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The UniProt accession P52020 corresponds to rat Sqle (synonym Erg1) encoding squalene monooxygenase / squalene epoxidase (SQLE), the sterol-pathway enzyme that epoxidizes squalene to oxidosqualene. The central biochemical function, enzyme family features (FAD-dependent monooxygenase), and endomembrane localization described in mammalian SQLE studies match the provided UniProt description, so the literature summarized below is aligned with the intended target. (padyana2019structureandinhibition pages 1-2, zhang2024squaleneepoxidaseits pages 2-4)
SQLE catalyzes the stereospecific epoxidation of squalene to 2,3(S)-oxidosqualene (also termed 2,3-epoxysqualene), which is the first oxygenation step and a committed transformation within the sterol branch of the mevalonate–cholesterol pathway. (padyana2019structureandinhibition pages 1-2, padyana2019structureandinhibition pages 9-9)
SQLE is widely described as one of the key rate-limiting control points in cholesterol synthesis (often discussed downstream of HMG-CoA reductase), so changes in its abundance/activity can substantially redirect pathway flux. (padyana2019structureandinhibition pages 1-2, zhang2024squaleneepoxidaseits pages 1-2)
Cofactor: SQLE is FAD-dependent; crystal structures of the human catalytic domain show SQLE bound to FAD. (padyana2019structureandinhibition pages 9-9, zhang2024squaleneepoxidaseits pages 2-4)
Electron donor system: SQLE is an electron-requiring microsomal (ER) enzyme. The principal electron donation route is NADPH → NADPH–cytochrome P450 reductase (POR/CPR/P450R) → SQLE. POR is an ER-associated flavoprotein that uses NADPH exclusively and transfers electrons to SQLE in cholesterol synthesis. (porter2015electrontransferpathways pages 2-4, porter2015electrontransferpathways pages 1-2)
Physiological nuance: Although POR is classically considered the key donor, hepatic POR-null mouse experiments indicate that ~40% of hepatic microsomal SQLE activity can persist, implying an additional microsomal NADPH-dependent reductase may contribute under some conditions. (porter2015electrontransferpathways pages 4-5)
SQLE is an endoplasmic reticulum (ER) membrane-associated protein. A regulatory N-terminal ~100 aa (N100) region mediates lipid sensing and degradation, while the catalytic domain spans the C-terminus (approximately aa 101–574 in human; highly conserved across mammals). (zhang2024squaleneepoxidaseits pages 2-4)
Topological features described for mammalian SQLE include an N-terminal re-entrant loop (aa 24–33) and an amphipathic helix (aa 62–73) that reversibly associates with the ER membrane and functions as a cholesterol-responsive structural element (degron mechanism). (zhang2024squaleneepoxidaseits pages 2-4, zhang2024squaleneepoxidaseits pages 4-6)
SQLE is a transcriptional target of SREBP2, the master transcriptional regulator of cholesterol biosynthesis genes. Under low cholesterol, SREBP2 activation increases SQLE expression; promoter-level regulation involves cooperating transcription factors including NF-Y, Sp1, and YY1. (zhang2024squaleneepoxidaseits pages 8-9, zhang2024squaleneepoxidaseits pages 6-8)
A central contemporary concept is that SQLE abundance is tuned by cholesterol-accelerated, proteasome-dependent degradation mediated by ER-associated degradation (ERAD) machinery.
Mechanistically, the ER E3 ubiquitin ligase MARCH6 (TEB4/RNF176) promotes SQLE ubiquitination and degradation. A CRISPR/Cas9 screen identified UBE2J2 as a principal E2 supporting MARCH6-dependent SQLE degradation, and the process involves VCP. (zhang2024squaleneepoxidaseits pages 8-9)
Noncanonical ubiquitination is emphasized: SQLE degradation does not strictly require lysine ubiquitination; serine residues in N100 (including Ser59, Ser61, Ser83, Ser87) are critical, and Ser83 is described as a ubiquitination site. (zhang2024squaleneepoxidaseits pages 8-9)
At the membrane-structural level, increased cholesterol triggers conformational changes in the N100 region and deformation/ejection of the amphipathic helix, exposing a hydrophobic signal that targets SQLE for proteasomal turnover. (zhang2024squaleneepoxidaseits pages 4-6, zhang2024squaleneepoxidaseits pages 2-4)
SQLE’s substrate, squalene, can bind the N100 region and reduce interaction/ubiquitination by MARCH6, stabilizing SQLE at the ER—an example of feedback where upstream metabolite accumulation buffers enzyme degradation. (zhang2024squaleneepoxidaseits pages 4-6)
A 2023 study in Communications Biology reports that cholesterol alters mevalonate-pathway flux by promoting SQLE degradation (described as a rate-limiting step), which increases levels of squalene and CoQ10 and thereby suppresses ferroptosis vulnerability. The authors further report that simultaneous inhibition of both CoQ10 and squalene biosynthesis abrogates cholesterol’s ferroptosis-protective effect, and mouse injury models (ischemia–reperfusion and doxorubicin-induced hepatotoxicity) support physiological relevance. (sun2023cholesterolmediatedferroptosis pages 1-2)
Wen et al. (May 2024, Gut) used hepatocyte-specific Sqle transgenic and hepatocyte-specific Sqle knockout mouse models under a choline-deficient high-fat diet plus DEN to induce MASH-HCC and showed that SQLE promotes tumor burden and immunosuppression. Specifically, Sqle transgenic mice showed increased tumor burden with reduced functional CD8+ T cell markers (IFN-γ+, Granzyme B+) and increased Arg-1+ MDSCs, whereas hepatocyte-specific Sqle knockout suppressed tumor growth and reversed these immune features. (wen2024targetingsqualeneepoxidase pages 1-2)
In orthotopic models (RIL-175, Hepa1-6), the excerpt provides group sizes (e.g., n=5/group) and dosing/depletion regimens for mechanistic immune tests, and in humanized CD34+ mice, treatment with the SQLE inhibitor terbinafine reduced tumor burden (n=8/group) and increased cytotoxic CD8+ markers. The authors conclude that targeting SQLE (genetic or terbinafine) can restore anti-PD-1 efficacy in MASH-HCC models. (wen2024targetingsqualeneepoxidase pages 5-6, wen2024targetingsqualeneepoxidase pages 1-2)
A 2024 study in Frontiers in Immunology frames SQLE as an enzyme whose activity removes squalene (by converting it to oxidosqualene), and reports that SQLE knockdown in pancreatic tumor models increases intracellular squalene and reshapes immune infiltration. In an immune-competent C57BL/6 model, KPC tumors were generated by injecting 1.8×10^6 cells (n=5/group). Direct administration of squalene 200 mg/kg intraperitoneally every two days reduced tumor growth; the excerpt notes one tumor disappeared in the SQLE-knockdown group and reports highly significant differences (*, *p<0.0001 for some comparisons). (pan2024sqlemediatedsqualenemetabolism pages 5-8)
Mechanistically, elevated squalene was linked to reduced NF-κB activity (p65 and p65 S536 phosphorylation) and reduced CXCL1 expression, with downstream effects on recruitment of immune-suppressive myeloid populations. (pan2024sqlemediatedsqualenemetabolism pages 5-8)
Wang et al. (Feb 2024, Clinical and Translational Medicine) identify SQLE as a metabolic vulnerability in high-risk osteosarcoma using an AI-derived prognostic index and multi-cohort validation. The excerpt reports that SQLE and MYC are overexpressed and correlated with copy-number amplification and that SQLE and MYC mRNA are independent predictors of mortality by multivariate Cox regression; in a 77-sample TMA, an outcome association is reported (p=0.037). Functionally, SQLE knockdown reduced malignant phenotypes and lowered tumor cholesterol, and the SQLE inhibitor FR194738 showed in vivo anti-osteosarcoma effects and synergy with chemotherapy in the reported study. (wang2024identifyingsqualeneepoxidase pages 14-17)
SQLE inhibition is a clinically proven strategy in fungi; the allylamine terbinafine targets fungal squalene epoxidase. Human SQLE structural work provides mechanistic rationale for inhibitor specificity and helps interpret clinically encountered terbinafine-resistant mutants (in fungi) as well as informing next-generation inhibitor design. (padyana2019structureandinhibition pages 1-2)
Recent in vivo work supports repurposing/leveraging SQLE inhibition to modulate tumor immunity and therapy response. In MASH-HCC models, terbinafine (pharmacologic SQLE inhibition) combined with immunotherapy is reported to restore anti-PD-1 efficacy. (wen2024targetingsqualeneepoxidase pages 1-2)
Multiple SQLE inhibitors are used as research tools (e.g., NB-598, Cmpd-4; and FR194738 in osteosarcoma work), enabling mechanistic dissection of cholesterol synthesis dependency versus squalene-mediated effects. (padyana2019structureandinhibition pages 1-2, wang2024identifyingsqualeneepoxidase pages 14-17)
A 2024 review in International Journal of Molecular Sciences synthesizes SQLE regulation across transcriptional control (SREBP2 and co-regulators) and post-translational ERAD (MARCH6 axis) and contextualizes SQLE as both a metabolic control node and a cancer-linked enzyme with therapeutic potential. This review also highlights less intuitive regulatory features such as N100-based cholesterol sensing and truncation mechanisms that may yield constitutively active forms. (zhang2024squaleneepoxidaseits pages 1-2, zhang2024squaleneepoxidaseits pages 8-9)
A domain-focused review in Lipids (2015) provides a mechanistic framework for electron transfer pathways on the ER supporting sterol synthesis enzymes, emphasizing POR as a central NADPH-dependent electron donor for SQLE while noting evidence for additional donors based on knockout/residual activity observations. (porter2015electrontransferpathways pages 4-5, porter2015electrontransferpathways pages 2-4)
Because the tool-accessible excerpts do not include full numeric effect sizes for many endpoints (e.g., hazard ratios, AUC values, tumor volumes), the quantitative highlights below are restricted to explicit numbers present in the retrieved text chunks:
Rat Sqle/Erg1 encodes an ER-associated, FAD-dependent monooxygenase that epoxidizes squalene to 2,3(S)-oxidosqualene, receiving reducing equivalents mainly through NADPH-dependent POR/CPR on the ER membrane. Its N-terminal regulatory region implements cholesterol-responsive ERAD (MARCH6/UBE2J2/VCP axis), making SQLE a metabolic “valve” controlling sterol pathway flux and altering levels of squalene and downstream cholesterol-dependent cellular states. Recent 2023–2024 studies extend SQLE’s relevance to ferroptosis modulation and tumor immunity, with pharmacologic inhibition (notably terbinafine) being evaluated in vivo for cancer-immunity contexts. (padyana2019structureandinhibition pages 1-2, zhang2024squaleneepoxidaseits pages 4-6, sun2023cholesterolmediatedferroptosis pages 1-2, wen2024targetingsqualeneepoxidase pages 1-2, pan2024sqlemediatedsqualenemetabolism pages 5-8, porter2015electrontransferpathways pages 4-5, porter2015electrontransferpathways pages 2-4)
| Aspect | Key points | Best supporting citations (pqac ids) | Key sources with URL and pub date |
|---|---|---|---|
| Enzyme function | Rat Sqle (UniProt P52020; synonym Erg1) matches mammalian squalene monooxygenase/squalene epoxidase, the first oxygenation step in sterol biosynthesis and a major rate-limiting control point downstream of HMGCR. Evidence is primarily from mammalian SQLE literature and is consistent with the UniProt family/domain assignment for rat. | (padyana2019structureandinhibition pages 1-2, zhang2024squaleneepoxidaseits pages 2-4, zhang2024squaleneepoxidaseits pages 1-2) | Padyana et al., Nat Commun (Jan 2019), https://doi.org/10.1038/s41467-018-07928-x; Zhang et al., Int J Mol Sci (Mar 2024), https://doi.org/10.3390/ijms25073874 |
| Reaction | SQLE catalyzes the stereospecific epoxidation of squalene to 2,3(S)-oxidosqualene (also called 2,3-epoxysqualene), the committed oxygenation step preceding cyclization to lanosterol in animals. | (padyana2019structureandinhibition pages 1-2, padyana2019structureandinhibition pages 9-9, zhang2024squaleneepoxidaseits pages 2-4) | Padyana et al., Nat Commun (Jan 2019), https://doi.org/10.1038/s41467-018-07928-x; Zhang et al., Int J Mol Sci (Mar 2024), https://doi.org/10.3390/ijms25073874 |
| Substrate/product | Substrate: squalene. Immediate product: 2,3-oxidosqualene. Structural and biochemical studies show a defined substrate/inhibitor-binding pocket for squalene, supporting strong substrate specificity for the sterol branch of the mevalonate pathway. | (zhang2024squaleneepoxidaseits pages 2-4, padyana2019structureandinhibition pages 9-9, pan2024sqlemediatedsqualenemetabolism pages 5-8) | Zhang et al., Int J Mol Sci (Mar 2024), https://doi.org/10.3390/ijms25073874; Padyana et al., Nat Commun (Jan 2019), https://doi.org/10.1038/s41467-018-07928-x; Pan et al., Front Immunol (Dec 2024), https://doi.org/10.3389/fimmu.2024.1512981 |
| Cofactors/electron donors | SQLE is an FAD-dependent monooxygenase. In mammalian ER membranes, reducing equivalents are supplied mainly from NADPH via NADPH-cytochrome P450 reductase (POR/CPR/P450R). Reconstitution assays used recombinant P450R; review evidence indicates POR is the major donor, although residual SQLE activity in hepatic POR-null mice suggests an additional microsomal NADPH-dependent reductase may contribute in some contexts. | (padyana2019structureandinhibition pages 1-2, porter2015electrontransferpathways pages 4-5, padyana2019structureandinhibition pages 9-9, porter2015electrontransferpathways pages 2-4) | Porter, Lipids (Sep 2015), https://doi.org/10.1007/s11745-015-4065-1; Padyana et al., Nat Commun (Jan 2019), https://doi.org/10.1038/s41467-018-07928-x |
| Subcellular localization/topology | SQLE is an ER membrane-associated protein. The protein has an N-terminal regulatory region (N100) with a re-entrant loop (aa 24-33) and amphipathic helix (aa 62-73) that reversibly associate with the ER membrane, plus a C-terminal catalytic domain (aa 101-574). This topology underlies cholesterol sensing and degradation control. | (zhang2024squaleneepoxidaseits pages 2-4, zhang2024squaleneepoxidaseits pages 4-6) | Zhang et al., Int J Mol Sci (Mar 2024), https://doi.org/10.3390/ijms25073874 |
| Regulation | SQLE is regulated both transcriptionally and post-translationally. SREBP2 activates SQLE transcription under low-cholesterol conditions, with NF-Y, Sp1, YY1 as promoter-associated regulators. Excess cholesterol triggers ER-associated degradation (ERAD) through MARCH6, UBE2J2, and VCP, acting on the N100 degron; critical residues include Ser59, Ser61, Ser83, Ser87. Squalene itself can stabilize SQLE by reducing MARCH6-dependent ubiquitination. | (zhang2024squaleneepoxidaseits pages 4-6, zhang2024squaleneepoxidaseits pages 6-8, zhang2024squaleneepoxidaseits pages 8-9) | Zhang et al., Int J Mol Sci (Mar 2024), https://doi.org/10.3390/ijms25073874 |
| Pathway role | SQLE functions in the mevalonate-cholesterol pathway after squalene synthase and before oxidosqualene cyclase, controlling flux into sterol production. Because it is one of the principal regulated steps in cholesterol synthesis, altered SQLE activity changes levels of cholesterol, squalene, and related metabolites such as CoQ pathway outputs indirectly via pathway flux redistribution. | (zhang2024squaleneepoxidaseits pages 1-2, sun2023cholesterolmediatedferroptosis pages 1-2, porter2015electrontransferpathways pages 1-2) | Zhang et al., Int J Mol Sci (Mar 2024), https://doi.org/10.3390/ijms25073874; Sun et al., Commun Biol (Nov 2023), https://doi.org/10.1038/s42003-023-05477-8; Porter, Lipids (Sep 2015), https://doi.org/10.1007/s11745-015-4065-1 |
| Inhibitors/applications | SQLE is a validated drug target. Terbinafine clinically targets fungal squalene epoxidase and human SQLE structures explain selectivity/resistance. Experimental mammalian SQLE inhibitors include NB-598, Cmpd-4 and FR194738. Current application areas include antifungal therapy, investigation of hypercholesterolemia/cholesterol metabolism, and emerging oncology/immunotherapy combinations. | (padyana2019structureandinhibition pages 1-2, zhang2024squaleneepoxidaseits pages 2-4, wen2024targetingsqualeneepoxidase pages 5-6, wang2024identifyingsqualeneepoxidase pages 14-17) | Padyana et al., Nat Commun (Jan 2019), https://doi.org/10.1038/s41467-018-07928-x; Wen et al., Gut (May 2024), https://doi.org/10.1136/gutjnl-2023-331117; Wang et al., Clin Transl Med (Feb 2024), https://doi.org/10.1002/ctm2.1586 |
| Recent disease/cancer findings (2023-2024) with quantitative details | 2023 ferroptosis: cholesterol promoted SQLE degradation, increasing squalene/CoQ and suppressing ferroptosis in mouse injury models (Sun 2023). 2024 MASH-HCC: hepatocyte-specific Sqle transgenic/knockout mouse models showed that Sqle promotes tumor burden and immunosuppression; orthotopic and humanized mouse experiments used n=5/group and n=8/group, respectively, and terbinafine restored anti-PD-1 response (Wen 2024). 2024 pancreatic cancer: shRNA SQLE knockdown with 1.8×10^6 cells injected, n=5/group, and squalene 200 mg/kg i.p. every 2 days suppressed tumor growth; one SQLE-KD tumor disappeared and some effects reached p<0.0001 (Pan 2024). 2024 osteosarcoma: SQLE high expression associated with poorer prognosis; TMA analysis reported p=0.037, and SQLE knockdown reduced xenograft growth and chemotherapy IC50 values (Wang 2024). | (sun2023cholesterolmediatedferroptosis pages 1-2, wen2024targetingsqualeneepoxidase pages 5-6, wen2024targetingsqualeneepoxidase pages 1-2, pan2024sqlemediatedsqualenemetabolism pages 5-8, wang2024identifyingsqualeneepoxidase pages 14-17) | Sun et al., Commun Biol (Nov 2023), https://doi.org/10.1038/s42003-023-05477-8; Wen et al., Gut (May 2024), https://doi.org/10.1136/gutjnl-2023-331117; Pan et al., Front Immunol (Dec 2024), https://doi.org/10.3389/fimmu.2024.1512981; Wang et al., Clin Transl Med (Feb 2024), https://doi.org/10.1002/ctm2.1586 |
Table: This table summarizes the best-supported functional annotation points for rat Sqle/ERG1 (UniProt P52020), integrating core mammalian biochemistry with recent 2023-2024 disease-focused evidence. It highlights enzyme chemistry, ER localization, regulation, pathway context, pharmacology, and recent quantitative findings relevant to interpretation.
References
(padyana2019structureandinhibition pages 1-2): Anil K. Padyana, Stefan Gross, Lei Jin, Giovanni Cianchetta, Rohini Narayanaswamy, Feng Wang, Rui Wang, Cheng Fang, Xiaobing Lv, Scott A. Biller, Lenny Dang, Christopher E. Mahoney, Nelamangala Nagaraja, David Pirman, Zhihua Sui, Janeta Popovici-Muller, and Gromoslaw A. Smolen. Structure and inhibition mechanism of the catalytic domain of human squalene epoxidase. Nature Communications, Jan 2019. URL: https://doi.org/10.1038/s41467-018-07928-x, doi:10.1038/s41467-018-07928-x. This article has 160 citations and is from a highest quality peer-reviewed journal.
(zhang2024squaleneepoxidaseits pages 2-4): Lin Zhang, Zheng Cao, Yuheng Hong, Haihua He, Leifeng Chen, Zhentao Yu, and Yibo Gao. Squalene epoxidase: its regulations and links with cancers. International Journal of Molecular Sciences, 25:3874, Mar 2024. URL: https://doi.org/10.3390/ijms25073874, doi:10.3390/ijms25073874. This article has 17 citations.
(padyana2019structureandinhibition pages 9-9): Anil K. Padyana, Stefan Gross, Lei Jin, Giovanni Cianchetta, Rohini Narayanaswamy, Feng Wang, Rui Wang, Cheng Fang, Xiaobing Lv, Scott A. Biller, Lenny Dang, Christopher E. Mahoney, Nelamangala Nagaraja, David Pirman, Zhihua Sui, Janeta Popovici-Muller, and Gromoslaw A. Smolen. Structure and inhibition mechanism of the catalytic domain of human squalene epoxidase. Nature Communications, Jan 2019. URL: https://doi.org/10.1038/s41467-018-07928-x, doi:10.1038/s41467-018-07928-x. This article has 160 citations and is from a highest quality peer-reviewed journal.
(zhang2024squaleneepoxidaseits pages 1-2): Lin Zhang, Zheng Cao, Yuheng Hong, Haihua He, Leifeng Chen, Zhentao Yu, and Yibo Gao. Squalene epoxidase: its regulations and links with cancers. International Journal of Molecular Sciences, 25:3874, Mar 2024. URL: https://doi.org/10.3390/ijms25073874, doi:10.3390/ijms25073874. This article has 17 citations.
(porter2015electrontransferpathways pages 2-4): Todd D. Porter. Electron transfer pathways in cholesterol synthesis. Lipids, 50:927-936, Sep 2015. URL: https://doi.org/10.1007/s11745-015-4065-1, doi:10.1007/s11745-015-4065-1. This article has 36 citations and is from a domain leading peer-reviewed journal.
(porter2015electrontransferpathways pages 1-2): Todd D. Porter. Electron transfer pathways in cholesterol synthesis. Lipids, 50:927-936, Sep 2015. URL: https://doi.org/10.1007/s11745-015-4065-1, doi:10.1007/s11745-015-4065-1. This article has 36 citations and is from a domain leading peer-reviewed journal.
(porter2015electrontransferpathways pages 4-5): Todd D. Porter. Electron transfer pathways in cholesterol synthesis. Lipids, 50:927-936, Sep 2015. URL: https://doi.org/10.1007/s11745-015-4065-1, doi:10.1007/s11745-015-4065-1. This article has 36 citations and is from a domain leading peer-reviewed journal.
(zhang2024squaleneepoxidaseits pages 4-6): Lin Zhang, Zheng Cao, Yuheng Hong, Haihua He, Leifeng Chen, Zhentao Yu, and Yibo Gao. Squalene epoxidase: its regulations and links with cancers. International Journal of Molecular Sciences, 25:3874, Mar 2024. URL: https://doi.org/10.3390/ijms25073874, doi:10.3390/ijms25073874. This article has 17 citations.
(zhang2024squaleneepoxidaseits pages 8-9): Lin Zhang, Zheng Cao, Yuheng Hong, Haihua He, Leifeng Chen, Zhentao Yu, and Yibo Gao. Squalene epoxidase: its regulations and links with cancers. International Journal of Molecular Sciences, 25:3874, Mar 2024. URL: https://doi.org/10.3390/ijms25073874, doi:10.3390/ijms25073874. This article has 17 citations.
(zhang2024squaleneepoxidaseits pages 6-8): Lin Zhang, Zheng Cao, Yuheng Hong, Haihua He, Leifeng Chen, Zhentao Yu, and Yibo Gao. Squalene epoxidase: its regulations and links with cancers. International Journal of Molecular Sciences, 25:3874, Mar 2024. URL: https://doi.org/10.3390/ijms25073874, doi:10.3390/ijms25073874. This article has 17 citations.
(sun2023cholesterolmediatedferroptosis pages 1-2): Qi Sun, Diming Liu, Weiwei Cui, Huimin Cheng, Ruihao Zhang, Junlian Gu, Shuo Liu, Lixia Huang, Xiao Zhuang, Yi Lu, Bo Chu, and jian Li. Cholesterol mediated ferroptosis suppression reveals essential roles of coenzyme q and squalene. Communications Biology, Nov 2023. URL: https://doi.org/10.1038/s42003-023-05477-8, doi:10.1038/s42003-023-05477-8. This article has 79 citations and is from a peer-reviewed journal.
(wen2024targetingsqualeneepoxidase pages 1-2): Jun Wen, Xiang Zhang, Chi Chun Wong, Yating Zhang, Yasi Pan, Yunfei Zhou, Alvin Ho-Kwan Cheung, Yali Liu, Fenfen Ji, Xing Kang, Dabin Liu, and Jun Yu. Targeting squalene epoxidase restores anti-pd-1 efficacy in metabolic dysfunction-associated steatohepatitis-induced hepatocellular carcinoma. Gut, 73:2023-2036, May 2024. URL: https://doi.org/10.1136/gutjnl-2023-331117, doi:10.1136/gutjnl-2023-331117. This article has 64 citations and is from a highest quality peer-reviewed journal.
(wen2024targetingsqualeneepoxidase pages 5-6): Jun Wen, Xiang Zhang, Chi Chun Wong, Yating Zhang, Yasi Pan, Yunfei Zhou, Alvin Ho-Kwan Cheung, Yali Liu, Fenfen Ji, Xing Kang, Dabin Liu, and Jun Yu. Targeting squalene epoxidase restores anti-pd-1 efficacy in metabolic dysfunction-associated steatohepatitis-induced hepatocellular carcinoma. Gut, 73:2023-2036, May 2024. URL: https://doi.org/10.1136/gutjnl-2023-331117, doi:10.1136/gutjnl-2023-331117. This article has 64 citations and is from a highest quality peer-reviewed journal.
(pan2024sqlemediatedsqualenemetabolism pages 5-8): Junchen Pan, Haixi Liang, Lin Zhou, Wenhua Lu, Bitao Huo, Rui Liu, and Peng Huang. Sqle-mediated squalene metabolism promotes tumor immune evasion in pancreatic cancer. Frontiers in Immunology, Dec 2024. URL: https://doi.org/10.3389/fimmu.2024.1512981, doi:10.3389/fimmu.2024.1512981. This article has 6 citations and is from a peer-reviewed journal.
(wang2024identifyingsqualeneepoxidase pages 14-17): Yongjie Wang, Xiaolong Ma, Enjie Xu, Zhen Huang, Chen Yang, Kunpeng Zhu, Yang Dong, and Chunlin Zhang. Identifying squalene epoxidase as a metabolic vulnerability in high‐risk osteosarcoma using an artificial intelligence‐derived prognostic index. Clinical and Translational Medicine, Feb 2024. URL: https://doi.org/10.1002/ctm2.1586, doi:10.1002/ctm2.1586. This article has 35 citations and is from a peer-reviewed journal.