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Malik, W.

Publications and source records attributed to Malik, W..

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Conserved folds enable immune antagonism across the tree of life

Many components of human innate immunity are conserved in prokaryotes 1,2. While pathogens are known to evade host defenses 3, whether mechanisms of immune evasion share a similarly deep evolutionary or functional conservation across the tree of life remains largely unresolved. Here, we systematically explore this question by establishing The Viral Compendium (TVC), a database of over 350,000 proteins and 790,000 domains from eukaryotic, bacterial, and archaeal viruses. We find that protein structure alignments identify pan-viral clusters of proteins and domains, vastly increasing viral protein annotation rates compared to sequence-based methods. Domain co-association analysis revealed 1,351 combinations of domains that are conserved across archaeal, eukaryotic, and bacterial viruses, including fusion proteins that reconstitute the nuclease-ATPase core of the Mre11-Rad50 multiprotein complex involved in cellular DNA repair 4. Leveraging structural comparisons, we identify widely shared structural folds that mediate immune suppression: conserved phosphodiesterase folds encoded by both viral and bacterial pathogens that degrade nucleotide messengers, and double-stranded RNA binding domains employed across eukaryotic and prokaryotic viruses to suppress cellular sensing. Together, our results demonstrate that pathogen immune evasion is built upon conserved structural building blocks, revealing unified mechanisms and effectors of immune antagonism spanning all domains of life.

microbiology↗

Dual inhibition of GTP-bound (ON) and GDP-bound (OFF) KRASG12C suppresses PI3Kα and leads to potent tumor inhibition

Current approved KRASG12C inhibitors covalently bind the inactive GDP-bound (OFF) form of KRASG12C. Recently, KRASG12C inhibitors that selectively bind to the GTP-bound (ON) form of both KRASG12C (ON) and (OFF) forms have been reported and entered clinical testing. In principle, KRASG12C (ON) inhibitors may be less susceptible to adaptive mechanisms that promote resistance to (OFF) inhibitors, however the specific mechanisms that differentiate the activity of (ON) versus (OFF) inhibition are not well understood. We profiled the activity of BBO-8520, a covalent dual inhibitor of GTP-bound (ON) and GDP-bound (OFF) KRASG12C, in KRASG12C-mutant non-small cell lung cancer models. BBO-8520 exerted more potent and sustained inhibition of KRASG12C and anti-tumor activity in vitro and in vivo compared with sotorasib, a KRASG12C (OFF)-only inhibitor. While cells treated with BBO-8520 or sotorasib both exhibited feedback reactivation of MAPK signaling driven by wild-type HRAS/NRAS isoforms, more durable suppression of KRASG12C by BBO-8520 was associated with decreased PI3K-AKT activation in vitro. Disruption of the interaction between RAS and PI3K using a novel protein:protein interaction inhibitor suppressed PI3K-AKT activation and increased the tumor response to sotorasib to a similar level as BBO-8520. Moreover, in some contexts, disruption of RAS-PI3K further increased the anti-tumor activity of BBO-8520 monotherapy. These results reveal mechanistic differences between KRAS (ON) and (OFF) inhibitors, highlight the importance of PI3K-AKT signaling in driving resistance to KRAS inhibition in lung cancer, and suggest combination strategies that suppress PI3K-AKT to improve the response to KRAS inhibitors.

cancer biology↗