L755507 is a derivative of 4-acylaminobenzenesulfonamide.[1]
Aplicación
L755507 has been shown to enhance CRISPR genome editing efficiency. To see other small molecule CRISPR enhancers, visit sigma.com/CRISPR-enhancers.
Acciones bioquímicas o fisiológicas
L755507 is a potent β3-adrenergic receptor partial agonist with an EC50 value of 0.43 nM for β3 receptors with over 440-fold selectivity for β3 compared to β1 and β2-adrenergic receptor binding. L755507 has been shown to enhance CRISPR-mediated homology-directed repair (HDR) efficiency in human induced pluripotent stem cells (iPSCs), increasing the efficiency of GFP insertion by 3-fold compared to control cells.
L755507 is a potent β3-adrenergic receptor partial agonist.
L755507 is found to stimulate the breakdown of lipids in human adipose tissues. L755507 also promotes urinary bladder relaxation.[1]
British journal of pharmacology, 135(8), 1903-1914 (2002-04-18)
1. This study characterizes the mouse beta(3a)-adrenoceptor (AR) and the splice variant of the beta(3)-AR (beta(3b)-AR) expressed in Chinese hamster ovary cells (CHO-K1). 2. Stable clones with high (approximately 1200), medium (approximately 500) or low receptor expression (approximately 100 fmol
Tools to study β 3-adrenoceptors.
Vrydag W and Michel M C
Naunyn-Schmiedeberg'S Archives of Pharmacology, 374(5-6), 385-398 (2007)
A study of 4-acylaminobenzenesulfonamides in a cloned human beta 3 adrenergic receptor assay resulted in the discovery of n-hexylurea, L-755,507 (22). This 0.43 nM beta 3 agonist, which is > 440-fold selective over both beta 1 and beta 2 binding
This study identifies signaling pathways activated by the beta(2)-/beta(3)-adrenoceptor (AR) agonist zinterol, the selective beta(3)-AR agonist L755507, and the selective beta(3)-AR antagonist L748337 in CHO-K1 cells expressing human beta(3)-adrenoceptors. Zinterol and L755507 caused a robust concentration-dependent increase in cAMP accumulation
The Journal of biological chemistry, 297(1), 100903-100903 (2021-06-23)
c-Myc is a transcription factor that plays a crucial role in cellular homeostasis, and its deregulation is associated with highly aggressive and chemotherapy-resistant cancers. After binding with partner MAX, the c-Myc-MAX heterodimer regulates the expression of several genes, leading to
Modulation of homology-directed repair (HDR) within the context of CRISPR-genome editing has led to the identification of small molecules that enhance CRISPR-mediated HDR efficiency in various cell types.
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