Publications by authors named "S DJOKIC"

Host factors that define the cellular tropism of SARS-CoV-2 beyond the cognate ACE2 receptor are poorly defined. Here we report that SARS-CoV-2 replication is restricted at a post-entry step in a number of ACE2-positive airway-derived cell lines due to tonic activation of the cGAS-STING pathway mediated by mitochondrial DNA leakage and naturally occurring cGAS and STING variants. Genetic and pharmacological inhibition of the cGAS-STING and type I/III IFN pathways as well as ACE2 overexpression overcome these blocks.

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Article Synopsis
  • A new total synthesis of the natural δ-lactone cleistenolide and its (6S)-stereoisomer was accomplished using d-glucose, involving key steps like oxidative cleavage and Wittig olefination.
  • The synthesis of several new 4-substituted cleistenolide analogues was conducted using molecular hybridization and bioisosterism methods, with many showing stronger anti-cancer activity than the original compound.
  • Notably, the strongest antiproliferative effects were observed in K562 cells, particularly with derivatives 3 and 17, while a structure-activity relationship (SAR) analysis identified crucial structural elements for their effectiveness.
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The first total synthesis and absolute configuration assignment of asperilactone B (I) have been accomplished. Additionally, a revision of the absolute stereochemistry of asperilactone C has been done. The first total synthesis of the opposite enantiomer of asperilactone B (-I) has also been achieved, as well as that of C-7 epimers of both asperilactones B (8) and C (9).

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Ten new thiophene derivatives related to goniofufurone have been obtained by multistep synthesis starting from d-glucose. The critical step of the synthesis was the Grignard reaction of 2-thienyl magnesium bromide with a protected dialdose, yielding the C-5 epimeric thiophene derivatives 9 and 10. The mixture was oxidized to the 5-keto derivative 11, which after deprotection was converted to the corresponding keto-lactone 14.

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Host factors that define the cellular tropism of SARS-CoV-2 beyond the cognate ACE2 receptor are poorly defined. Here we report that SARS-CoV-2 replication is restricted at a post-entry step in a number of ACE2-positive airway-derived cell lines due to tonic activation of the cGAS-STING pathway mediated by mitochondrial DNA leakage and naturally occurring cGAS and STING variants. Genetic and pharmacological inhibition of the cGAS-STING and type I/III IFN pathways as well as ACE2 overexpression overcome these blocks.

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