bioRxiv Science⌕ Search

Biology subjects

Abranyi-Balogh, P.

Publications and source records attributed to Abranyi-Balogh, P..

3 recordsLinked to original sources

Efficient detection of cryptic pockets on challenging drug targets using MD-free co-vibrational modes

Allosteric and cryptic binding sites provide unique opportunities in drug discovery for achieving selectivity, reducing toxicity and unlocking challenging therapeutical targets. Yet, cryptic pockets are particularly elusive in that they are difficult to capture with experimental methodologies, and therefore often remain undetected. Computational approaches for flexible cryptic site detection traditionally involve extensive unbiased molecular dynamics simulations, or more efficient but computationally still highly demanding biased MD alternatives that make use of enhanced sampling along low-frequency motions of the protein structure. Here we utilize a new variant of the recently introduced and orders of magnitude faster, MD-free COVIB algorithm to identify cryptic pockets efficiently in two challenging targets, the KRAS oncoprotein and the N-terminal domain of the STAT5B transcription factor. Using experimental and AI-modelled structures, respectively, we identify numerous cryptic sites, some of which have not yet been reported. The sites are prioritized and validated with our pharmacophore optimized photoaffinity-tagged fragment library via MS-based peptide mapping and NMR spectroscopy. Besides identifying new, targetable regions on the surface of these important oncotargets, we have established a protocol combining COVIB-based cryptic pocket detection and photoaffinity-based experimental peptide mapping as a robust approach for exploring unique and tractable cryptic pockets.

biophysics↗

Covalent activation of the C-type lectin DC-SIGN

Dendritic Cell-Specific Intercellular adhesion molecule-3-Grabbing Non-integrin (DC-SIGN) is a C-type lectin receptor expressed on antigen-presenting cells, crucial for pathogen recognition and immune modulation. The shallow and polar carbohydrate binding site of DC-SIGN presents challenges for ligand design. Here, we explored covalent modification targeting specific lysine residues as a novel strategy to modulate DC-SIGN function. Screening a lysine-targeted electrophilic fragment library using orthogonal functional assays identified two potent activators. Structural analyses via NMR spectroscopy, mass spectrometry and computational modeling confirmed structural perturbations of the carbohydrate recognition domain and revealed distinct mechanisms of activation. While both activators significantly enhanced DC-SIGNs affinity for monosaccharide ligands, one compound induced oligomerization via covalent coupling and non-covalent secondary site interactions, whereas the other selectively modified lysine K373 directly within the primary carbohydrate-binding site. These findings demonstrate the potential of lysine-targeted covalent compounds as a novel therapeutic strategy for modulating DC-SIGN function and potentially C-type lectins in general. Table of contents O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=50 SRC="FIGDIR/small/674704v1_ufig1.gif" ALT="Figure 1"> View larger version (19K): org.highwire.dtl.DTLVardef@1b44543org.highwire.dtl.DTLVardef@2f3feaorg.highwire.dtl.DTLVardef@d48e1org.highwire.dtl.DTLVardef@2baee1_HPS_FORMAT_FIGEXP M_FIG C_FIG We introduce the first covalent activators of a C-type lectin. Using GCI, NMR, MS/MS and computational modeling, we delineate mechanisms from a functional electrophile-first screen on DC-SIGN that yields two modes: NHS-ester 11 modifies K379 to induce CRD oligomerization via a secondary site, and squarate 33 modifies K373 in the carbohydrate site to strengthen glycan binding.

pharmacology and toxicology↗

Crystallographic and electrophilic fragment screening of the SARS-CoV-2 main protease

COVID-19, caused by SARS-CoV-2, lacks effective therapeutics. Additionally, no antiviral drugs or vaccines were developed against the closely related coronavirus, SARS-CoV-1 or MERS-CoV, despite previous zoonotic outbreaks. To identify starting points for such therapeutics, we performed a large-scale screen of electrophile and non-covalent fragments through a combined mass spectrometry and X-ray approach against the SARS-CoV-2 main protease, one of two cysteine viral proteases essential for viral replication. Our crystallographic screen identified 71 hits that span the entire active site, as well as 3 hits at the dimer interface. These structures reveal routes to rapidly develop more potent inhibitors through merging of covalent and non-covalent fragment hits; one series of low-reactivity, tractable covalent fragments was progressed to discover improved binders. These combined hits offer unprecedented structural and reactivity information for on-going structure-based drug design against SARS-CoV-2 main protease.

biophysics↗