bioRxiv Science⌕ Search

Biology subjects

Shabunya, P.

Publications and source records attributed to Shabunya, P..

3 recordsLinked to original sources

Intermolecular interactions of CYP3A enzymes and cytosolic sulfotransferases (SULT1E1, SULT2A1)

Cytochrome P450 enzymes of the CYP3A subfamily (CYP3A4 and CYP3A5) and cytosolic sulfotransferases (SULT1E1 and SULT2A1) play key roles in the sequential oxidative and conjugative metabolism of steroid hormones and xenobiotics. While their coordinated transcriptional regulation and co-expression patterns are well documented, direct physical interactions between these phase I and phase II enzymes have not previously been demonstrated. In this study, we combined systems biology analysis, SPR biosensing, activity assays, and AlphaFold2 modeling to investigate PPIs between CYP3A4/3A5 and SULT1E1/2A1. STRINGdb and transcriptomic data suggested potential associations, but direct evidence was lacking. SPR confirmed high-affinity binding (Kd 0.29-1.8 nM); the SULT2A1-CYP3A5 pair gave 0.29 nM, while SULT2A1-CYP3A4 gave 1.8 nM. Notably, the presence of the sulfo group donor SULT PAPS, had minimal effect on binding affinity. Functional assays demonstrated that SULTs slightly inhibited CYP3A4 activity while moderately enhancing CYP3A5 activity in the presence of SULT1E1, both with and without PAPS, whereas the addition of CYPs leads to selectively increase in SULT2A1 activity in vitro by 38% (CYP3A4) and 108% (CYP3A5), without affecting SULT1E1. AlphaFold2 models revealed stable interfaces (715-1856 square angstroms) with 10-16 H-bonds and salt bridges. The results of our in silico tunnel analysis suggested a plausible alignment of substrate exit channels from CYPs with entry pathways to SULTs, supporting a mechanistic basis for substrate channeling in CYP-SULT complexes. These results indicate that the enzymes may form functional multienzyme complexes, offering new insights into coordinated steroid/xenobiotic metabolism and drug clearance.

molecular biology↗

Hydroxylation of antitubercular drug candidate, SQ109, by mycobacterial cytochrome P450

Spreading of the multidrug-resistant (MDR) strains of the deadliest pathogen Mycobacterium tuberculosis (Mtb) generates the need for new effective drugs. SQ109 showed activity against resistant Mtb and already advanced to Phase II/III clinical trials. Fast SQ109 degradation is attributed to the human liver Cytochrome P450s (CYPs). However, no information is available about interactions of the drug with Mtb CYPs. Here, we show that Mtb CYP124, previously assigned as a methyl-branched lipid monooxygenase, binds and hydroxylates SQ109 in vitro. A 1.25 [A]-resolution crystal structure of the CYP124-SQ109 complex unambiguously shows two conformations of the drug, both positioned for hydroxylation of the {omega}-methyl group in the trans position. The hydroxylated SQ109 presumably forms stabilizing H-bonds with its target, the Mycobacterial membrane protein Large 3 (MmpL3). We anticipate that Mtb CYPs could function as analogs of drug-metabolizing human CYPs affecting pharmacokinetics and pharmacodynamics of antitubercular (anti-TB) drugs.

biochemistry↗

Metabolic fate of human immunoactive sterols in Mycobacterium tuberculosis

Mycobacterium tuberculosis (Mtb) infection is among top ten causes of death worldwide, and the number of drug-resistant strains is increasing. The direct interception of human immune signaling molecules by Mtb remains elusive, limiting drug discovery. Oxysterols and secosteroids regulate both innate and adaptive immune responses. Here we report a functional, structural, and bioinformatics study of Mtb enzymes initiating cholesterol catabolism and demonstrated their interrelation with human immunity. We show that these enzymes metabolize human immune oxysterol messengers. Rv2266, the most potent among them, can also metabolize vitamin D3 (VD3) derivatives. High-resolution structures show common patterns of sterols binding and reveal a site for oxidative attack during catalysis. Finally, we designed a compound that binds and inhibits three studied proteins. The compound shows activity against Mtb H37Rv residing in macrophages. Our findings contribute to molecular understanding of suppression of immunity and suggest that Mtb has its own transformation system resembling the human phase I drug-metabolizing system.Competing Interest StatementA.Gi. and E.S. are employees of MT-Medicals LLC. The other authors declare no competing interests.View Full Text

biochemistry↗