bioRxiv Science⌕ Search

bioRxiv · 10.64898/2026.10.14.759113

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

Abstract

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.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Tumilovich, A., Yablokov, E., Gnedenko, O., Mednaia, D., Selin, V., Mezentsev, Y., Ershov, P., Kaluzhskiy, L., Tsybruk, T., Grabovec, I., Shabunya, P., Gilep, A., Ivanov, A.. 2026-10-16. Intermolecular interactions of CYP3A enzymes and cytosolic sulfotransferases (SULT1E1, SULT2A1). https://doi.org/10.64898/2026.10.14.759113

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

CRISPRa-mediated activation of Tfeb in a fibril-induced alpha-synuclein aggregation model

Accumulation of misfolded alpha-synuclein (a-syn) is a key hallmark of Parkinson's disease (PD), making it a key target for novel therapeutic strategies. Here, we use a previously described screening assay to select multiple efficient single guide RNA (sgRNA) combinations targeting transcription factor EB (TFEB) for CRISPR-activation (CRISPRa) using a nuclease-deficient Staphylococcus aureus Cas9 coupled to a truncated VP64-p53-Rta (VPR) activator complex. Selected sgRNA are applied in a rat neuroblastoma in-vitro model of fibril-induced a-syn aggregation with the goal of inducing autophagy and reduce protein aggregation. We successfully induce a-syn aggregation in this model and observe a stagnation in phosphorylated a-syn (p-a-syn) compared to non-phosphorylated a-syn across treatment groups. While we achieve robust expression of Tfeb in the exogenous screening assay and at endogenous mRNA level, we did not observe proportional increase in protein expression. Additionally, we do not observe any additive effects of CRISPRa induction combined with media treatments inducing Tfeb nuclear translocation. Taken together, these findings illustrate difficulties in epigenetic induction of Tfeb using CRISPRa and highlights the need for additional studies exploring this application.

molecular biology↗

cBAF drives AR-V7 expression through regulation of transcriptional termination in castration-resistant prostate cancer

The androgen receptor splice variant AR-V7 drives resistance to androgen receptor-targeted therapies in castration-resistant prostate cancer (CRPC), but the mechanisms governing its expression remain incompletely understood. Here, we identify the canonical BAF (cBAF) chromatin remodeling complex as a selective regulator of AR-V7 expression. Pharmacologic and genetic disruption of cBAF reduced AR-V7 levels, suppressed AR-V7-dependent transcriptional programs, and impaired CRPC cell proliferation. Mechanistically, cBAF binds an intronic regulatory element downstream of AR cryptic exon 3, where it maintains chromatin accessibility, enhancer activity, and promoter-enhancer looping. cBAF loss decreases recruitment of transcription termination machinery, reduces RNA polymerase II Thr4 phosphorylation, and promotes transcriptional readthrough beyond the AR-V7 polyadenylation site. POINT-seq revealed that cBAF-dependent transcriptional termination is required for AR-V7 biogenesis and regulates termination at a subset of genes genome-wide. Together, these findings uncover a role for cBAF in chromatin-mediated control of transcriptional termination and establish this mechanism as a critical determinant of AR-V7 expression.

molecular biology↗

Stage-specific checkpoint signalling by ATM, ATR and DNA-PK safeguards oocyte genome integrity

In somatic cells, DNA double-strand breaks (DSBs) are potentially catastrophic lesions that activate phosphatidylinositol 3-kinase-related kinase (PIKK) signalling to promote DNA repair or eliminate damaged cells. During meiosis, however, DSBs are deliberately generated as essential intermediates in homologous recombination, raising the question of how DNA damage signalling distinguishes programmed recombination from genome instability. To define how PIKK signalling is adapted to these distinct contexts, we resolved the function of the three PIKKs ATM, ATR and DNA-PK in physiological meiotic recombination and the response to postnatal DNA damage in mouse oocytes. Following postnatal irradiation, ATM functions as the dominant response kinase, with ATR and DNA-PK acting redundantly to eliminate damaged oocytes. In contrast, meiotic surveillance is mediated by ATR, with ATR removal rescuing oocyte loss in response to asynapsis and, independently, to persistent meiotic DSBs. Our findings demonstrate that DNA damage signalling is developmentally reconfigured during oogenesis and highlight distinct pathways of oocyte elimination that may ultimately inform strategies to maintain the ovarian reserve in mammals.

molecular biology↗