The research report should be a detailed narrative explaining the function, biological processes, and localization of the gene product. Citations should be given for all claims.
You should prioritize authoritative reviews and primary scientific literature when conducting research. You can supplement
this with annotations you find in gene/protein databases, but these can be outdated or inaccurate.
We are specifically interested in the primary function of the gene - for enzymes, what reaction is catalyzed, and what is the substrate specificity? For transporters, what is the substrate? For structural proteins or adapters, what is the broader structural role? For signaling molecules, what is the role in the pathway.
We are interested in where in or outside the cell the gene product carries out its function.
We are also interested in the signaling or biochemical pathways in which the gene functions. We are less interested in broad pleiotropic effects, except where these elucidate the precise role.
Include evidence where possible. We are interested in both experimental evidence as well as inference from structure, evolution, or bioinformatic analysis. Precise studies should be prioritized over high-throughput, where available.
The target is human DHCR24 (UniProt Q15392), encoding Δ(24)-sterol reductase (also called 24-dehydrocholesterol reductase, 3β-hydroxysterol Δ24-reductase, and seladin-1). This identity is consistent across recent reviews and primary studies, including work that explicitly retrieved the sequence from UniProt Q15392 for modeling/inhibitor screening. (fu2024dhcr24intumor pages 1-2, wang2023virtualscreeningof pages 12-13)
| Category | Key points | Evidence |
|---|---|---|
| Identity and synonyms | Human delta(24)-sterol reductase; gene DHCR24; also known as seladin-1; UniProt Q15392 | (fu2024dhcr24intumor pages 12-13, fu2024dhcr24intumor pages 1-2) |
| Enzymatic reaction and substrates | FAD-dependent reduction of the Δ24(25) double bond in sterol intermediates; converts desmosterol to cholesterol (terminal Bloch step) | (wang2023virtualscreeningof pages 1-2, bai2022theroleof pages 3-5) |
| Required cofactors/electron donor | Flavin adenine dinucleotide (FAD) cofactor; in vitro conversion strictly dependent on reduced NADPH; activity increased by added FAD | (cocciadiferro2024exploitinginsilico pages 1-2, wang2023virtualscreeningof pages 1-2) |
| Pathway placement | Operates in the Bloch pathway (desmosterol → cholesterol) and links to the Kandutsch–Russell route; controls post-lanosterol flux | (bai2022theroleof pages 3-5, skubic2024knockoutsofcyp51a1 pages 8-10) |
| Subcellular localization/topology | ER/Golgi-associated single-pass membrane enzyme; N-terminus luminal; C-terminal cytosolic region harbors FAD-binding domain | (fu2024dhcr24intumor pages 1-2, fu2024dhcr24intumor pages 12-13) |
| Notable inhibitors/regulators (quantitative) | Irbesartan is a competitive DHCR24 inhibitor (IC50 ≈ 602 nM in vitro); SH-42 reported as potent probe inhibitor (IC50 ≈ 4 nM); U18666A inhibits DHCR24 | (wang2023virtualscreeningof pages 1-2, peeples2024chemicalinhibitionof pages 17-18) |
| Genetic disease: desmosterolosis | Autosomal recessive sterol biosynthesis disorder with elevated desmosterol; neurodevelopmental anomalies; recent case validated novel p.M169T variant affecting FAD interactions | (cocciadiferro2024exploitinginsilico pages 1-2, fu2024dhcr24intumor pages 12-13) |
| 2023–2024 finding: AD model | AAV-mediated hippocampal DHCR24 overexpression in 5xFAD mice increased cholesterol and reversed cognitive impairment and AD-like pathology | (zhang2023dhcr24reversesalzheimer’s pages 1-2, zhang2023dhcr24reversesalzheimer’s pages 14-15) |
| 2023–2024 finding: melanoma resistance | DHCR24/27HC axis promotes melanoma spheroid growth and vemurafenib resistance; 27-hydroxycholesterol increased by ~41.39% (from 89.784→129.240 ng/mL; p=0.0000751) upon DHCR24 overexpression | (wang2024cholesterolneutralizedvemurafenib pages 10-13, wang2024cholesterolneutralizedvemurafenib media 6e0d6af5) |
| 2023–2024 finding: diet-induced brain injury | High-fat diet downregulated DHCR24 protein in mouse brain, associated with neuronal apoptosis and ER-stress markers; DHCR24 overexpression rescued cholesterol-loading toxicity in N2a cells | (lu2023highfatdiet pages 9-12) |
Table: Compact functional-annotation table for human DHCR24 (Q15392), covering identity, reaction, cofactors, pathway position, localization, inhibitors, genetic disease, and recent 2023–2024 model findings with quantitative data. Each entry includes primary evidence citations for rapid reference.
DHCR24 is a flavin adenine dinucleotide (FAD)-dependent oxidoreductase in the distal cholesterol biosynthetic pathway that reduces the Δ24 double bond of sterol intermediates; in the canonical Bloch pathway it catalyzes desmosterol → cholesterol. (wang2023virtualscreeningof pages 1-2, bai2022theroleof pages 3-5)
Biochemical requirements include reduced NADPH (as electron donor) and FAD as cofactor; in vitro desmosterol→cholesterol conversion by DHCR24 is reported as strictly NADPH-dependent and ~2-fold increased by addition of FAD. (cocciadiferro2024exploitinginsilico pages 1-2)
DHCR24 is positioned at a late step of cholesterol synthesis and is described as acting on sterols in the Bloch arm, with sterol intermediates able to shift between Bloch and Kandutsch–Russell routes (post-lanosterol), making DHCR24 activity a key determinant of sterol intermediate pools (e.g., desmosterol accumulation upon loss/inhibition). (bai2022theroleof pages 3-5, fu2024dhcr24intumor pages 2-3)
DHCR24 is a membrane-associated enzyme localized to endoplasmic reticulum (ER) (and described in review sources as present in ER/Golgi-associated membranes), with a single-pass transmembrane segment and a largely cytosolic C-terminal region containing the FAD-binding domain and interaction regions (e.g., reported p53/Mdm2 binding regions in cancer-oriented reviews). (fu2024dhcr24intumor pages 1-2, fu2024dhcr24intumor pages 2-3)
| Year | Study (first author) | Publication (journal) | System/model | Key finding | Quantitative/statistical highlights | Potential application/implementation |
|---|---|---|---|---|---|---|
| 2023 | Wang | Molecules | HepG2 cells; high-fat-diet (HFD) mice | Repurposed DHCR24 inhibitors (incl. irbesartan) competitively inhibit DHCR24 and reduce cholesterol | Irbesartan IC50 = 602 nM in immune-complex assay; reduced cellular cholesterol and improved serum lipids in HFD mice (wang2023virtualscreeningof pages 1-2) | Cholesterol-lowering strategy; candidate repurposing for patients with hyperlipidemia and comorbidities (wang2023virtualscreeningof pages 1-2) |
| 2023 | Zhang | Acta Neuropathol Commun | 5xFAD Alzheimer’s mice; AAV-DHCR24 hippocampal delivery | DHCR24 overexpression raised hippocampal cholesterol and reversed cognitive deficits and AD-like pathology | Significant behavioral rescue; reduced amyloid-β; increased filipin cholesterol signal (zhang2023dhcr24reversesalzheimer’s pages 1-2, zhang2023dhcr24reversesalzheimer’s pages 14-15) | Gene therapy approach to restore neuronal cholesterol in AD (zhang2023dhcr24reversesalzheimer’s pages 1-2, zhang2023dhcr24reversesalzheimer’s pages 14-15) |
| 2023 | Lu | Cell Tissue Res | HFD mouse brain; N2a neuronal cells | HFD downregulated DHCR24 protein via ubiquitination (MDM2); DHCR24 overexpression rescued cholesterol-loading toxicity | ER-stress markers (BiP/CHOP) up; DHCR24 protein decreased despite mRNA unchanged; rescue by Ad-DHCR24 (lu2023highfatdiet pages 9-12) | Targeting MDM2/DHCR24 axis; neuroprotection under metabolic stress (lu2023highfatdiet pages 9-12) |
| 2024 | Wang | Cell Mol Life Sci | Melanoma (A375/A2058) spheroids; patient datasets | DHCR24-driven cholesterol elevates 27-hydroxycholesterol (27HC) to activate Rap1–PI3K/AKT and vemurafenib resistance | 27HC ↑41.39% (89.784 → 129.240 ng/mL; p=0.0000751) with DHCR24 overexpression; CYP27A1 inhibition (dafadine-A) attenuated resistance (wang2024cholesterolneutralizedvemurafenib pages 10-13, wang2024cholesterolneutralizedvemurafenib media 6e0d6af5) | Target CYP27A1/27HC to overcome BRAF inhibitor resistance (wang2024cholesterolneutralizedvemurafenib pages 10-13, wang2024cholesterolneutralizedvemurafenib media 6e0d6af5) |
| 2024 | Skubic | iScience | HepG2 DHCR24 knockout; sterolomics/transcriptomics | Desmosterol accumulation and sterol rewiring alter proliferation and WNT/LEF1 signaling | G0+G1 increased to 63% in DHCR24 KO vs 58% native; distinct pathway changes vs CYP51/SC5D KOs (skubic2024knockoutsofcyp51a1 pages 8-10, skubic2024knockoutsofcyp51a1 pages 10-12) | Pathway-informed targeting by sterol intermediates; cell-cycle modulation biomarkers (skubic2024knockoutsofcyp51a1 pages 8-10, skubic2024knockoutsofcyp51a1 pages 10-12) |
| 2024 | Cocciadiferro | Front Genet | Desmosterolosis patient (WES; MD sims; biochemical assay) | Novel DHCR24 variant p.M169T disrupts FAD interactions; genotype–phenotype expansion | In vitro desmosterol→cholesterol conversion strictly NADPH-dependent; +FAD doubles activity; variant validated deleterious (cocciadiferro2024exploitinginsilico pages 1-2) | Genetic diagnosis/variant interpretation; counseling and mechanistic insight (cocciadiferro2024exploitinginsilico pages 1-2) |
| 2024 | Peeples | Biomolecules (review) | Chemical inhibition landscape | Late-pathway druggability; SH42 probe; amiodarone and other FDA drugs can inhibit DHCR24; desmosterol links to LXR/pro-resolving mediators | SH42 highlighted as potent probe; catalog of inhibitors; translational/safety gaps noted (peeples2024chemicalinhibitionof pages 6-7, peeples2024chemicalinhibitionof pages 17-18) | Safety pharmacology; probe-led mechanistic and therapeutic development (peeples2024chemicalinhibitionof pages 6-7, peeples2024chemicalinhibitionof pages 17-18) |
Table: A concise table of 2023–2024 developments and applications for DHCR24, spanning biochemistry, disease models, genetics, and translational strategies. It includes quantitative metrics (e.g., IC50, 27HC change) and potential implementations, with inline citations to primary sources.
A 2024 study expanded DHCR24-related desmosterolosis by reporting a patient homozygous for DHCR24 p.M169T (c.506T>C) with functional validation and molecular dynamics evidence implicating disrupted interactions in/near the FAD/cofactor interaction network; this strengthens mechanistic interpretation of pathogenic alleles affecting the catalytic core. (cocciadiferro2024exploitinginsilico pages 1-2)
A 2023 inhibitor repurposing study identified multiple DrugBank candidates (irbesartan, risperidone, tolvaptan, conivaptan) that lowered cholesterol in HepG2 cells and improved lipid parameters in a mouse hyperlipidemia model; it quantified irbesartan inhibition of DHCR24 with IC50 = 602 nM using an in vitro enzymatic assay. (wang2023virtualscreeningof pages 1-2, wang2023virtualscreeningof pages 12-13)
A 2024 review emphasized the broader “chemical inhibition landscape” of post-lanosterol sterol synthesis and highlighted potent DHCR24 chemical probes (e.g., SH42) and the possibility that numerous FDA-approved medications can inhibit late sterol enzymes (including DHCR24), arguing that sterol pathway inhibition is underappreciated in safety contexts. (peeples2024chemicalinhibitionof pages 6-7, peeples2024chemicalinhibitionof pages 17-18)
A 2024 iScience study used HepG2 DHCR24 knockout (and other late-pathway KOs) to show that distinct sterol intermediate accumulation states drive distinct regulatory programs and cell-cycle phenotypes; in the DHCR24 KO, the G0+G1 fraction increased to 63% vs 58% in native cells, consistent with slower growth under some conditions and supporting the concept that distal intermediates (e.g., desmosterol) are not merely inert precursors. (skubic2024knockoutsofcyp51a1 pages 8-10)
Blocking DHCR24 is being investigated as a cholesterol-lowering approach. In a 2023 study, competitive DHCR24 inhibition by irbesartan was proposed as a repurposing strategy, supported by cell-based cholesterol lowering and an in vitro IC50 of 602 nM. (wang2023virtualscreeningof pages 1-2)
Real-world implementation remains preclinical for DHCR24-selective agents, but the concept intersects with pharmacovigilance: a 2024 review catalogued many chemical exposures and approved drugs that can inhibit post-lanosterol sterol biosynthesis, implying that off-target DHCR24 inhibition may already occur in clinical practice and could be relevant to safety (especially in pregnancy/neurodevelopment). (peeples2024chemicalinhibitionof pages 6-7)
In a 2023 Alzheimer’s mouse model study, hippocampal delivery of AAV-DHCR24 in 5xFAD mice increased filipin-detectable cholesterol in hippocampus and was reported to significantly reverse cognitive impairment and multiple AD-related pathological readouts (amyloid-β deposition, synaptic injury markers, glial activation, autophagy, apoptosis). This is a concrete preclinical implementation of DHCR24 modulation as a disease-modifying strategy. (zhang2023dhcr24reversesalzheimer’s pages 1-2, zhang2023dhcr24reversesalzheimer’s pages 14-15)
A 2024 melanoma study reported that reducing intracellular cholesterol by DHCR24 knockdown impaired proliferation/migration and reduced xenograft tumor volume, while DHCR24/cholesterol promoted spheroid growth and vemurafenib resistance through a cholesterol-metabolite mechanism involving 27-hydroxycholesterol (27HC) and Rap1–PI3K/AKT signaling. (wang2024cholesterolneutralizedvemurafenib pages 1-2, wang2024cholesterolneutralizedvemurafenib pages 10-13)
A 2024 cancer-focused review frames DHCR24 as both a cholesterol-synthesis enzyme and a regulator intersecting with oncogenic signaling (e.g., ROS, p53, Ras, PI3K/AKT) and emphasizes DHCR24’s membrane topology/interaction regions when interpreting non-enzymatic phenotypes; although narrative, it consolidates evidence linking cholesterol pathway flux to tumor progression and therapy response. (fu2024dhcr24intumor pages 1-2, fu2024dhcr24intumor pages 12-13)
A 2024 sterol-inhibition review argues that late-pathway sterol inhibition (including DHCR24) is an underrecognized mechanism by which diverse chemicals and medications can perturb homeostasis, and it highlights knowledge gaps in both mechanisms and long-term consequences—an expert consensus-style warning relevant for translational work. (peeples2024chemicalinhibitionof pages 6-7)
DHCR24 (Q15392) is best annotated as an ER-associated, single-pass membrane FAD-dependent oxidoreductase that performs Δ24(25) sterol double-bond reduction in distal cholesterol biosynthesis, most classically converting desmosterol to cholesterol in the Bloch pathway. (fu2024dhcr24intumor pages 1-2, wang2023virtualscreeningof pages 1-2)
Because DHCR24 sits at a distal branchpoint that shapes sterol intermediate pools, its perturbation can produce pleiotropic effects via (i) cholesterol availability (membrane structure, lipid rafts), and (ii) bioactive intermediates such as desmosterol and oxysterols (e.g., 27HC), which can engage nuclear receptors and signaling pathways. This mechanistic framing is directly supported by recent cell and disease-model studies showing DHCR24-dependent shifts to 27HC with downstream Rap1–PI3K/AKT activation in melanoma, and by sterol-intermediate-driven transcriptional/cell-cycle remodeling in engineered KO systems. (wang2024cholesterolneutralizedvemurafenib pages 10-13, skubic2024knockoutsofcyp51a1 pages 8-10)
Quantitative 27HC changes upon DHCR24 overexpression are supported by a table and figure panels extracted from Wang et al. 2024 (Table 2; Fig. 3J–K). (wang2024cholesterolneutralizedvemurafenib media 6e0d6af5, wang2024cholesterolneutralizedvemurafenib media ab69483a)
References
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(wang2023virtualscreeningof pages 12-13): Haozhen Wang, Ziyin Lu, Yang Li, Ting Liu, Linlin Zhao, Tianqi Gao, Xiuli Lu, and Bing Gao. Virtual screening of novel 24-dehydroxysterol reductase (dhcr24) inhibitors and the biological evaluation of irbesartan in cholesterol-lowering effect. Molecules, 28:2643, Mar 2023. URL: https://doi.org/10.3390/molecules28062643, doi:10.3390/molecules28062643. This article has 15 citations.
(fu2024dhcr24intumor pages 12-13): Xin Fu and Zhaosong Wang. Dhcr24 in tumor diagnosis and treatment: a comprehensive review. Technology in Cancer Research & Treatment, Jan 2024. URL: https://doi.org/10.1177/15330338241259780, doi:10.1177/15330338241259780. This article has 17 citations and is from a peer-reviewed journal.
(wang2023virtualscreeningof pages 1-2): Haozhen Wang, Ziyin Lu, Yang Li, Ting Liu, Linlin Zhao, Tianqi Gao, Xiuli Lu, and Bing Gao. Virtual screening of novel 24-dehydroxysterol reductase (dhcr24) inhibitors and the biological evaluation of irbesartan in cholesterol-lowering effect. Molecules, 28:2643, Mar 2023. URL: https://doi.org/10.3390/molecules28062643, doi:10.3390/molecules28062643. This article has 15 citations.
(bai2022theroleof pages 3-5): Xiaojing Bai, Meiting Mai, Kai Yao, MengQi Zhang, Yue Huang, Wenbin Zhang, Xiaorou Guo, Yixuan Xu, Ying Zhang, Atikam Qurban, Lijie Duan, Jimei Bu, Jianfeng Zhang, Junfeng Wu, Yong-fei Zhao, Xiangshan Yuan, and Heng-bing Zu. The role of dhcr24 in the pathogenesis of ad: re-cognition of the relationship between cholesterol and ad pathogenesis. Acta Neuropathologica Communications, Mar 2022. URL: https://doi.org/10.1186/s40478-022-01338-3, doi:10.1186/s40478-022-01338-3. This article has 55 citations and is from a peer-reviewed journal.
(cocciadiferro2024exploitinginsilico pages 1-2): Dario Cocciadiferro, Tommaso Mazza, Davide Vecchio, Tommaso Biagini, Francesco Petrizzelli, Emanuele Agolini, Andrea Villani, Daniele Minervino, Diego Martinelli, Cristiano Rizzo, Sara Boenzi, Filippo Maria Panfili, Paola Sabrina Buonuomo, Marina Macchiaiolo, Andrea Bartuli, and Antonio Novelli. Exploiting in silico structural analysis to introduce emerging genotype–phenotype correlations in dhcr24-related sterol biosynthesis disorder: a case study. Frontiers in Genetics, Jan 2024. URL: https://doi.org/10.3389/fgene.2023.1307934, doi:10.3389/fgene.2023.1307934. This article has 7 citations and is from a peer-reviewed journal.
(skubic2024knockoutsofcyp51a1 pages 8-10): Cene Skubic, Hana Trček, Petra Nassib, Tinkara Kreft, Andrew Walakira, Katka Pohar, Sara Petek, Tadeja Režen, Alojz Ihan, and Damjana Rozman. Knockouts of cyp51a1, dhcr24, or sc5d from cholesterol synthesis reveal pathways modulated by sterol intermediates. iScience, 27:110651, Sep 2024. URL: https://doi.org/10.1016/j.isci.2024.110651, doi:10.1016/j.isci.2024.110651. This article has 10 citations and is from a peer-reviewed journal.
(peeples2024chemicalinhibitionof pages 17-18): Eric Peeples, Karoly Mirnics, and Zeljka Korade. Chemical inhibition of sterol biosynthesis. Biomolecules, 14:410, Mar 2024. URL: https://doi.org/10.3390/biom14040410, doi:10.3390/biom14040410. This article has 17 citations.
(zhang2023dhcr24reversesalzheimer’s pages 1-2): Wen-bin Zhang, Yue Huang, Xiao-rou Guo, Meng-qi Zhang, Xiang-shan Yuan, and Heng-bing Zu. Dhcr24 reverses alzheimer’s disease-related pathology and cognitive impairment via increasing hippocampal cholesterol levels in 5xfad mice. Acta Neuropathologica Communications, Jun 2023. URL: https://doi.org/10.1186/s40478-023-01593-y, doi:10.1186/s40478-023-01593-y. This article has 38 citations and is from a peer-reviewed journal.
(zhang2023dhcr24reversesalzheimer’s pages 14-15): Wen-bin Zhang, Yue Huang, Xiao-rou Guo, Meng-qi Zhang, Xiang-shan Yuan, and Heng-bing Zu. Dhcr24 reverses alzheimer’s disease-related pathology and cognitive impairment via increasing hippocampal cholesterol levels in 5xfad mice. Acta Neuropathologica Communications, Jun 2023. URL: https://doi.org/10.1186/s40478-023-01593-y, doi:10.1186/s40478-023-01593-y. This article has 38 citations and is from a peer-reviewed journal.
(wang2024cholesterolneutralizedvemurafenib pages 10-13): Xiaohong Wang, Feiliang Zhong, Tingting Chen, Hongbo Wang, Weifang Wang, Hongkai Jin, Chouyang Li, Xuan Guo, Ying Liu, Yu Zhang, and Bo Li. Cholesterol neutralized vemurafenib treatment by promoting melanoma stem-like cells via its metabolite 27-hydroxycholesterol. Cellular and Molecular Life Sciences: CMLS, May 2024. URL: https://doi.org/10.1007/s00018-024-05267-3, doi:10.1007/s00018-024-05267-3. This article has 7 citations.
(wang2024cholesterolneutralizedvemurafenib media 6e0d6af5): Xiaohong Wang, Feiliang Zhong, Tingting Chen, Hongbo Wang, Weifang Wang, Hongkai Jin, Chouyang Li, Xuan Guo, Ying Liu, Yu Zhang, and Bo Li. Cholesterol neutralized vemurafenib treatment by promoting melanoma stem-like cells via its metabolite 27-hydroxycholesterol. Cellular and Molecular Life Sciences: CMLS, May 2024. URL: https://doi.org/10.1007/s00018-024-05267-3, doi:10.1007/s00018-024-05267-3. This article has 7 citations.
(lu2023highfatdiet pages 9-12): Ziyin Lu, Haozhen Wang, Xiujin Zhang, Xiuting Huang, Shan Jiang, Yang Li, Ting Liu, Xiuli Lu, and Bing Gao. High fat diet induces brain injury and neuronal apoptosis via down-regulating 3-β hydroxycholesterol 24 reductase (dhcr24). Cell and Tissue Research, 393:471-487, Jul 2023. URL: https://doi.org/10.1007/s00441-023-03804-3, doi:10.1007/s00441-023-03804-3. This article has 8 citations and is from a peer-reviewed journal.
(fu2024dhcr24intumor pages 2-3): Xin Fu and Zhaosong Wang. Dhcr24 in tumor diagnosis and treatment: a comprehensive review. Technology in Cancer Research & Treatment, Jan 2024. URL: https://doi.org/10.1177/15330338241259780, doi:10.1177/15330338241259780. This article has 17 citations and is from a peer-reviewed journal.
(skubic2024knockoutsofcyp51a1 pages 10-12): Cene Skubic, Hana Trček, Petra Nassib, Tinkara Kreft, Andrew Walakira, Katka Pohar, Sara Petek, Tadeja Režen, Alojz Ihan, and Damjana Rozman. Knockouts of cyp51a1, dhcr24, or sc5d from cholesterol synthesis reveal pathways modulated by sterol intermediates. iScience, 27:110651, Sep 2024. URL: https://doi.org/10.1016/j.isci.2024.110651, doi:10.1016/j.isci.2024.110651. This article has 10 citations and is from a peer-reviewed journal.
(peeples2024chemicalinhibitionof pages 6-7): Eric Peeples, Karoly Mirnics, and Zeljka Korade. Chemical inhibition of sterol biosynthesis. Biomolecules, 14:410, Mar 2024. URL: https://doi.org/10.3390/biom14040410, doi:10.3390/biom14040410. This article has 17 citations.
(wang2024cholesterolneutralizedvemurafenib pages 1-2): Xiaohong Wang, Feiliang Zhong, Tingting Chen, Hongbo Wang, Weifang Wang, Hongkai Jin, Chouyang Li, Xuan Guo, Ying Liu, Yu Zhang, and Bo Li. Cholesterol neutralized vemurafenib treatment by promoting melanoma stem-like cells via its metabolite 27-hydroxycholesterol. Cellular and Molecular Life Sciences: CMLS, May 2024. URL: https://doi.org/10.1007/s00018-024-05267-3, doi:10.1007/s00018-024-05267-3. This article has 7 citations.
(wang2024cholesterolneutralizedvemurafenib media ab69483a): Xiaohong Wang, Feiliang Zhong, Tingting Chen, Hongbo Wang, Weifang Wang, Hongkai Jin, Chouyang Li, Xuan Guo, Ying Liu, Yu Zhang, and Bo Li. Cholesterol neutralized vemurafenib treatment by promoting melanoma stem-like cells via its metabolite 27-hydroxycholesterol. Cellular and Molecular Life Sciences: CMLS, May 2024. URL: https://doi.org/10.1007/s00018-024-05267-3, doi:10.1007/s00018-024-05267-3. This article has 7 citations.