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this with annotations you find in gene/protein databases, but these can be outdated or inaccurate.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.
mfsd2aa encodes a vertebrate major facilitator superfamily (MFS) membrane transporter orthologous to mammalian MFSD2A, best known for (i) sodium-dependent transport (symport) of lysophosphatidylcholine (LPC)–linked fatty acids (notably omega-3 DHA) and (ii) suppression of endothelial transcytosis, a key mechanism for establishing/maintaining blood–brain barrier (BBB) integrity. In zebrafish, direct genetic evidence shows mfsd2aa (not mfsd2ab) is required to suppress brain endothelial transcytosis and maintain a tight BBB, with developmental upregulation in cerebral vessels coinciding with BBB maturation at ~5 days post fertilization (dpf). (o’brown2019suppressionoftranscytosis pages 8-10, o’brown2019suppressionoftranscytosis pages 7-8, o’brown2019suppressionoftranscytosis pages 12-12, o’brown2019suppressionoftranscytosis pages 12-13)
Target provided: UniProt Q5U3U7, Danio rerio protein “Sodium-dependent lysophosphatidylcholine symporter 1-A / MFSD2A-A”, gene mfsd2aa (synonyms mfsd2a, nls1a), MFS family transporter with MFS_2/MFS_trans_sf domains.
Zebrafish paralogy: Zebrafish has two mfsd2a paralogues, mfsd2aa and mfsd2ab, which are not functionally redundant for BBB barrier properties: mfsd2aa mutants show BBB leakage and increased vesicular trafficking, while mfsd2ab mutants do not show the vesicle-density phenotype and are concluded not to play the conserved BBB role. (o’brown2019suppressionoftranscytosis pages 12-12, o’brown2019suppressionoftranscytosis pages 12-13)
Important scope note: Multiple recent mechanistic/structural studies use Danio rerio Mfsd2a protein (drMfsd2a) and demonstrate Na+-coupled LPC-flipping transport, but those studies typically refer to “drMfsd2a” without mapping to mfsd2aa vs mfsd2ab. Therefore, the most paralog-specific functional claims in zebrafish herein are anchored to genetic/expression work explicitly labeling mfsd2aa. (o’brown2019suppressionoftranscytosis pages 8-10, o’brown2019suppressionoftranscytosis pages 12-12, o’brown2019suppressionoftranscytosis pages 12-13)
MFSD2A/Mfsd2a is an MFS transporter (12 transmembrane helices in two 6-helix bundles) enriched in barrier endothelia (BBB/BRB) and coupled to Na+ to drive lipid-lysophospholipid transport. (bergman2023substratebindinginducedconformational pages 1-2, sengottuvel2023deficiencyinthe pages 1-2)
In vertebrates, MFSD2A mediates uptake of omega-3 fatty acids (especially DHA) when esterified to LPC (e.g., LPC-DHA), and is described as Na+-dependent. (chua2023mfsd2autilizesa pages 1-2, sengottuvel2023deficiencyinthe pages 1-2)
A key modern conceptual advance is that MFSD2A behaves like a lysolipid flippase (a transporter that translocates a lysolipid from the outer to inner leaflet), rather than a classical soluble-substrate carrier. (chua2023mfsd2autilizesa pages 1-2, nguyen2023lipidflippingin pages 1-3)
BBB permeability can arise from (i) leaky tight junctions or (ii) excess vesicular trafficking (transcytosis) across endothelial cells. In zebrafish, BBB maturation is strongly associated with a developmental suppression of endothelial transcytosis (vesicle density dropping from 3 to 5 dpf), and mfsd2aa is required for that suppression. (o’brown2019suppressionoftranscytosis pages 7-8, o’brown2019suppressionoftranscytosis pages 11-12)
Recent primary mechanistic work on MFSD2A/Mfsd2a supports that the physiologically central substrates are LPC species carrying long-chain unsaturated fatty acids such as DHA (22:6) and α-linolenic acid (ALA, 18:3) (and also oleate, 18:1) attached to the LPC headgroup. (nguyen2023lipidflippingin pages 1-3, nguyen2023lipidflippingin pages 3-4)
Direct biochemical reconstitution experiments show Mfsd2a-mediated lysolipid flipping occurs in a sodium-dependent manner. In a proteoliposome flipping assay, sodium dependence was supported by (i) NaCl increasing activity, (ii) monensin (Na+ ionophore) abolishing activity, and (iii) sodium-binding site mutants reducing activity; an in vitro Na+ Km ~22 mM was reported. (chua2023mfsd2autilizesa pages 3-4)
Three complementary 2023 mechanistic lines converge on a “trap-and-flip” model:
Biochemical proof of flippase activity (PNAS 2023): Mfsd2a was shown to flip lysolipids from the outer to inner leaflet in a Na+-dependent manner, providing direct evidence for a flippase mechanism. Substrate preferences included a requirement for a zwitterionic headgroup and an acyl chain ≥14 carbons; reported apparent Km values include ~3 μM for LPC-16:1-NBD and 244 μM for LPC-12:0-NBD, supporting the chain-length requirement. (chua2023mfsd2autilizesa pages 1-2, chua2023mfsd2autilizesa pages 2-3)
MD + cryo-EM-guided model (Nat Commun 2023): simulations suggest substrates enter laterally from the membrane outer leaflet; the headgroup engages Na+-bridged interactions (with a conserved acidic residue), triggering a transition to an occluded state consistent with trap-and-flip. (bergman2023substratebindinginducedconformational pages 1-2)
Zebrafish structural snapshots (bioRxiv 2023): five cryo-EM structures of Danio rerio Mfsd2a captured multiple ALA-LPC positions along a translocation route consistent with stepwise flipping; Mfsd2a is described as ATP-independent and Na+-dependent. Mutational analysis identified residues whose substitution abolished or reduced transport. (nguyen2023lipidflippingin pages 3-4, nguyen2023lipidflippingin pages 18-20)
Inference for mfsd2aa: While the above mechanistic studies strongly establish MFSD2A/Mfsd2a’s biochemical transport function, the paralog-specific mapping to UniProt Q5U3U7 (mfsd2aa) is best treated as orthology-supported rather than directly proven in those studies. (o’brown2019suppressionoftranscytosis pages 8-10, nguyen2023lipidflippingin pages 3-4)
In zebrafish brain vasculature, fluorescent in situ hybridization showed mfsd2aa vascular signal is low/undetectable at 3 dpf but higher at 5 dpf, while mfsd2ab is high at both 3 and 5 dpf (and both are low in adult vessels). Neither paralogue is exclusively vascular, indicating expression beyond endothelium. (o’brown2019suppressionoftranscytosis pages 7-8, o’brown2019suppressionoftranscytosis pages 8-10, o’brown2019suppressionoftranscytosis media 640df88c)
The timing of increased mfsd2aa vascular expression aligns with the developmental switch to lower transcytosis and functional barrier properties. (o’brown2019suppressionoftranscytosis pages 7-8)
The zebrafish BBB phenotype and TEM findings indicate the key site of action for mfsd2aa in this context is brain endothelial cells, where it regulates vesicular trafficking/transcytosis. (o’brown2019suppressionoftranscytosis pages 12-13, o’brown2019suppressionoftranscytosis pages 11-12)
From ortholog literature, MFSD2A/Mfsd2a is generally described as a transporter enriched in barrier endothelium and functioning at the plasma membrane. For example, liver work reports basolateral plasma-membrane localization when overexpressed in hepatocytes, consistent with blood-facing uptake. (chin2023bloodderivedlysophospholipidsustains pages 1-2)
In mfsd2aa CRISPR mutants (e.g., predicted early stop at aa82), BBB permeability assays at 5 dpf showed ≥2-fold increased parenchymal tracer leakage (e.g., 1 kDa NHS tracer; also leakage of endogenous ~80 kDa DBP-EGFP serum protein) in midbrain and hindbrain compared with wild-type. (o’brown2019suppressionoftranscytosis pages 8-10, o’brown2019suppressionoftranscytosis media 640df88c)
Time-lapse imaging further showed that at 5 dpf, when siblings have a sealed BBB, mfsd2aa mutants show continued diffuse tracer leakage similar to earlier leaky developmental stages, consistent with failure to suppress transcytosis. (o’brown2019suppressionoftranscytosis pages 12-13, o’brown2019suppressionoftranscytosis pages 11-12)
TEM analyses showed BBB maturation correlates with a major reduction in endothelial vesicle density from 3 to 5 dpf: 0.21 ± 0.03 (luminal) and 0.17 ± 0.02 (abluminal) vesicles/mm at 3 dpf vs 0.08 ± 0.01 and 0.07 ± 0.01 at 5 dpf (and similarly low at 7 dpf). Tight junctions were functional at these stages, implicating transcytosis rather than junction maturation as the critical process. (o’brown2019suppressionoftranscytosis pages 7-8)
In adult mfsd2aa mutants, vesicular density was markedly increased: wild-type ~0.10 (luminal) and 0.11 (abluminal) vesicles/mm vs mfsd2aa mutants 0.29 and 0.27 vesicles/mm, with increased tracer leakage highly significant (p < 0.0001). (o’brown2019suppressionoftranscytosis pages 12-12, o’brown2019suppressionoftranscytosis pages 11-12)
mfsd2ab mutants did not show increased vesicular pit density and were concluded not to play the conserved role in determining zebrafish barrier properties. (o’brown2019suppressionoftranscytosis pages 12-12, o’brown2019suppressionoftranscytosis pages 12-13)
A key 2023 advance was a proteoliposome assay showing Na+-dependent lysolipid flipping by Mfsd2a, enabling quantification such as apparent substrate Km values and Na+ coupling parameters. These experiments provide mechanistic grounding to interpret mfsd2aa as a sodium-dependent LPC symporter. (chua2023mfsd2autilizesa pages 2-3, chua2023mfsd2autilizesa pages 3-4)
2023 simulations and structural interpretations detailed how substrates may enter from the outer leaflet via lateral openings and use Na+-bridged interactions to initiate conformational transitions, strengthening an atomistic view of how a lipid-like substrate is handled by an MFS scaffold. (bergman2023substratebindinginducedconformational pages 1-2)
Although not zebrafish, 2023 work expanded MFSD2A’s functional scope beyond endothelial transport to oligodendrocyte lineage biology: OPC-specific knockout changed oligodendrocyte state distributions and caused hypomyelination. Quantitative cellular data included ~80% reduction in Pdgfra+ OPC fraction (5.4% to 0.9%) with no significant change in total Olig2+ fraction (23.7% vs 29.2%). (sengottuvel2023deficiencyinthe pages 2-3)
These findings are relevant to annotation because they link Mfsd2a-mediated LPC uptake to membrane lipid composition and Srebp-1 signaling, offering plausible downstream pathway hypotheses when interpreting vertebrate mfsd2aa biology. (sengottuvel2023deficiencyinthe pages 1-2, sengottuvel2023deficiencyinthe pages 8-9)
A 2024 nutrition-focused paper summarizes the concept that Mfsd2a contributes to BBB/BRB integrity by suppressing transcytosis and discusses manipulating this axis as a potential way to influence barrier properties relevant to drug delivery or barrier repair. (macura2024thesupplementationof pages 8-10)
The zebrafish mfsd2aa mutant provides a practical experimental platform for BBB research: it is viable, shows measurable BBB leakage at 5 dpf via injected tracers, and allows combined live imaging and TEM quantification of transcytosis. This supports real-world implementation for screening barrier modulators and studying barrier development dynamics. (o’brown2019suppressionoftranscytosis pages 15-17, o’brown2019suppressionoftranscytosis pages 11-12)
A high-citation 2023 review positions MFSD2A as an endothelial BBB transporter regulating transcytosis and discusses clinical correlations, including proposals that serum MFSD2A levels decline with Alzheimer’s pathology while BBB MFSD2A expression may remain unchanged. It also summarizes interventions where increased MFSD2A is associated with reduced BBB damage and improved cognitive outcomes in animal models, interpreted as transcytosis inhibition rather than tight-junction regulation. (alkhalifa2023blood–brainbarrierbreakdown pages 8-10)
Two authoritative 2023–2024 “expert synthesis” sources are particularly useful:
Perez (PNAS 2023 commentary) contextualizes MFSD2A as a pharmacologically relevant MFS lipid transporter and emphasizes the methodological importance of reliable lipid-flipping assays; it notes the ability to estimate affinity constants and the potential for inhibitor screening. (perez2023howtomeasure pages 1-2)
Alkhalifa et al. (IJMS 2023 review; high citation count) integrates genetic, mechanistic, and disease evidence and frames MFSD2A as both a BBB functional determinant and a potential translational target/biomarker in neurodegenerative disease. (alkhalifa2023blood–brainbarrierbreakdown pages 8-10)
The following table consolidates zebrafish-specific evidence and ortholog-informed mechanistic understanding.
| Evidence area | Key finding | Species/system | Experimental approach | Key quantitative/statistical details | Primary citation (with year, journal, URL) |
|---|---|---|---|---|---|
| Molecular function | MFSD2A/Mfsd2a is a sodium-dependent lysophosphatidylcholine (LPC) transporter that mediates uptake of omega-3 fatty acids, especially DHA, as LPC; substrate recognition favors a zwitterionic headgroup and acyl chains ≥14 carbons. | Recombinant chicken/mammalian Mfsd2a in proteoliposomes; orthology used for zebrafish annotation | In vitro liposome flipping assay; cryo-EM-guided biochemical analysis | Apparent Km ~3 μM for LPC-16:1-NBD and 244 μM for LPC-12:0-NBD; NaCl stimulation constant ~10 mM in one assay; in vitro Na+ Km ~22 mM in LPS flipping assay, supporting Na+-coupled transport. | Chua et al., 2023, PNAS, https://doi.org/10.1073/pnas.2215290120 (chua2023mfsd2autilizesa pages 1-2, chua2023mfsd2autilizesa pages 2-3, chua2023mfsd2autilizesa pages 3-4) |
| Mechanistic model | Mfsd2a acts as a lysolipid flippase: substrate enters laterally from the outer leaflet, the LPC headgroup engages Na+-bridged interactions, then the lipid is flipped and released toward the inner leaflet/cytoplasmic side. | MFSD2A/Mfsd2a structural models; zebrafish drMfsd2a structural study included | Cryo-EM, molecular dynamics, mutagenesis, structural modeling | Conserved residues highlighted for function include D92, E312, R85; zebrafish drMfsd2a structures captured multiple ALA-LPC positions consistent with a stepwise trap-and-flip pathway. | Bergman et al., 2023, Nature Communications, https://doi.org/10.1038/s41467-023-39088-y; Nguyen et al., 2023, bioRxiv, https://doi.org/10.1101/2022.05.31.494244 (bergman2023substratebindinginducedconformational pages 1-2, nguyen2023lipidflippingin pages 3-4, nguyen2023lipidflippingin pages 1-3, nguyen2023lipidflippingin pages 12-14) |
| Expression/localization | In zebrafish cerebral vessels, mfsd2aa vascular expression is low at 3 dpf and higher at 5 dpf, whereas mfsd2ab is high at both 3 and 5 dpf; neither paralogue is exclusively vascular. This timing matches BBB maturation. | Danio rerio (zebrafish) | HCR FISH on larval/adult brain sections; vascular transcript quantification | Expression timing correlates with the drop in endothelial vesicular trafficking from 3 dpf to 5 dpf during BBB acquisition. | O’Brown et al., 2019, eLife, https://doi.org/10.7554/eLife.47326 (o’brown2019suppressionoftranscytosis pages 8-10, o’brown2019suppressionoftranscytosis pages 7-8, o’brown2019suppressionoftranscytosis media 640df88c) |
| Zebrafish phenotype | mfsd2aa, but not mfsd2ab, is required for normal zebrafish BBB integrity; loss of mfsd2aa causes increased BBB permeability without obvious angiogenic defects. | Danio rerio mfsd2aa and mfsd2ab CRISPR mutants | Stable CRISPR mutants, F0 crispants, intracardiac fluorescent tracer assays, endogenous DBP-EGFP leakage assays | mfsd2aa mutants showed ≥2-fold increased parenchymal tracer leakage in midbrain/hindbrain at 5 dpf; both mutant lines were viable/fertile, and mfsd2aa mutants had reduced adult survival but no larval brain-size decrease reported here. | O’Brown et al., 2019, eLife, https://doi.org/10.7554/eLife.47326 (o’brown2019suppressionoftranscytosis pages 8-10, o’brown2019suppressionoftranscytosis pages 1-2, o’brown2019suppressionoftranscytosis media 640df88c) |
| Zebrafish phenotype / ultrastructure | The BBB defect in mfsd2aa mutants is attributable to increased transcytosis, not obvious tight-junction failure; mfsd2ab mutants do not show this vesicular phenotype. | Adult and larval Danio rerio brain endothelium | TEM with gold nanoparticle tracers; vesicle-density quantification; time-lapse dextran leakage imaging | Developmentally, vesicle densities fall from 0.21 ± 0.03 (luminal) and 0.17 ± 0.02 (abluminal) vesicles/mm at 3 dpf to 0.08 ± 0.01 and 0.07 ± 0.01 at 5 dpf; adult mfsd2aa mutants rise to 0.29 (luminal) and 0.27 (abluminal) vesicles/mm versus WT 0.10 and 0.11; tracer leakage increase p < 0.0001. | O’Brown et al., 2019, eLife, https://doi.org/10.7554/eLife.47326 (o’brown2019suppressionoftranscytosis pages 7-8, o’brown2019suppressionoftranscytosis pages 12-12, o’brown2019suppressionoftranscytosis pages 12-13, o’brown2019suppressionoftranscytosis pages 11-12, o’brown2019suppressionoftranscytosis media 640df88c) |
| Expression/localization outside zebrafish | In mammals, MFSD2A is enriched in BBB and BRB endothelium and is also expressed in oligodendrocyte precursor cells (OPCs) and periportal hepatocytes, supporting orthology-based annotation of a plasma-membrane lipid importer. | Mouse/human | Cell-type expression profiling, conditional knockouts, tissue analysis | OPC-lineage expression is enriched in OPC/COP/NFOL populations; hepatic Mfsd2a localizes to the basolateral membrane when overexpressed in hepatocytes. | Sengottuvel et al., 2023, JCI, https://doi.org/10.1172/JCI164118; Chin et al., 2023, JCI, https://doi.org/10.1172/JCI171267 (sengottuvel2023deficiencyinthe pages 1-2, chin2023bloodderivedlysophospholipidsustains pages 1-2, sengottuvel2023deficiencyinthe pages 2-3) |
| Biological pathway/function | MFSD2A-driven LPC uptake helps maintain brain phospholipid composition, suppresses Srebp-1-driven compensatory lipogenesis, and is important for postnatal myelination in oligodendrocyte lineage cells. | Mouse OPC-specific knockout | scRNA-seq, lipidomics, RNA-seq, conditional genetics | In 2aOKO brains, Pdgfra+ OPCs fell from 5.4% to 0.9% while total Olig2+ fraction was not significantly changed (23.7% vs 29.2%); lipidomics showed reduced DHA-containing phospholipids and increased mono-unsaturated species (n=3/genotype, significant at P < 0.05). | Sengottuvel et al., 2023, JCI, https://doi.org/10.1172/JCI164118 (sengottuvel2023deficiencyinthe pages 1-2, sengottuvel2023deficiencyinthe pages 2-3, sengottuvel2023deficiencyinthe pages 8-9) |
| Biological pathway/function | In liver, Mfsd2a imports abundant blood LPC species (not only LPC-DHA), sustaining hepatic phospholipid pools and protecting against overnutrition-associated injury. | Mouse liver-specific knockout; human NAFLD context | Tissue-specific knockout, diet challenge, lipidomics, expression analysis | Hepatic Mfsd2a induction was detectable by 2 weeks and significantly elevated by 8 and 16 weeks of high-fat/NASH diet; liver-specific KO developed a rapid NASH-like phenotype within 2 weeks with reduced linoleate-containing phospholipids. | Chin et al., 2023, JCI, https://doi.org/10.1172/JCI171267 (chin2023bloodderivedlysophospholipidsustains pages 1-2) |
| Applications / translational relevance | MFSD2A is a major regulator of BBB/BRB transcytosis, making it relevant to barrier repair, disease biomarkers, and CNS drug-delivery strategies. | Human disease reviews, mouse/rat disease models | Review synthesis of genetic, expression, and intervention studies | Reported in AD-related contexts: BBB MFSD2A expression may remain unchanged while serum MFSD2A declines with pathology; MFSD2A overexpression in chronic cerebral hypoperfusion models reduced BBB damage and cognitive decline, with benefit attributed to reduced transcytosis. | Alkhalifa et al., 2023, IJMS, https://doi.org/10.3390/ijms242216288; Macura et al., 2024, Frontiers in Nutrition, https://doi.org/10.3389/fnut.2023.1330414 (alkhalifa2023blood–brainbarrierbreakdown pages 8-10, macura2024thesupplementationof pages 8-10) |
Table: This table summarizes the strongest currently gathered evidence for functional annotation of zebrafish mfsd2aa (UniProt Q5U3U7), integrating zebrafish-specific mutant data with recent mechanistic and orthology-supported MFSD2A studies. It highlights what is directly shown in zebrafish versus what is inferred from closely studied vertebrate orthologs.
High-confidence zebrafish-specific function: mfsd2aa is required in zebrafish for BBB integrity by suppressing endothelial transcytosis, with developmental vascular upregulation around the time BBB function is established (~5 dpf). (o’brown2019suppressionoftranscytosis pages 8-10, o’brown2019suppressionoftranscytosis pages 7-8, o’brown2019suppressionoftranscytosis pages 11-12)
High-confidence ortholog function relevant to zebrafish annotation: Vertebrate MFSD2A/Mfsd2a is a Na+-coupled transporter/flippase for LPC-linked fatty acids (including LPC-DHA and LPC-ALA), with a trap-and-flip/lateral entry mechanism supported by biochemical and structural work. (chua2023mfsd2autilizesa pages 2-3, bergman2023substratebindinginducedconformational pages 1-2, nguyen2023lipidflippingin pages 1-3)
Moderate-confidence inference for mfsd2aa substrate transport: Because zebrafish mfsd2aa is the paralogue required for BBB properties and because ortholog Mfsd2a is a Na+-dependent LPC transporter, it is reasonable to annotate mfsd2aa as a sodium-dependent lysophosphatidylcholine symporter (LPC transporter), but paralog-specific direct transport assays for Q5U3U7 were not identified in the retrieved text corpus. (o’brown2019suppressionoftranscytosis pages 8-10, chua2023mfsd2autilizesa pages 2-3)
References
(o’brown2019suppressionoftranscytosis pages 8-10): Natasha M. O’Brown, Sean Gregory Megason, and Chenghua Gu. Suppression of transcytosis regulates zebrafish blood-brain barrier function. eLife, Aug 2019. URL: https://doi.org/10.7554/elife.47326, doi:10.7554/elife.47326. This article has 123 citations and is from a domain leading peer-reviewed journal.
(o’brown2019suppressionoftranscytosis pages 7-8): Natasha M. O’Brown, Sean Gregory Megason, and Chenghua Gu. Suppression of transcytosis regulates zebrafish blood-brain barrier function. eLife, Aug 2019. URL: https://doi.org/10.7554/elife.47326, doi:10.7554/elife.47326. This article has 123 citations and is from a domain leading peer-reviewed journal.
(o’brown2019suppressionoftranscytosis pages 12-12): Natasha M. O’Brown, Sean Gregory Megason, and Chenghua Gu. Suppression of transcytosis regulates zebrafish blood-brain barrier function. eLife, Aug 2019. URL: https://doi.org/10.7554/elife.47326, doi:10.7554/elife.47326. This article has 123 citations and is from a domain leading peer-reviewed journal.
(o’brown2019suppressionoftranscytosis pages 12-13): Natasha M. O’Brown, Sean Gregory Megason, and Chenghua Gu. Suppression of transcytosis regulates zebrafish blood-brain barrier function. eLife, Aug 2019. URL: https://doi.org/10.7554/elife.47326, doi:10.7554/elife.47326. This article has 123 citations and is from a domain leading peer-reviewed journal.
(bergman2023substratebindinginducedconformational pages 1-2): Shana Bergman, Rosemary J. Cater, Ambrose Plante, Filippo Mancia, and George Khelashvili. Substrate binding-induced conformational transitions in the omega-3 fatty acid transporter mfsd2a. Nature Communications, Jun 2023. URL: https://doi.org/10.1038/s41467-023-39088-y, doi:10.1038/s41467-023-39088-y. This article has 24 citations and is from a highest quality peer-reviewed journal.
(sengottuvel2023deficiencyinthe pages 1-2): Vetrivel Sengottuvel, Monalisa Hota, Jeongah Oh, Dwight L. Galam, Bernice H. Wong, Markus R. Wenk, Sujoy Ghosh, Federico Torta, and David L. Silver. Deficiency in the omega-3 lysolipid transporter mfsd2a leads to aberrant oligodendrocyte lineage development and hypomyelination. Journal of Clinical Investigation, Jun 2023. URL: https://doi.org/10.1172/jci164118, doi:10.1172/jci164118. This article has 22 citations and is from a highest quality peer-reviewed journal.
(chua2023mfsd2autilizesa pages 1-2): Geok-Lin Chua, Bryan C. Tan, Randy Y. J. Loke, Menglan He, Cheen-Fei Chin, Bernice H. Wong, Alvin C. Y. Kuk, Mei Ding, Markus R. Wenk, Lan Guan, Federico Torta, and David L. Silver. Mfsd2a utilizes a flippase mechanism to mediate omega-3 fatty acid lysolipid transport. Proceedings of the National Academy of Sciences of the United States of America, Feb 2023. URL: https://doi.org/10.1073/pnas.2215290120, doi:10.1073/pnas.2215290120. This article has 38 citations and is from a highest quality peer-reviewed journal.
(nguyen2023lipidflippingin pages 1-3): Chi Nguyen, Hsiang-Ting Lei, Louis Tung Faat Lai, Marc J. Gallenito, Doreen Matthies, and Tamir Gonen. Lipid flipping in the omega-3 fatty-acid transporter. BioRxiv, Jun 2023. URL: https://doi.org/10.1101/2022.05.31.494244, doi:10.1101/2022.05.31.494244. This article has 41 citations.
(o’brown2019suppressionoftranscytosis pages 11-12): Natasha M. O’Brown, Sean Gregory Megason, and Chenghua Gu. Suppression of transcytosis regulates zebrafish blood-brain barrier function. eLife, Aug 2019. URL: https://doi.org/10.7554/elife.47326, doi:10.7554/elife.47326. This article has 123 citations and is from a domain leading peer-reviewed journal.
(nguyen2023lipidflippingin pages 3-4): Chi Nguyen, Hsiang-Ting Lei, Louis Tung Faat Lai, Marc J. Gallenito, Doreen Matthies, and Tamir Gonen. Lipid flipping in the omega-3 fatty-acid transporter. BioRxiv, Jun 2023. URL: https://doi.org/10.1101/2022.05.31.494244, doi:10.1101/2022.05.31.494244. This article has 41 citations.
(chua2023mfsd2autilizesa pages 3-4): Geok-Lin Chua, Bryan C. Tan, Randy Y. J. Loke, Menglan He, Cheen-Fei Chin, Bernice H. Wong, Alvin C. Y. Kuk, Mei Ding, Markus R. Wenk, Lan Guan, Federico Torta, and David L. Silver. Mfsd2a utilizes a flippase mechanism to mediate omega-3 fatty acid lysolipid transport. Proceedings of the National Academy of Sciences of the United States of America, Feb 2023. URL: https://doi.org/10.1073/pnas.2215290120, doi:10.1073/pnas.2215290120. This article has 38 citations and is from a highest quality peer-reviewed journal.
(chua2023mfsd2autilizesa pages 2-3): Geok-Lin Chua, Bryan C. Tan, Randy Y. J. Loke, Menglan He, Cheen-Fei Chin, Bernice H. Wong, Alvin C. Y. Kuk, Mei Ding, Markus R. Wenk, Lan Guan, Federico Torta, and David L. Silver. Mfsd2a utilizes a flippase mechanism to mediate omega-3 fatty acid lysolipid transport. Proceedings of the National Academy of Sciences of the United States of America, Feb 2023. URL: https://doi.org/10.1073/pnas.2215290120, doi:10.1073/pnas.2215290120. This article has 38 citations and is from a highest quality peer-reviewed journal.
(nguyen2023lipidflippingin pages 18-20): Chi Nguyen, Hsiang-Ting Lei, Louis Tung Faat Lai, Marc J. Gallenito, Doreen Matthies, and Tamir Gonen. Lipid flipping in the omega-3 fatty-acid transporter. BioRxiv, Jun 2023. URL: https://doi.org/10.1101/2022.05.31.494244, doi:10.1101/2022.05.31.494244. This article has 41 citations.
(o’brown2019suppressionoftranscytosis media 640df88c): Natasha M. O’Brown, Sean Gregory Megason, and Chenghua Gu. Suppression of transcytosis regulates zebrafish blood-brain barrier function. eLife, Aug 2019. URL: https://doi.org/10.7554/elife.47326, doi:10.7554/elife.47326. This article has 123 citations and is from a domain leading peer-reviewed journal.
(chin2023bloodderivedlysophospholipidsustains pages 1-2): Cheen Fei Chin, Dwight L.A. Galam, Liang Gao, Bryan C. Tan, Bernice H. Wong, Geok-Lin Chua, Randy Y.J. Loke, Yen Ching Lim, Markus R. Wenk, Miao-Shan Lim, Wei-Qiang Leow, George B.B. Goh, Federico Torta, and David L. Silver. Blood-derived lysophospholipid sustains hepatic phospholipids and fat storage necessary for hepatoprotection in overnutrition. Journal of Clinical Investigation, Sep 2023. URL: https://doi.org/10.1172/jci171267, doi:10.1172/jci171267. This article has 28 citations and is from a highest quality peer-reviewed journal.
(sengottuvel2023deficiencyinthe pages 2-3): Vetrivel Sengottuvel, Monalisa Hota, Jeongah Oh, Dwight L. Galam, Bernice H. Wong, Markus R. Wenk, Sujoy Ghosh, Federico Torta, and David L. Silver. Deficiency in the omega-3 lysolipid transporter mfsd2a leads to aberrant oligodendrocyte lineage development and hypomyelination. Journal of Clinical Investigation, Jun 2023. URL: https://doi.org/10.1172/jci164118, doi:10.1172/jci164118. This article has 22 citations and is from a highest quality peer-reviewed journal.
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