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this with annotations you find in gene/protein databases, but these can be outdated or inaccurate.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.
Zebrafish flvcr2a (syn. mfsd7c-a; UniProt: A0A0R4ILB2) encodes a predicted Major Facilitator Superfamily (MFS) / SLC49 (FLVCR1/2-like) multipass membrane transporter. The strongest current mechanistic and physiological evidence across vertebrates supports facilitative (uniporter-like), concentration-driven transport of choline (and, context-dependently, ethanolamine) across the plasma membrane, with particular relevance to blood–brain barrier (BBB)/CNS endothelial choline handling and neurovascular development (nguyen2024mfsd7cfunctionsas pages 3-4, nguyen2024mfsd7cfunctionsas pages 7-8, ri2024molecularmechanismof pages 7-7).
A key zebrafish-relevant experimental point is that zebrafish MFSD7c isoforms “DaMfsd7c_a” and “DaMfsd7c_b” show choline transport activity in heterologous assays, supporting conservation of substrate specificity in Danio rerio and directly connecting the vertebrate FLVCR2/MFSD7C functional model to zebrafish (nguyen2024mfsd7cfunctionsas pages 3-4).
Earlier literature proposed heme import by FLVCR2 based on hemin-binding and heme-analog uptake assays (duffy2010thefowlersyndromeassociated pages 2-3), and recent heme-focused reviews still cite that work (belot2024updateonheme pages 19-20). However, 2023–2024 structural/functional work in humans and 2024 BBB physiology work in mice strongly “de-orphanize” FLVCR2/MFSD7C as a choline/ethanolamine transporter, and explicitly note that a physiological role for FLVCR2-mediated heme uptake is not confirmed (ri2024molecularmechanismof pages 7-7, nguyen2024mfsd7cfunctionsas pages 3-4).
Gene/protein in scope:
- Organism: Danio rerio (zebrafish). (User-provided UniProt context)
- Gene symbol: flvcr2a; synonym mfsd7c-a. (User-provided UniProt context)
- Protein family/domains: MFS transporter; FLVCR1/2 (SLC49)-like transporter family. This matches vertebrate MFSD7C/FLVCR2 literature describing FLVCR2/MFSD7C as an MFS-domain membrane transporter (kalailingam2020deficiencyofmfsd7c pages 1-2, ri2024molecularmechanismof pages 7-7).
- Ambiguity check: The major risk is confusing zebrafish flvcr2a with mammalian FLVCR2. Here, the linkage is supported because a 2024 Cell Research study explicitly tested zebrafish orthologs/isoforms (DaMfsd7c_a, DaMfsd7c_b) for transport activity, confirming the zebrafish entity is a bona fide FLVCR2/MFSD7C-family transporter (nguyen2024mfsd7cfunctionsas pages 3-4).
MFS proteins are secondary transporters that often perform facilitated diffusion (uniport) or coupled transport across membranes, using alternating-access conformational changes. For FLVCR2-family proteins, the current leading model is uniport (“downhill”) transport for specific organic cations (choline/ethanolamine) rather than ATP-driven pumping (ri2024molecularmechanismof pages 7-7).
FLVCR2/MFSD7C had long-standing uncertainty about its physiological substrate(s) (often discussed as heme). 2023–2024 work provides direct biochemical transport evidence and structures with bound substrates to identify its transported solutes (ri2024molecularmechanismof pages 7-7, nguyen2024mfsd7cfunctionsas pages 3-4).
Choline and ethanolamine are precursors for phosphatidylcholine (PC) and phosphatidylethanolamine (PE) (Kennedy pathway), central to membrane biogenesis. BBB transport/recycling of choline is therefore plausibly important for neurodevelopmental lipid metabolism. In vivo BBB data for MFSD7C show that altering endothelial MFSD7C changes brain choline flux and choline metabolite levels (nguyen2024mfsd7cfunctionsas pages 7-8).
Choline transport (strong evidence):
- In HEK293 cells, overexpression of human or mouse MFSD7c increases radiolabeled choline uptake by ~1.5–2-fold (nguyen2024mfsd7cfunctionsas pages 3-4).
- Import is concentration- and time-dependent (nguyen2024mfsd7cfunctionsas pages 3-4).
- Zebrafish isoforms DaMfsd7c_a and DaMfsd7c_b exhibit choline transport activity, directly supporting conservation in zebrafish (nguyen2024mfsd7cfunctionsas pages 3-4).
Ethanolamine transport (supported but more conditional in MFSD7C-focused work):
- MFSD7c did not increase ethanolamine uptake alone, but ethanolamine transport became significant when ethanolamine kinase (ETNK1) was co-expressed—consistent with metabolic “sink” effects and facilitative transport (nguyen2024mfsd7cfunctionsas pages 7-8).
Independent 2024 mechanistic evidence in humans:
- A 2024 Nature study concludes that human FLVCR1 and FLVCR2 mediate cellular transport of choline and ethanolamine and that both operate as uniporters (ri2024molecularmechanismof pages 7-7). The authors conclude downhill transport independent of sodium or pH gradients, with selectivity mediated by conserved aromatic residues (cation–π interactions) (ri2024molecularmechanismof pages 7-7).
MFSD7c displays properties of a facilitative transporter and can mediate release/export of intracellular choline as well as import, consistent with an equilibrative uniporter/channel-like mechanism rather than an obligate importer (nguyen2024mfsd7cfunctionsas pages 7-8). In a BBB context, the authors propose MFSD7c can act as a choline exporter from brain parenchyma-derived pools into endothelial cells (recycling) (nguyen2024mfsd7cfunctionsas pages 7-8).
In the Cell Research 2024 study, when MFSD7c was co-expressed with choline kinase A (ChKA) (lowering intracellular free choline), choline uptake increased ~9-fold and the inferred kinetics were Km ~100 µM and Vmax ~0.117 µmol/well/60 min (nguyen2024mfsd7cfunctionsas pages 7-8). A disease-associated mutant (S203Y) showed severely impaired kinetics (Km ~1197 µM; Vmax ~0.039 µmol/well/60 min) (nguyen2024mfsd7cfunctionsas pages 7-8).
Both the human preprint (2023) and the 2024 Nature study report plasma-membrane localization in HEK293 assays used for transport measurements (ri2023structuralandmechanistic pages 1-4, ri2024molecularmechanismof pages 7-7). In the Cell Research 2024 MFSD7c study, a transport-deficient mutant (S203Y) was stated not to have defective plasma membrane localization, supporting that transport phenotypes reflect functional impairment rather than mislocalization (nguyen2024mfsd7cfunctionsas pages 3-4).
Multiple mouse studies identify MFSD7c/FLVCR2 as a CNS endothelial/BBB-expressed gene, and knockout produces neurovascular developmental phenotypes (kalailingam2020deficiencyofmfsd7c pages 1-2, santander2020lackofflvcr2 pages 1-3). In endothelial-conditional knockout mice, loss of MFSD7c reduces brain uptake of injected radiolabeled choline while leaving peripheral organ signals comparable (nguyen2024mfsd7cfunctionsas pages 7-8).
Quantitative BBB-related statistic: In the choline-injection experiment (supraphysiological dose), the brain accounted for ~2–3% of total radioactive signal, and this brain signal was significantly reduced upon endothelial MFSD7c knockout (nguyen2024mfsd7cfunctionsas pages 7-8).
Because direct in vivo zebrafish phenotypes for flvcr2a were not retrieved in the accessible corpus, the most defensible zebrafish annotation is built from: (i) direct zebrafish ortholog transport activity, and (ii) conserved vertebrate BBB/endothelial roles.
The 2024 Cell Research study integrates metabolomics and isotope tracing to argue MFSD7c regulates brain choline levels and participates in LPC-derived choline recycling at the BBB (nguyen2024mfsd7cfunctionsas pages 7-8, nguyen2024mfsd7cfunctionsas pages 3-4). These processes connect mechanistically to membrane lipid homeostasis (PC synthesis) and neurodevelopment.
Two independent 2020 JCI papers provide strong phenotype evidence that FLVCR2/MFSD7c is required for normal brain angiogenic sprouting:
- Global Mfsd7c knockout embryos display inhibited CNS vessel growth (ventricular/subventricular zones), vessel tip dilation/fusion (glomeruloid), hypoxia, neuronal death, and microcephaly/ventriculomegaly (kalailingam2020deficiencyofmfsd7c pages 1-2).
- Flvcr2 inactivation impairs brain angiogenesis while reportedly not disrupting BBB integrity, indicating uncoupling of vessel morphogenesis from BBB formation (santander2020lackofflvcr2 pages 1-3).
These data support a working model: in vertebrates, FLVCR2/MFSD7C-mediated metabolite transport (now strongly linked to choline) is intertwined with CNS endothelial metabolic state and angiogenic signaling programs (kalailingam2020deficiencyofmfsd7c pages 1-2, nguyen2024mfsd7cfunctionsas pages 7-8).
Nguyen et al. (Cell Research, Feb 2024) identify MFSD7c as a BBB choline transporter using metabolomics (>520 metabolites), electrophysiology (electrogenic transport), and isotope-tracing paradigms; importantly, they show zebrafish MFSD7c isoforms have choline transport activity, directly informing zebrafish functional annotation (nguyen2024mfsd7cfunctionsas pages 3-4, nguyen2024mfsd7cfunctionsas pages 7-8). URL: https://doi.org/10.1038/s41422-023-00923-y (nguyen2024mfsd7cfunctionsas pages 3-4).
Ri et al. (Nature, Jun 2024) present cryo-EM and functional transport assays establishing that human FLVCR2 transports choline and ethanolamine and operates as a uniporter. The study defines binding-pocket residues (conserved aromatic side chains and cation–π interactions) and emphasizes that physiological specialization between FLVCR paralogs still requires confirmation in vivo (ri2024molecularmechanismof pages 7-7). URL: https://doi.org/10.1038/s41586-024-07444-7 (ri2024molecularmechanismof pages 7-7).
A 2023 bioRxiv preprint reported choline/ethanolamine transport and plasma membrane localization for human FLVCR1/2, providing early support for the 2024 model (ri2023structuralandmechanistic pages 1-4). URL: https://doi.org/10.1101/2023.09.15.557925 (ri2023structuralandmechanistic pages 1-4).
Duffy et al. (Molecular and Cellular Biology, Nov 2010) reported hemin-agarose binding by FLVCR2 and functional uptake assays (e.g., ZnMP uptake; Xenopus oocyte [55Fe]hemin uptake). Hemin competition reduced hemin-agarose binding by ~23% (25 µM) and 36% (50 µM) (duffy2010thefowlersyndromeassociated pages 2-3). URL: https://doi.org/10.1128/MCB.00690-10 (duffy2010thefowlersyndromeassociated pages 2-3).
The 2024 Nature paper explicitly notes that FLVCR2-mediated heme uptake “has not been confirmed” and that prior biochemical evidence for heme roles was not definitive; it concludes choline and ethanolamine are the primary substrates supported by multiple lines of evidence (ri2024molecularmechanismof pages 7-7).
Implication for zebrafish flvcr2a annotation: annotate choline transporter (facilitative/uniporter) as the primary molecular function, and treat heme transport as a historical/contested hypothesis that would require direct zebrafish testing under physiological conditions.
Mouse genetic models (global or endothelial loss) are used to define how FLVCR2/MFSD7C loss causes microcephaly-associated vasculopathy and hydrocephalus-like phenotypes, providing a translational framework for vertebrate developmental vascular biology (kalailingam2020deficiencyofmfsd7c pages 1-2, santander2020lackofflvcr2 pages 1-3).
The 2024 BBB-focused work provides implementable experimental frameworks:
- Radiotracer choline injection with organ distribution measurements to quantify BBB import defects (nguyen2024mfsd7cfunctionsas pages 7-8).
- Stable-isotope tracing to follow LPC-derived choline and infer recycling/export steps at the BBB (nguyen2024mfsd7cfunctionsas pages 7-8).
These approaches can be adapted to zebrafish (e.g., tracer exposures in larvae, endothelial reporters, CRISPR mutants) to directly test whether flvcr2a supports choline flux in CNS endothelium.
The 2024 Nature structural mechanism identifies conserved binding-pocket features (e.g., aromatic residues mediating cation–π interactions), enabling structure-guided testing of zebrafish residues and variants for substrate binding/transport hypotheses (ri2024molecularmechanismof pages 7-7).
Key extracted quantitative points:
- Zebrafish relevance: zebrafish DaMfsd7c_a and DaMfsd7c_b show choline transport activity in heterologous assays (qualitative, but direct) (nguyen2024mfsd7cfunctionsas pages 3-4).
- Transport amplification by metabolic sink: ~9-fold increased uptake with ChKA co-expression (nguyen2024mfsd7cfunctionsas pages 7-8).
- Kinetics (with ChKA co-expression): Km 100 µM; Vmax 0.117 µmol/well/60 min (nguyen2024mfsd7cfunctionsas pages 7-8).
- BBB radiotracer distribution: brain ~2–3% of total signal; reduced in endothelial KO (nguyen2024mfsd7cfunctionsas pages 7-8).
- Heme-binding competition (historical): hemin reduced FLVCR2 pulldown binding by 23% (25 µM) and 36% (50 µM) (duffy2010thefowlersyndromeassociated pages 2-3).
- Structural cavity volumes: FLVCR2 ~579 ų vs FLVCR1 ~513 ų (ri2024molecularmechanismof pages 7-7).
Primary molecular function (most supported):
- Facilitative transporter (uniporter-like) for choline across the plasma membrane; can support bidirectional flux depending on concentration gradients and intracellular metabolic trapping. (nguyen2024mfsd7cfunctionsas pages 7-8, ri2024molecularmechanismof pages 7-7, nguyen2024mfsd7cfunctionsas pages 3-4)
Secondary/conditional function (supported but less direct):
- Ethanolamine transport is plausible and strongly supported for human FLVCR2 in structural/transport assays; MFSD7c-mediated ethanolamine flux may require metabolic trapping (ETNK1) in some contexts. (ri2024molecularmechanismof pages 7-7, nguyen2024mfsd7cfunctionsas pages 7-8)
Cellular component/localization (most supported):
- Plasma membrane; enriched/functional in CNS endothelial (BBB) contexts in mammals; zebrafish localization remains to be measured directly. (nguyen2024mfsd7cfunctionsas pages 3-4, kalailingam2020deficiencyofmfsd7c pages 1-2)
Biological process (inferred and cross-vertebrate supported):
- Choline homeostasis at the BBB; contribution to brain choline availability/recycling and lipid precursor metabolism; neurovascular development/angiogenesis. (nguyen2024mfsd7cfunctionsas pages 7-8, kalailingam2020deficiencyofmfsd7c pages 1-2, santander2020lackofflvcr2 pages 1-3)
Legacy/contested hypothesis (should be labeled as such):
- Heme import has historical experimental support in heterologous systems but is not confirmed as the primary physiological function in newer mechanistic work. (duffy2010thefowlersyndromeassociated pages 2-3, ri2024molecularmechanismof pages 7-7)
Within the currently retrieved corpus, there is no direct in vivo zebrafish mutant phenotype, tissue expression map, or subcellular localization imaging for flvcr2a. The strongest zebrafish-specific evidence is conserved choline transport activity of zebrafish MFSD7c isoforms in a heterologous assay (nguyen2024mfsd7cfunctionsas pages 3-4). Therefore, zebrafish annotations beyond molecular function (e.g., exact larval phenotypes, spatial expression domains) should be treated as hypotheses derived from vertebrate conservation until validated experimentally in zebrafish.
| Claim (function/substrate/localization/role) | Species/system | Evidence type | Key quantitative/statistical details | Main takeaway for zebrafish flvcr2a annotation | Citation (include DOI URL and year) |
|---|---|---|---|---|---|
| MFSD7c/FLVCR2 is a choline transporter, and zebrafish orthologs are active | Human and mouse MFSD7c in HEK293; zebrafish DaMfsd7c_a and DaMfsd7c_b; medaka; frog | Radioactive choline transport assays across vertebrate orthologs | Overexpression of hMFSD7c or mMfsd7c increased intracellular [3H]-choline by ~1.5- to 2-fold; zebrafish isoforms a and b also showed choline transport activity | Direct cross-species evidence supports annotating zebrafish flvcr2a/MFSD7C-a as a choline transporter rather than an uncharacterized orphan transporter | Nguyen et al., 2024, Cell Research, https://doi.org/10.1038/s41422-023-00923-y (nguyen2024mfsd7cfunctionsas pages 3-4) |
| MFSD7c is a facilitative plasma-membrane choline transporter with BBB relevance | Human MFSD7c in HEK293; mouse embryos/BBB | Transport assay; metabolomics; physiological inference | Choline uptake was concentration- and time-dependent; fetal brain metabolomics covered >520 metabolites; Mfsd7c loss increased brain choline while reducing CDP-choline; heme and bilirubin in fetal brains were comparable between WT and KO | For zebrafish flvcr2a, the strongest current annotation is plasma-membrane choline transport linked to choline metabolism, not a primary heme-transport role | Nguyen et al., 2024, Cell Research, https://doi.org/10.1038/s41422-023-00923-y (nguyen2024mfsd7cfunctionsas pages 3-4) |
| MFSD7c behaves as a facilitative/electrogenic transporter and can mediate bidirectional choline movement | Human MFSD7c in HEK293 | Transport assay; patch clamp; release assay | Co-expression with choline kinase A increased choline uptake ~9-fold; apparent Km for choline import under this condition was 100 µM and Vmax 0.117 µmol/well/60 min; expression was required for intracellular choline release; choline import increased membrane potential | Zebrafish flvcr2a is best inferred to function as a gradient-driven choline transporter/uniporter-like protein capable of import and export depending on context | Nguyen et al., 2024, Cell Research, https://doi.org/10.1038/s41422-023-00923-y (nguyen2024mfsd7cfunctionsas pages 4-7, nguyen2024mfsd7cfunctionsas pages 7-8) |
| Ethanolamine can also be transported, but less strongly supported than choline in MFSD7c study | Human MFSD7c in HEK293 | Transport assay with metabolic trapping | Ethanolamine uptake was not increased by MFSD7c alone but became significant with ETNK1 co-expression; L-carnitine increase was slight and considered a weak ligand | Zebrafish flvcr2a may transport ethanolamine, but choline is the best-supported substrate from MFSD7c-specific vertebrate data | Nguyen et al., 2024, Cell Research, https://doi.org/10.1038/s41422-023-00923-y (nguyen2024mfsd7cfunctionsas pages 4-7) |
| MFSD7c localizes to plasma membrane and is expressed in CNS endothelial cells/BBB | Mouse embryos/adult brain; human/mouse cell systems | Immunohistochemistry; localization controls; functional cell assays | S203Y reduced transport without loss of plasma-membrane localization; prior and current data place MFSD7c in CNS endothelial cells and plasma membrane | For zebrafish flvcr2a, the likely cellular location is plasma membrane of endothelial/BBB-like cells rather than an exclusively mitochondrial compartment | Nguyen et al., 2024, Cell Research, https://doi.org/10.1038/s41422-023-00923-y (nguyen2024mfsd7cfunctionsas pages 3-4); Kalailingam et al., 2020, JCI, https://doi.org/10.1172/JCI136727 (kalailingam2020deficiencyofmfsd7c pages 1-2) |
| MFSD7c is required for BBB choline handling in vivo | Endothelial-specific Mfsd7c knockout mice | Conditional knockout; radiotracer uptake; stable-isotope tracing | Brain radioactive choline signal was significantly reduced in endothelial KO mice, whereas peripheral organs were comparable; brain accounted for ~2%–3% of total radioactive signal; endogenous and labeled choline accumulated in KO brain | Zebrafish flvcr2a likely contributes to endothelial/brain choline flux and could influence brain phospholipid precursor supply during development | Nguyen et al., 2024, Cell Research, https://doi.org/10.1038/s41422-023-00923-y (nguyen2024mfsd7cfunctionsas pages 7-8) |
| MFSD7c is implicated in export/recycling of LPC-derived choline at the BBB | Endothelial-specific Mfsd7c knockout mice | Stable-isotope lipid tracing | After LPC-d49 tracing, deuterated choline-d13 accumulated in KO brains, supporting a defect in choline export/recycling from brain parenchyma to endothelium | Zebrafish flvcr2a annotation should mention a role in choline recycling/homeostasis, not just uptake | Nguyen et al., 2024, Cell Research, https://doi.org/10.1038/s41422-023-00923-y (nguyen2024mfsd7cfunctionsas pages 7-8) |
| Human FLVCR2 is structurally and biochemically a choline/ethanolamine transporter | Human FLVCR2 in HEK293 and cryo-EM structural studies | Radioligand transport assays; cryo-EM; mutagenesis; MD simulation | FLVCR1 cavity ~513 Å3, FLVCR2 cavity ~579 Å3; conserved W102/F324/Y325 in FLVCR2 coordinate ligand; authors conclude FLVCR1/2 are uniporters enabling downhill transport independent of sodium or pH gradients | Because zebrafish flvcr2a belongs to the same conserved FLVCR2/MFS family, current best inference is choline/ethanolamine uniport activity with conserved aromatic binding chemistry | Ri et al., 2024, Nature, https://doi.org/10.1038/s41586-024-07444-7 (ri2024molecularmechanismof pages 7-7) |
| The 2024 FLVCR2 model revises the earlier heme-import hypothesis | Human FLVCR1/FLVCR2 | Expert synthesis within primary structural paper | Authors explicitly state that FLVCR2-mediated heme uptake has not been confirmed and that choline and ethanolamine are the primary transport substrates | For zebrafish flvcr2a, annotation should prioritize choline/ethanolamine transport and treat heme transport as an older, less secure model | Ri et al., 2024, Nature, https://doi.org/10.1038/s41586-024-07444-7 (ri2024molecularmechanismof pages 7-7) |
| Earlier literature supported FLVCR2 as a cell-surface heme importer | Human FLVCR2 in CHO cells, TE671 cells, Xenopus oocytes | Hemin-agarose binding; ZnMP uptake; [55Fe]hemin uptake; siRNA knockdown | Free hemin reduced hemin-agarose binding by ~23% (25 µM) and ~36% (50 µM); FY981 Env reduced ZnMP uptake by ~40%; FLVCR2 knockdown disrupted heme uptake | Heme-import activity remains part of the historical literature for FLVCR2-family proteins, but for zebrafish flvcr2a it should be considered secondary/contested versus newer choline data | Duffy et al., 2010, Mol Cell Biol, https://doi.org/10.1128/MCB.00690-10 (duffy2010thefowlersyndromeassociated pages 2-3) |
| Loss of MFSD7c causes CNS vascular-development defects relevant to Fowler syndrome | Global Mfsd7c knockout mice; comparison to human FLVCR2 disease | Knockout phenotype; histology; transcriptomics | KO caused late-gestation lethality; impaired angiogenic growth in ventricular/subventricular zones; dilated/fused vascular tips, glomeruloid vessels, hypoxia, neuronal cell death, reduced cortical layers, enlarged ventricles, microcephaly | For zebrafish flvcr2a, likely biological roles include CNS endothelial function, angiogenic brain vascular development, and neurodevelopmental support through metabolite transport | Kalailingam et al., 2020, JCI, https://doi.org/10.1172/JCI136727 (kalailingam2020deficiencyofmfsd7c pages 1-2) |
Table: This table compiles the strongest retrieved evidence relevant to zebrafish flvcr2a/MFSD7C-a, emphasizing direct vertebrate transport data, family-level structural mechanisms, and knockout phenotypes. It is useful for assigning a cautious, evidence-weighted functional annotation that prioritizes choline transport and BBB/CNS vascular roles while noting the older contested heme-import model.
References
(nguyen2024mfsd7cfunctionsas pages 3-4): Xuan Thi Anh Nguyen, Thanh Nha Uyen Le, Toan Q. Nguyen, Hoa Thi Thuy Ha, Anna Artati, Nancy C. P. Leong, Dat T. Nguyen, Pei Yen Lim, Adelia Vicanatalita Susanto, Qianhui Huang, Ling Fam, Lo Ngah Leong, Isabelle Bonne, Angela Lee, Jorge L. Granadillo, Catherine Gooch, Dejie Yu, Hua Huang, Tuck Wah Soong, Matthew Wook Chang, Markus R. Wenk, Jerzy Adamski, Amaury Cazenave-Gassiot, and Long N. Nguyen. Mfsd7c functions as a transporter of choline at the blood–brain barrier. Cell Research, 34:245-257, Feb 2024. URL: https://doi.org/10.1038/s41422-023-00923-y, doi:10.1038/s41422-023-00923-y. This article has 27 citations and is from a domain leading peer-reviewed journal.
(nguyen2024mfsd7cfunctionsas pages 7-8): Xuan Thi Anh Nguyen, Thanh Nha Uyen Le, Toan Q. Nguyen, Hoa Thi Thuy Ha, Anna Artati, Nancy C. P. Leong, Dat T. Nguyen, Pei Yen Lim, Adelia Vicanatalita Susanto, Qianhui Huang, Ling Fam, Lo Ngah Leong, Isabelle Bonne, Angela Lee, Jorge L. Granadillo, Catherine Gooch, Dejie Yu, Hua Huang, Tuck Wah Soong, Matthew Wook Chang, Markus R. Wenk, Jerzy Adamski, Amaury Cazenave-Gassiot, and Long N. Nguyen. Mfsd7c functions as a transporter of choline at the blood–brain barrier. Cell Research, 34:245-257, Feb 2024. URL: https://doi.org/10.1038/s41422-023-00923-y, doi:10.1038/s41422-023-00923-y. This article has 27 citations and is from a domain leading peer-reviewed journal.
(ri2024molecularmechanismof pages 7-7): Keiken Ri, Tsai-Hsuan Weng, Ainara Claveras Cabezudo, Wiebke Jösting, Yu Zhang, Andre Bazzone, Nancy C. P. Leong, Sonja Welsch, Raymond T. Doty, Gonca Gursu, Tiffany Jia Ying Lim, Sarah Luise Schmidt, Janis L. Abkowitz, Gerhard Hummer, Di Wu, Long N. Nguyen, and Schara Safarian. Molecular mechanism of choline and ethanolamine transport in humans. Nature, 630:501-508, May 2024. URL: https://doi.org/10.1038/s41586-024-07444-7, doi:10.1038/s41586-024-07444-7. This article has 36 citations and is from a highest quality peer-reviewed journal.
(duffy2010thefowlersyndromeassociated pages 2-3): Simon P. Duffy, Jennifer Shing, Punit Saraon, Lloyd C. Berger, Maribeth V. Eiden, Andrew Wilde, and Chetankumar S. Tailor. The fowler syndrome-associated protein flvcr2 is an importer of heme. Nov 2010. URL: https://doi.org/10.1128/mcb.00690-10, doi:10.1128/mcb.00690-10. This article has 160 citations and is from a domain leading peer-reviewed journal.
(belot2024updateonheme pages 19-20): Audrey Belot, Herve Puy, Iqbal Hamza, and Herbert L. Bonkovsky. Update on heme biosynthesis, tissue‐specific regulation, heme transport, relation to iron metabolism and cellular energy. Liver International, 44:2235-2250, Jun 2024. URL: https://doi.org/10.1111/liv.15965, doi:10.1111/liv.15965. This article has 53 citations and is from a peer-reviewed journal.
(kalailingam2020deficiencyofmfsd7c pages 1-2): Pazhanichamy Kalailingam, Kai Qi Wang, Xiu Ru Toh, Toan Q. Nguyen, Madhuvanthi Chandrakanthan, Zafrul Hasan, Clair Habib, Aharon Schif, Francesca Clementina Radio, Bruno Dallapiccola, Karin Weiss, and Long N. Nguyen. Deficiency of mfsd7c results in microcephaly-associated vasculopathy in fowler syndrome. Journal of Clinical Investigation, Jun 2020. URL: https://doi.org/10.1172/jci136727, doi:10.1172/jci136727. This article has 32 citations and is from a highest quality peer-reviewed journal.
(ri2023structuralandmechanistic pages 1-4): Keiken Ri, Tsai-Hsuan Weng, Ainara Claveras Cabezudo, Wiebke Jösting, Zhang Yu, Andre Bazzone, Nancy C.P. Leong, Sonja Welsch, Raymond T. Doty, Gonca Gursu, Tiffany Jia Ying Lim, Sarah Luise Schmidt, Janis L. Abkowitz, Gerhard Hummer, Di Wu, Long N Nguyen, and Schara Safarian. Structural and mechanistic insights into human choline and ethanolamine transport. bioRxiv, Dec 2023. URL: https://doi.org/10.1101/2023.09.15.557925, doi:10.1101/2023.09.15.557925. This article has 4 citations.
(santander2020lackofflvcr2 pages 1-3): Nicolas Santander, Carlos O. Lizama, Eman Meky, Gabriel L. McKinsey, Bongnam Jung, Dean Sheppard, Christer Betsholtz, and Thomas D. Arnold. Lack of flvcr2 impairs brain angiogenesis without affecting the blood-brain barrier. Journal of Clinical Investigation, Jun 2020. URL: https://doi.org/10.1172/jci136578, doi:10.1172/jci136578. This article has 33 citations and is from a highest quality peer-reviewed journal.
(nguyen2024mfsd7cfunctionsas pages 4-7): Xuan Thi Anh Nguyen, Thanh Nha Uyen Le, Toan Q. Nguyen, Hoa Thi Thuy Ha, Anna Artati, Nancy C. P. Leong, Dat T. Nguyen, Pei Yen Lim, Adelia Vicanatalita Susanto, Qianhui Huang, Ling Fam, Lo Ngah Leong, Isabelle Bonne, Angela Lee, Jorge L. Granadillo, Catherine Gooch, Dejie Yu, Hua Huang, Tuck Wah Soong, Matthew Wook Chang, Markus R. Wenk, Jerzy Adamski, Amaury Cazenave-Gassiot, and Long N. Nguyen. Mfsd7c functions as a transporter of choline at the blood–brain barrier. Cell Research, 34:245-257, Feb 2024. URL: https://doi.org/10.1038/s41422-023-00923-y, doi:10.1038/s41422-023-00923-y. This article has 27 citations and is from a domain leading peer-reviewed journal.