF2α[2]. CRF is released from hypothalamic-pituitary-adrenal (HPA) axis induced by stress, and leads to production of glucocorticoids which down regulate immune responses. CRF also has proinflammatory effects. CRF affects brain microvessel endothelial cells (BMEC) structure or function, CRF (100 nM) significantly increases cAMP in BMEC[3].
[1]. CRF, bovine is a potent agonist of CRF receptor, and displaces [125I-Tyr]ovine CRF with a Ki of 3.52 nM[1]. CRF shows pEC50s of 11.16, 8.53 and 8.70 for human CRF1, human CRF2 and rat CRF2α[2]. CRF is released from hypothalamic-pituitary-adrenal (HPA) axis induced by stress, and leads to production of glucocorticoids which down regulate immune responses. CRF also has proinflammatory effects. CRF affects brain microvessel endothelial cells (BMEC) structure or function, CRF (100 nM) significantly increases cAMP in BMEC[3]. [2]. Smart D, et al. Characterisation using microphysiometry of CRF receptor pharmacology. Eur J Pharmacol. 1999 Aug 27;379(2-3):229-35. [3]. Esposito P, et al. Corticotropin-releasing factor (CRF) can directly affect brain microvessel endothelial cells. Brain Res. 2003 Apr 11;968(2):192-8.