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Mistry, S. N.

Publications and source records attributed to Mistry, S. N..

2 recordsLinked to original sources

Development of fluorescent peptide G Protein Coupled Receptor activation biosensors for NanoBRET characterisation of intracellular allosteric modulators

G protein coupled receptors (GPCRs) are widely therapeutically targeted, and recent advances in allosteric modulator development at this class of receptors offer further potential for exploitation. In particular GPCR intracellular allosteric modulators (IAM) represent a class of ligands that bind to the receptor-effector interface (e.g. G protein) and so inhibit agonist responses non-competitively. This potentially offers a tailored mode of action and greater selectivity between conserved receptor subtypes compared to classical orthosteric ligands. However, while specific examples of the IAM class of ligands are well described (particularly for chemokine receptors), a more general methodology for assessing compound interactions at the GPCR IAM site is lacking. Here fluorescent labelled peptides based on the G peptide C terminus are developed as novel binding and activation biosensors for the GPCR IAM binding site. In TR-FRET binding studies, unlabelled peptides derived from the GS subunit C-terminus were first characterised for their ability to positively modulate agonist affinity at the {beta}2-adrenoceptor. On this basis, a tetramethylrhodamine (TMR) labelled tracer was synthesized based on the 19 amino acid C terminal GS peptide (TMR-GS19cha18, where cha=cyclohexylalanine). Using NanoBRET technology to detect binding, TMR-GS19cha18 was recruited to Gs coupled {beta}2-adrenoceptor and EP2 receptors in an agonist dependent manner (correlated with ligand efficacy), but not to the Gi coupled CXCR2 receptor. Moreover, NanoBRET competition binding assays using TMR-GS19cha18 enabled direct assessment of the affinity of unlabelled ligands for {beta}2-adrenoceptor IAM site. Thus the NanoBRET platform using fluorescent-labelled G protein peptide mimetics offers novel potential for medium-throughput affinity screens to identify new IAMs, applicable across GPCRs coupled to a G protein class. Using the same platform, Gs peptide biosensors also represent useful tools to probe orthosteric agonist efficacy and the dynamics of receptor activation.

pharmacology and toxicology↗

Activation of M1 muscarinic receptors reduce pathology and slow progression of neurodegenerative disease.

The most prevalent types of dementias, including Alzheimers disease, are those that are propagated via the spread of "prion-like" misfolded proteins. Despite considerable effort no treatments are available to slow or stop the progression of these dementias. Here we investigate the possibility that activation of the M1-muscarinic receptor (M1-receptor), which is highly expressed in the brain and that shows pro-cognitive properties, might present a novel disease modifying target. We demonstrate that the progression of murine prion disease, which we show here displays many of the pathological, behavioural and biochemical hallmarks of human neurodegenerative disease, is slowed and normal behaviour maintained by the activation of the M1-receptor with a highly tolerated positive allosteric modulator (VU846). This correlates with a reduction in both neuroinflammation and indicators of mitochondrial dysregulation, as well as a normalisation in the expression of markers associated with neurodegeneration and Alzheimers disease. Furthermore, VU846 preserves expression of synaptic proteins and post-synaptic signalling components that are altered in disease. We conclude that allosteric regulation of M1-receptors has the potential to reduce the severity of neurodegenerative diseases caused by the prion-like propagation of misfolded protein in a manner that extends life span and maintains normal behaviour.

neuroscience↗