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this with annotations you find in gene/protein databases, but these can be outdated or inaccurate.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 UniProt target provided (Q6DRD3) is annotated as DNA polymerase beta (Pol β) in Danio rerio, encoded by polb, and classified in the DNA polymerase type-X family with an N-terminal 5′-deoxyribose-phosphate (5′-dRP) lyase domain and a C-terminal DNA polymerase/nucleotidyltransferase domain. The literature captured here consistently uses “Pol β / polb” to denote the base excision repair (BER) gap-filling polymerase in zebrafish and other vertebrates, matching the UniProt-provided identity rather than an unrelated gene symbol reuse. In particular, Pol β is described as a dual-function enzyme with dRP lyase and polymerase activities and conserved active-site architecture, supporting that zebrafish polb is the orthologous BER polymerase. (sobol2024mousemodelsto pages 1-3, almohdar2024impactofdna pages 1-2)
Base excision repair (BER) is the dominant pathway for repair of small, non-helix-distorting base lesions and abasic (AP) sites generated by oxidation, deamination, alkylation, and spontaneous base loss. In the canonical sequence, a DNA glycosylase excises a damaged base to form an AP site, an AP endonuclease (APE1/Apex1) cleaves the backbone, and downstream enzymes restore the correct nucleotide and seal the strand break. (dey2023dnarepairgenes pages 4-5, scalera2024investigationsofthe pages 27-29, gohil2023baseexcisionrepair pages 6-8)
DNA polymerase β (Pol β) is a core BER enzyme that performs two coupled downstream reactions:
1) Gap-filling DNA synthesis: Pol β catalyzes template-directed insertion of the correct nucleotide into the repair gap (classically a 1-nt gap in “short-patch” BER). (dey2023dnarepairgenes pages 4-5, scalera2024investigationsofthe pages 27-29, almohdar2024impactofdna pages 1-2)
2) 5′-dRP lyase reaction: Pol β removes the 5′-deoxyribose phosphate (5′-dRP) blocking group left at the 5′ end after incision at an AP site, enabling final ligation. (almohdar2024impactofdna pages 1-2, shahi2026harnessingdnapolymerase pages 1-2)
Mechanistically, recent synthesis sources describe Pol β as having separable domains for these activities (N-terminal dRP lyase and C-terminal nucleotidyltransferase), with conserved catalytic residues in mammalian Pol β including K72 (dRP lyase) and the polymerase active-site Asp triad (D190/D192/D256)—information that supports functional inference for the zebrafish ortholog. (sobol2024mousemodelsto pages 1-3)
BER is often partitioned into:
- Short-patch BER (SN-BER): typically replaces one nucleotide, with Pol β performing gap filling and then ligation commonly by XRCC1–LIG3α (in many vertebrate models). (dey2023dnarepairgenes pages 4-5, scalera2024investigationsofthe pages 27-29)
- Long-patch BER (LP-BER): replaces a longer tract; synthesis can involve polymerase switching and downstream processing of flap intermediates (e.g., FEN1, PCNA, RPA, and ligases). A recent review summarizes LP-BER patch sizes as 2–11 nt and also describes a distinct 5′-gap LP-BER model with a 9-nt gap and 8-nt flap intermediate, with reported incorporation of ~20 nt in that pathway context. (gohil2023baseexcisionrepair pages 6-8)
Zebrafish-focused synthesis sources place polb in BER with the conserved step order: lesion recognition/excision → AP site incision by Apex1 → nucleotide replacement by Pol β → nick sealing by XRCC1–LIG3α. (dey2023dnarepairgenes pages 4-5, scalera2024investigationsofthe pages 27-29)
A 2024 Journal of Biological Chemistry study focusing on downstream BER coordination emphasizes that Pol β function depends critically on handoffs and protein–protein interactions with ligases and APE1. It highlights that Pol β performs both the 5′-dRP lyase step and gap-filling synthesis, and that ligase interactions (LIG1 or LIGIIIα) strongly influence successful nick sealing; defects in coordination can yield abortive intermediates that block ligation and contribute to genome instability. (almohdar2024impactofdna pages 1-2)
A 2024 review of Pol β mouse models also catalogs many interaction partners reported for Pol β regulation and recruitment in mammalian systems, including PARP1 and XRCC1, and other factors (e.g., NEIL1/2). These interactions are relevant to zebrafish primarily by orthology-based inference rather than being directly demonstrated in the zebrafish-specific sources retrieved here. (sobol2024mousemodelsto pages 1-3, sobol2024mousemodelsto pages 12-14)
For zebrafish polb, the retrieved zebrafish-focused sources support its assignment to BER but do not provide direct subcellular localization experiments (e.g., immunofluorescence or biochemical fractionation). Thus:
- Nuclear function is strongly supported by the canonical BER role described for Pol β. (dey2023dnarepairgenes pages 4-5, scalera2024investigationsofthe pages 27-29)
- Mitochondrial BER participation is supported in vertebrate literature syntheses (mouse/human-focused) indicating Pol β can also function in mitochondria, but this remains inferred for zebrafish based on conservation rather than directly shown in the zebrafish-specific evidence captured here. (sobol2024mousemodelsto pages 1-3, ong2025structurefunctionanalysisa pages 108-110)
A fish-embryo DNA repair review reports that BER operates across fish development, but emphasizes that BER in zebrafish eggs and early embryos appears less efficient than in adults. It specifically notes that in zebrafish, polb mRNA is present at all embryonic stages, yet Pol β protein is reportedly absent in eggs and early embryos until gastrulation, suggesting an early developmental stage where canonical Pol β-dependent SN-BER capacity may be limited. The same synthesis describes lower BER enzyme activities in early embryos (e.g., Udg and Ape1 activities lower in 3.5 hpf embryos than in adults), and discusses regulatory connections involving Apex/Creb1 that may influence Pol β expression prior to gastrulation. (dey2023dnarepairgenes pages 4-5)
A 2024 zebrafish DNA-damage-response synthesis likewise lists pol β among core BER genes/proteins in zebrafish and reiterates a zebrafish-embryo distinction: embryos lack Pol β and rely more on replicative polymerases and Mg2+-dependent endonuclease activity early, whereas Apex1/Apex2 are highly expressed in embryos and participate in early oxidative-damage repair. (scalera2024investigationsofthe pages 27-29)
Interpretation: these sources together support a model in which zebrafish polb is a canonical BER factor but may be developmentally limited at the protein level before gastrulation, implying stage-specific reliance on alternative polymerase activities early in embryogenesis. (dey2023dnarepairgenes pages 4-5, scalera2024investigationsofthe pages 27-29)
Zebrafish embryos are widely used to evaluate environmental genotoxicants and oxidative stress. In one well-cited experimental study, zebrafish embryos exposed to 100 nm polystyrene nanoplastics (0, 100, 200, 400 mg/L) showed altered expression of BER-pathway genes including polb, consistent with BER pathway engagement during oxidative stress. (feng2022polystyrenenanoplasticexposure pages 1-2)
In that study, exposure of embryos starting at 24 hpf for 24 h led to oxidative stress with ROS increases of 1.27-fold, 1.47-fold, and 2.23-fold at 100, 200, and 400 mg/L, respectively, and the authors reported that polb expression increased at lower concentrations (<200 mg/L) and slightly decreased at 400 mg/L. (feng2022polystyrenenanoplasticexposure pages 5-6)
Figure-level evidence from the paper (BER gene-expression panel including polb) is shown in Figure 6, which visually supports the reported directional trend for polb across doses. (feng2022polystyrenenanoplasticexposure media 1eee0503, feng2022polystyrenenanoplasticexposure media e296e8ed)
Recent reviews emphasize that BER is not a single linear pathway but a set of subpathways (SN-BER, LP-BER, replication- and transcription-associated BER) with coordinated “handoffs” among enzymes and scaffolds. Quantitative pathway descriptors (e.g., typical 2–11 nt LP-BER patch sizes; 5′-gap pathway intermediates including a 9-nt gap and 8-nt flap) help constrain expectations for the kinds of BER intermediates that Pol β-related assays may measure. (gohil2023baseexcisionrepair pages 6-8)
A 2024 mechanistic study directly analyzes how DNA ligases (LIG1, LIGIIIα) and APE1 influence the efficiency and fidelity of Pol β’s downstream BER steps, underscoring that functional annotation of Pol β should include not only catalytic activities but also ligase-coupled coordination and avoidance of abortive repair intermediates. (almohdar2024impactofdna pages 1-2)
A 2024 review of Pol β mouse models consolidates evidence that Pol β is essential at the organismal level (loss leads to early lethality in mouse), and highlights new knock-in models that separate recruitment/stability from catalytic function (e.g., disruption of binding to XRCC1 affecting recruitment/stability). While not zebrafish-specific, this provides an authoritative framework for what phenotypes might be expected from strong loss-of-function or recruitment-defective polb alleles in vertebrates and highlights XRCC1 as an obligate functional partner in vivo. (sobol2024mousemodelsto pages 1-3, sobol2024mousemodelsto pages 12-14)
The most relevant quantitative and semi-quantitative data points captured in the retrieved evidence include:
- Developmental timing (zebrafish): reduced BER enzyme activities noted in embryos at 3.5 hpf; Pol β protein reported absent until gastrulation despite polb mRNA presence. (dey2023dnarepairgenes pages 4-5)
- LP-BER tract sizes (mechanistic review): typical LP-BER patches of 2–11 nt, and a distinct LP-BER 5′-gap pathway with a 9-nt gap, 8-nt flap, and reported incorporation of ~20 nt. (gohil2023baseexcisionrepair pages 6-8)
- Environmental exposure and oxidative stress (zebrafish embryos): polystyrene nanoplastic exposures at 0/100/200/400 mg/L; ROS increased 1.27×, 1.47×, 2.23× at 100/200/400 mg/L, respectively; polb expression directionally increased at lower doses and slightly decreased at the highest dose (as described in text and supported by the figure). (feng2022polystyrenenanoplasticexposure pages 5-6, feng2022polystyrenenanoplasticexposure media 1eee0503, feng2022polystyrenenanoplasticexposure media e296e8ed)
In practice, zebrafish polb is used primarily as:
- A BER pathway marker gene in embryo toxicology and environmental-genotoxicity studies, where altered polb expression is interpreted as engagement of BER under oxidative stress conditions (e.g., nanoplastic exposure). (feng2022polystyrenenanoplasticexposure pages 5-6, feng2022polystyrenenanoplasticexposure pages 1-2, feng2022polystyrenenanoplasticexposure media 1eee0503)
- A component in developmental DNA repair frameworks, where early embryo reliance on alternative polymerases and developmental control of DNA repair capacity is studied to understand embryo susceptibility to genotoxins. (dey2023dnarepairgenes pages 4-5, scalera2024investigationsofthe pages 27-29)
The following table consolidates zebrafish-specific evidence and conserved mechanistic annotation for zebrafish Pol β.
| Category | Key points | Best supporting sources (with citation IDs) | Links (DOI/URL + publication date when available) |
|---|---|---|---|
| Identity/domains | Target identity is Danio rerio polb / DNA polymerase beta (UniProt Q6DRD3), a type-X family DNA polymerase. Conserved Pol β architecture supports the UniProt annotation: an N-terminal 5'-dRP lyase domain and C-terminal nucleotidyl-transferase/polymerase domain. Mammalian Pol β is a 335 aa, ~39 kDa protein; active-site residues defining these activities include K72 for dRP lyase and D190/D192/D256 for polymerase catalysis, supporting functional inference for zebrafish ortholog Q6DRD3. (sobol2024mousemodelsto pages 1-3, almohdar2024impactofdna pages 1-2) | Sobol 2024 review (sobol2024mousemodelsto pages 1-3); Almohdar et al. 2024 JBC (almohdar2024impactofdna pages 1-2) | Sobol 2024, Environ Mol Mutagen (Apr 2024): https://doi.org/10.1002/em.22593 ; Almohdar et al. 2024, J Biol Chem (Jun 2024): https://doi.org/10.1016/j.jbc.2024.107355 |
| Core reactions | Primary biochemical role in base excision repair (BER): Pol β (1) performs template-directed single-nucleotide gap filling and (2) removes the 5'-deoxyribose phosphate (5'-dRP) blocking group via its dRP lyase/AP lyase activity before ligation. Pol β has highest catalytic activity on 5'-phosphorylated 1-nt gapped DNA and typically inserts the first nucleotide in repair intermediates. (gohil2023baseexcisionrepair pages 6-8, almohdar2024impactofdna pages 1-2, shahi2026harnessingdnapolymerase pages 1-2) | Gohil et al. 2023 review (gohil2023baseexcisionrepair pages 6-8); Almohdar et al. 2024 (almohdar2024impactofdna pages 1-2); Shahi et al. 2026 review summary (shahi2026harnessingdnapolymerase pages 1-2) | Gohil et al. 2023, Int J Mol Sci (Sep 2023): https://doi.org/10.3390/ijms241814186 ; Almohdar et al. 2024 (Jun 2024): https://doi.org/10.1016/j.jbc.2024.107355 ; Shahi et al. 2026 (Jan 2026): https://doi.org/10.3389/jpps.2025.15360 |
| Pathway context | In canonical short-patch BER, a damaged base is removed by a glycosylase, APE1/Apex1 cleaves the AP site, Pol β fills the gap, and the nick is sealed by XRCC1-LIG3α. Pol β also contributes to long-patch BER (LP-BER), where it may add the first nucleotide before Pol δ/ε extension; downstream factors include FEN1, PCNA, RPA, LIG1/LIG3. Reviews also note roles in nucleotide incision repair, replication-stress responses, and TET-mediated DNA demethylation. (dey2023dnarepairgenes pages 4-5, scalera2024investigationsofthe pages 27-29, sobol2024mousemodelsto pages 1-3, gohil2023baseexcisionrepair pages 6-8) | Dey et al. 2023 fish embryo review (dey2023dnarepairgenes pages 4-5); Scalera 2024 thesis/review material (scalera2024investigationsofthe pages 27-29); Sobol 2024 (sobol2024mousemodelsto pages 1-3); Gohil et al. 2023 (gohil2023baseexcisionrepair pages 6-8) | Dey et al. 2023, Front Cell Dev Biol (Mar 2023): https://doi.org/10.3389/fcell.2023.1119229 ; Scalera 2024 (Jan 2024): https://doi.org/10.25358/openscience-10606 ; Sobol 2024: https://doi.org/10.1002/em.22593 ; Gohil et al. 2023: https://doi.org/10.3390/ijms241814186 |
| Key protein partners | Best-supported conserved partners around Pol β include XRCC1, LIG3α, LIG1, APE1, PARP1, FEN1, PCNA, RPA, Neil1/Neil2, APC, P300, PRMT1/PRMT6, and TRF2. Recent work emphasizes that ligase–Pol β coordination is critical: disrupted interplay lowers nick-sealing efficiency and can generate abortive repair intermediates. (sobol2024mousemodelsto pages 1-3, almohdar2024impactofdna pages 1-2, sobol2024mousemodelsto pages 12-14) | Sobol 2024 (sobol2024mousemodelsto pages 1-3, sobol2024mousemodelsto pages 12-14); Almohdar et al. 2024 (almohdar2024impactofdna pages 1-2) | Sobol 2024 (Apr 2024): https://doi.org/10.1002/em.22593 ; Almohdar et al. 2024 (Jun 2024): https://doi.org/10.1016/j.jbc.2024.107355 |
| Subcellular localization | Functional inference from vertebrate Pol β literature indicates predominant action in the nucleus during BER, with evidence that Pol β also functions in mitochondrial BER. For zebrafish polb specifically, the retrieved evidence supports BER pathway assignment but does not provide direct zebrafish subcellular-localization experiments; thus nuclear localization is strongly inferred, and mitochondrial participation remains plausible by orthology rather than directly shown here. (sobol2024mousemodelsto pages 1-3, ong2025structurefunctionanalysisa pages 108-110) | Sobol 2024 review (sobol2024mousemodelsto pages 1-3); compiled Pol β structure/function references (ong2025structurefunctionanalysisa pages 108-110) | Sobol 2024 (Apr 2024): https://doi.org/10.1002/em.22593 ; Ong 2025 summary/references (2025): journal unspecified |
| Zebrafish embryogenesis evidence | Fish/zebrafish reviews consistently place polb in BER during embryogenesis. In zebrafish, polb mRNA is reported at all embryonic stages, but Pol β protein is absent in eggs and early embryos until gastrulation; early embryos appear to rely on an aphidicolin-sensitive replicative polymerase instead. Udg and Ape1 activities are lower in 3.5 hpf embryos than in adults, indicating reduced BER capacity early in development. Apex1/creb1 regulatory relationships have been proposed to influence Pol β expression before gastrulation. (dey2023dnarepairgenes pages 4-5, scalera2024investigationsofthe pages 27-29) | Dey et al. 2023 review of fish embryo DNA repair (dey2023dnarepairgenes pages 4-5); Scalera 2024 zebrafish DNA-damage-response synthesis (scalera2024investigationsofthe pages 27-29) | Dey et al. 2023 (Mar 2023): https://doi.org/10.3389/fcell.2023.1119229 ; Scalera 2024 (Jan 2024): https://doi.org/10.25358/openscience-10606 |
| Zebrafish environmental/toxicant response evidence | In zebrafish embryos exposed to 100 nm polystyrene nanoplastics, polb mRNA changed significantly as part of a BER-response signature. The text reports polb increased at lower concentrations (<200 mg/L) and slightly decreased at 400 mg/L after exposure of 24 hpf embryos for 24 h. The same study linked BER-gene changes with developmental toxicity and oxidative stress. (feng2022polystyrenenanoplasticexposure pages 5-6, feng2022polystyrenenanoplasticexposure pages 1-2, feng2022polystyrenenanoplasticexposure pages 7-8, feng2022polystyrenenanoplasticexposure media 1eee0503) | Feng et al. 2022 ACS Omega (feng2022polystyrenenanoplasticexposure pages 5-6, feng2022polystyrenenanoplasticexposure pages 1-2, feng2022polystyrenenanoplasticexposure pages 7-8); Figure 6 image summary (feng2022polystyrenenanoplasticexposure media 1eee0503) | Feng et al. 2022, ACS Omega (Aug 2022): https://doi.org/10.1021/acsomega.2c03378 |
| Quantitative datapoints | Available quantitative values from retrieved evidence: 3.5 hpf marks reduced BER enzyme activity relative to adults in zebrafish embryos; gastrulation marks the stage after which Pol β protein becomes detectable in zebrafish reviews. In BER mechanism reviews, LP-BER repair patches are typically 2–11 nt; a distinct 5'-gap LP-BER model includes a 9-nt gap, 8-nt flap, and reported incorporation of 20 nt. In nanoplastic-exposed zebrafish embryos, exposure concentrations were 0, 100, 200, 400 mg/L; ROS increased 1.27-fold, 1.47-fold, and 2.23-fold at 100, 200, and 400 mg/L, respectively. Figure-based extraction suggests the polb qPCR bars are modestly elevated at 100 and 200 mg/L and near/below control at 400 mg/L, but exact fold values are not readable with confidence from the available image crop, so they should not be over-interpreted. (dey2023dnarepairgenes pages 4-5, gohil2023baseexcisionrepair pages 6-8, feng2022polystyrenenanoplasticexposure pages 5-6, feng2022polystyrenenanoplasticexposure media 1eee0503, feng2022polystyrenenanoplasticexposure media e296e8ed) | Dey et al. 2023 (dey2023dnarepairgenes pages 4-5); Gohil et al. 2023 (gohil2023baseexcisionrepair pages 6-8); Feng et al. 2022 and figure/image summaries (feng2022polystyrenenanoplasticexposure pages 5-6, feng2022polystyrenenanoplasticexposure media 1eee0503, feng2022polystyrenenanoplasticexposure media e296e8ed) | Dey et al. 2023 (Mar 2023): https://doi.org/10.3389/fcell.2023.1119229 ; Gohil et al. 2023 (Sep 2023): https://doi.org/10.3390/ijms241814186 ; Feng et al. 2022 (Aug 2022): https://doi.org/10.1021/acsomega.2c03378 |
Table: This table summarizes functional annotation for zebrafish polb (UniProt Q6DRD3) by integrating zebrafish-specific evidence with conserved Pol β biochemistry. It highlights what is directly shown in zebrafish versus what is inferred from broader vertebrate DNA repair literature.
polb encodes DNA polymerase beta (Pol β), the principal BER gap-filling polymerase that (i) fills short DNA gaps created during BER and (ii) removes the 5′-dRP blocking group via intrinsic lyase activity to enable ligation. In zebrafish, polb is part of the conserved BER module (Apex1 → Pol β → XRCC1/LIG3α) and appears developmentally regulated, with evidence that early embryos may lack Pol β protein until gastrulation despite polb mRNA presence. Pol β also functions in broader vertebrate contexts including LP-BER coordination and (by inference) may participate in mitochondrial BER, but direct zebrafish localization data were not captured in the retrieved sources. (dey2023dnarepairgenes pages 4-5, scalera2024investigationsofthe pages 27-29, sobol2024mousemodelsto pages 1-3, almohdar2024impactofdna pages 1-2)
References
(sobol2024mousemodelsto pages 1-3): Robert W. Sobol. Mouse models to explore the biological and organismic role of dna polymerase beta. Environmental and Molecular Mutagenesis, 65:57-71, Apr 2024. URL: https://doi.org/10.1002/em.22593, doi:10.1002/em.22593. This article has 3 citations and is from a peer-reviewed journal.
(almohdar2024impactofdna pages 1-2): Danah Almohdar, David Murcia, Qun Tang, Abigail Ortiz, Ernesto Martinez, Tanay Parwal, Pradnya R. Kamble, and Melike Çağlayan. Impact of dna ligase 1 and iiiα interactions with ape1 and polβ on the efficiency of base excision repair pathway at the downstream steps. Journal of Biological Chemistry, 300:107355, Jun 2024. URL: https://doi.org/10.1016/j.jbc.2024.107355, doi:10.1016/j.jbc.2024.107355. This article has 15 citations and is from a domain leading peer-reviewed journal.
(dey2023dnarepairgenes pages 4-5): Abhipsha Dey, Martin Flajšhans, Martin Pšenička, and Ievgeniia Gazo. Dna repair genes play a variety of roles in the development of fish embryos. Frontiers in Cell and Developmental Biology, Mar 2023. URL: https://doi.org/10.3389/fcell.2023.1119229, doi:10.3389/fcell.2023.1119229. This article has 26 citations.
(scalera2024investigationsofthe pages 27-29): Claudia Scalera. Investigations of the uv-induced dna damage response in human cells and zebrafish embryos. Text, Jan 2024. URL: https://doi.org/10.25358/openscience-10606, doi:10.25358/openscience-10606. This article has 1 citations and is from a peer-reviewed journal.
(gohil2023baseexcisionrepair pages 6-8): Dhara Gohil, Altaf H. Sarker, and Rabindra Roy. Base excision repair: mechanisms and impact in biology, disease, and medicine. International Journal of Molecular Sciences, 24:14186, Sep 2023. URL: https://doi.org/10.3390/ijms241814186, doi:10.3390/ijms241814186. This article has 124 citations.
(shahi2026harnessingdnapolymerase pages 1-2): Aashirwad Shahi, Shengyuan Zhao, and Dawit Kidane. Harnessing dna polymerase beta defect enhances synthetic lethality and treatment response in gastric cancer cells: implication for immunotherapy. Journal of Pharmacy & Pharmaceutical Sciences, Jan 2026. URL: https://doi.org/10.3389/jpps.2025.15360, doi:10.3389/jpps.2025.15360. This article has 0 citations and is from a peer-reviewed journal.
(sobol2024mousemodelsto pages 12-14): Robert W. Sobol. Mouse models to explore the biological and organismic role of dna polymerase beta. Environmental and Molecular Mutagenesis, 65:57-71, Apr 2024. URL: https://doi.org/10.1002/em.22593, doi:10.1002/em.22593. This article has 3 citations and is from a peer-reviewed journal.
(ong2025structurefunctionanalysisa pages 108-110): V Ong. Structure function analysis of dna polymerase β and discovery of novel interactors. Unknown journal, 2025.
(feng2022polystyrenenanoplasticexposure pages 1-2): Mei-ling Feng, Juanjuan Luo, Y. Wan, Jiannan Zhang (张剑南), Chunjiao Lu, Maya Wang, Lu Dai, Xiaoqian Cao, Xiaojun Yang, and Yajun Wang. Polystyrene nanoplastic exposure induces developmental toxicity by activating the oxidative stress response and base excision repair pathway in zebrafish (danio rerio). ACS Omega, 7:32153-32163, Aug 2022. URL: https://doi.org/10.1021/acsomega.2c03378, doi:10.1021/acsomega.2c03378. This article has 108 citations and is from a peer-reviewed journal.
(feng2022polystyrenenanoplasticexposure pages 5-6): Mei-ling Feng, Juanjuan Luo, Y. Wan, Jiannan Zhang (张剑南), Chunjiao Lu, Maya Wang, Lu Dai, Xiaoqian Cao, Xiaojun Yang, and Yajun Wang. Polystyrene nanoplastic exposure induces developmental toxicity by activating the oxidative stress response and base excision repair pathway in zebrafish (danio rerio). ACS Omega, 7:32153-32163, Aug 2022. URL: https://doi.org/10.1021/acsomega.2c03378, doi:10.1021/acsomega.2c03378. This article has 108 citations and is from a peer-reviewed journal.
(feng2022polystyrenenanoplasticexposure media 1eee0503): Mei-ling Feng, Juanjuan Luo, Y. Wan, Jiannan Zhang (张剑南), Chunjiao Lu, Maya Wang, Lu Dai, Xiaoqian Cao, Xiaojun Yang, and Yajun Wang. Polystyrene nanoplastic exposure induces developmental toxicity by activating the oxidative stress response and base excision repair pathway in zebrafish (danio rerio). ACS Omega, 7:32153-32163, Aug 2022. URL: https://doi.org/10.1021/acsomega.2c03378, doi:10.1021/acsomega.2c03378. This article has 108 citations and is from a peer-reviewed journal.
(feng2022polystyrenenanoplasticexposure media e296e8ed): Mei-ling Feng, Juanjuan Luo, Y. Wan, Jiannan Zhang (张剑南), Chunjiao Lu, Maya Wang, Lu Dai, Xiaoqian Cao, Xiaojun Yang, and Yajun Wang. Polystyrene nanoplastic exposure induces developmental toxicity by activating the oxidative stress response and base excision repair pathway in zebrafish (danio rerio). ACS Omega, 7:32153-32163, Aug 2022. URL: https://doi.org/10.1021/acsomega.2c03378, doi:10.1021/acsomega.2c03378. This article has 108 citations and is from a peer-reviewed journal.
(feng2022polystyrenenanoplasticexposure pages 7-8): Mei-ling Feng, Juanjuan Luo, Y. Wan, Jiannan Zhang (张剑南), Chunjiao Lu, Maya Wang, Lu Dai, Xiaoqian Cao, Xiaojun Yang, and Yajun Wang. Polystyrene nanoplastic exposure induces developmental toxicity by activating the oxidative stress response and base excision repair pathway in zebrafish (danio rerio). ACS Omega, 7:32153-32163, Aug 2022. URL: https://doi.org/10.1021/acsomega.2c03378, doi:10.1021/acsomega.2c03378. This article has 108 citations and is from a peer-reviewed journal.