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this with annotations you find in gene/protein databases, but these can be outdated or inaccurate.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 requested identity is verified: Q56JH6 corresponds to zebrafish Kit ligand a, encoded by kitlga (historical alias kitla), not the paralog kitlgb and not a similarly named gene from another organism. It is a co-ortholog of mammalian KITLG/stem cell factor (SCF) generated by teleost gene duplication. Cloning, phylogenetic analysis, chromosome mapping, expression, and paralog-specific genetic experiments all support this assignment. The literature therefore agrees with the supplied UniProt description and with assignment to the SCF family and four-helix-cytokine-like structural class. (yao2010kitsystemin pages 2-3, hultman2007geneduplicationof pages 2-3)
Functionally, Kitlga is a signaling cytokine rather than an enzyme, transporter, or structural protein. Its best-established role is to activate the receptor tyrosine kinase Kita on neighboring target cells. This promotes embryonic melanocyte migration and survival and, after pigment-cell injury, activates RAS–MAPK/ERK signaling in melanocyte progenitors to drive regeneration. Additional context-dependent functions include a follicle-cell-to-oocyte signal in the ovary and cooperation with erythropoietin in erythroid progenitor expansion. (hultman2007geneduplicationof pages 1-2, yao2013spatialdistributionand pages 1-2, frantz2023pigmentcellprogenitor pages 11-13, oltova2020zebrafishkitligands pages 4-7)
| Annotation aspect | Best-supported conclusion | Direct evidence/method | Evidence strength/caveat |
|---|---|---|---|
| Identity and paralogy | kitlga, historically kitla, is the Danio rerio Kit-ligand-a co-ortholog of mammalian KITLG/SCF and is distinct from zebrafish kitlgb. The two paralogs arose through teleost duplication; reported sequence identity is approximately 30%. | Cloning from 24-hpf cDNA, 5′/3′ RACE, phylogenetic analysis, chromosome mapping, and paralog-specific expression and loss-of-function studies. (yao2010kitsystemin pages 2-3, hultman2007geneduplicationof pages 2-3) | Strong. Exact-organism molecular and functional evidence supports the identification. The literature does not independently map every experiment to UniProt Q56JH6, but the gene name and aliases match that record. |
| Protein class and location | Kitlga is an SCF-family cytokine ligand, not an enzyme or transporter. It is synthesized as a membrane-associated ligand and can be released extracellularly; alternative transcripts differ around exon 6 and cleavage-associated sequence. Its operative compartment is therefore the producing-cell surface and extracellular or paracrine space. | Sequence and splice-form analysis found exon-6-containing Kitlga transcripts and predicted membrane-cleavage sites; recombinant soluble extracellular Kitlga was biologically active in cell and marrow assays. (hultman2007geneduplicationof pages 2-3, hultman2007geneduplicationof pages 10-11, oltova2020zebrafishkitligands pages 4-7) | Moderate to strong. Cytokine identity and soluble activity are experimentally supported, but direct zebrafish protein-topology imaging, cleavage-site mutagenesis, and endogenous protein-localization data are limited. The four-helix cytokine and SCF-domain assignment is chiefly sequence-based. |
| Receptor specificity and pathway | Kitlga preferentially activates the receptor tyrosine kinase Kita; Kitlgb preferentially activates Kitb. Kitlga–Kita signaling can activate MAPK/ERK, although weak Kitb cross-activation is possible in ovarian assays. | Recombinant ligands, Kita or Kitb expression in COS cells, receptor-phosphorylation Western blots, MAPK assays, and denuded-oocyte or follicle-cell assays established preferential Kitlga-to-Kita and Kitlgb-to-Kitb signaling. (yao2013spatialdistributionand pages 1-2, yao2013spatialdistributionand pages 13-14) | Strong for preferential, not absolute, specificity. Genetic Kita dependence in pigmentation and erythropoiesis independently supports the biochemical result. |
| Embryonic melanocytes | The principal established developmental function is Kita-dependent control of melanocyte number, migration, growth, and survival. Signaling is required before 2 dpf mainly for migration and after 2 dpf for survival. | kitlga, but not kitlgb, morphants phenocopied kita loss; low-dose kitlga knockdown genetically enhanced a sensitized kita allele; kitlga overexpression caused Kita-dependent hyperpigmentation through increased melanocyte number and size. In situ hybridization placed kitlga along the medial trunk migration route at 18–30 hpf and in skin at 4–5 dpf. (hultman2007geneduplicationof pages 1-2, hultman2007geneduplicationof pages 2-3, hultman2007geneduplicationof pages 10-11) | Strong. Convergent expression, loss-of-function, genetic-interaction, overexpression, and receptor-dependence evidence assign this role directly to kitlga rather than kitlgb. |
| Adult melanocyte regeneration and RAS–MAPK | Injury-induced kitlga–Kita signaling drives melanocyte-progenitor differentiation, especially direct differentiation, and increases progenitor ERK activity. Kita loss caused more than an eightfold reduction in direct differentiation and an approximately twofold reduction in asymmetric divisions; kitlga mutants showed similar defects. | scRNA-seq and NicheNetR, three-replicate qRT-PCR, mutant analysis, longitudinal single-cell imaging, melanocyte-lineage ERKKTR imaging, and downstream BRAFV600E rescue were used. After ablation, kitlga rose transiently in skin; ERK activation failed in kita mutants, while BRAFV600E restored regeneration toward wild-type levels. Imaging cohorts were WT n=10, kita(lf) n=9, and kitlga(lf) n=11. (frantz2023pigmentcellprogenitor pages 11-13, frantz2023pigmentcellprogenitor pages 17-19, frantz2023pigmentcellprogenitor pages 9-11, frantz2023pigmentcellprogenitor pages 7-9) | Strong and recent (2023). Wild type restored the full stripe complement within two weeks, whereas kita mutants regenerated a mean 51.4%; an earlier report gave 65.2% for kitlga mutants. Exact kitlga transcript fold change and ERK-sensor magnitude were unavailable in the extracted evidence. (frantz2022stemcellheterogeneity pages 14-20, frantz2023pigmentcellprogenitor pages 7-9) |
| Ovarian localization and function | In preovulatory follicles, kitlga is produced by somatic follicle cells, whereas Kita is oocyte-localized, establishing a follicle-cell-to-oocyte paracrine axis. Kitlga activates oocyte MAPK and suppresses spontaneous oocyte maturation in vitro. | RT-PCR and qPCR across follicular stages, spatial localization, recombinant-ligand assays, receptor phosphorylation, MAPK measurement, and germinal-vesicle-breakdown assays were used. Expression rose from primary to secondary growth, peaked in early vitellogenesis, then declined and was marginal in ovulated oocytes lacking follicle cells. (yao2010kitsystemin pages 2-3, yao2013spatialdistributionand pages 1-2, yao2013spatialdistributionand pages 13-14) | Strong for cell-type localization and in vitro signaling; moderate for whole-animal physiological necessity. Kitlga did not significantly enhance DHP-induced maturation, unlike Kitlgb, demonstrating paralog specialization. |
| Erythroid progenitors and Epo | Kitlga cooperates with erythropoietin (Epo) to expand erythroid progenitors and requires Kita for this response. It acts mainly as a growth or survival co-signal rather than as an enzyme or transporter. | Adult whole-kidney-marrow cultures started at 3×10⁶ cells/ml and were maintained at 2×10⁶ cells/ml; Epo and Kitlga were tested at 100 ng/ml. Kitlga alone had a mild nonsignificant effect, whereas Kitlga plus Epo significantly increased day-7 cell numbers over Epo alone; dexamethasone further enhanced expansion. Embryonic mRNA injection, lcr:EGFP FACS, benzidine staining, gata1a and hbbe1 qPCR, and sparse or kita mutants showed loss of Epo–Kit-ligand cooperation without Kita. (oltova2020zebrafishkitligands pages 12-15, oltova2020zebrafishkitligands pages 9-12, oltova2020zebrafishkitligands pages 7-9, oltova2020zebrafishkitligands pages 4-7) | Moderate. Results combine ex vivo and in vivo evidence but derive from a 2020 bioRxiv preprint; exact effect sizes and P values were unavailable in the extracted text. Soluble and full-length ligand forms differ, and Kitlgb also contributes in vivo. |
| HSC signaling: distinction from Kitlgb and Kitb | kitlga should not be annotated as the principal embryonic HSC-specification ligand. Evidence instead assigns that role mainly to Kitlgb–Kitb, while kitlga–Kita is dominant in pigmentation and contributes to erythropoiesis. | Injected kitlga mRNA did not alter cmyb at 4 dpf; kitb knockdown reduced aortic runx1 and cmyb and caudal-hematopoietic-tissue cmyb. Combined subthreshold kitlgb and osm increased cmyb (p=0.0001), and combined kitb and osmr inhibition reduced HSC markers (p=0.0000009). (mahony2018oncostatinmand pages 1-2, mahony2018oncostatinmand pages 8-11) | Strong caution against paralog conflation. Low Kita expression in HSCs and possible receptor cross-activation mean a minor or context-dependent kitlga contribution cannot be excluded, but direct evidence favors Kitlgb–Kitb for embryonic HSC control. |
Table: Evidence-based annotation of zebrafish kitlga/kitla, separating direct molecular and genetic findings from inference and distinguishing Kitlga–Kita from the paralogous Kitlgb–Kitb system.
Zebrafish retained two Kit-ligand genes following teleost duplication: kitlga/kitla and kitlgb/kitlb. The corresponding receptors are Kita and Kitb. The two ligand paralogs have only approximately 30% sequence identity and have undergone substantial functional partitioning. kitlga was cloned from 24-hours-post-fertilization zebrafish cDNA using RACE and exon-spanning PCR; phylogenetic analysis identified both zebrafish proteins as Kit-ligand co-orthologs, with kitlga and kitlgb located on chromosomes 25 and 4, respectively. (yao2010kitsystemin pages 2-3, hultman2007geneduplicationof pages 2-3)
This distinction is critical. Much of the pigmentation evidence belongs specifically to Kitlga–Kita, whereas embryonic hematopoietic-stem-cell regulation has been assigned predominantly to Kitlgb–Kitb. Results for mammalian KITLG or zebrafish Kitlgb should not automatically be transferred to Q56JH6. (hultman2007geneduplicationof pages 1-2, mahony2018oncostatinmand pages 1-2, mahony2018oncostatinmand pages 8-11)
Kitlga is an SCF-family cytokine that binds and activates a Kit-family receptor tyrosine kinase. Recombinant-ligand experiments, receptor-expression assays in COS cells, receptor-phosphorylation Western blots, and MAPK assays demonstrate a preferred pairing of Kitlga with Kita. Kitlgb preferentially activates Kitb. The specificity is not necessarily absolute: weak Kitlga activation of Kitb was observed in ovarian follicle-cell assays, but the dominant biochemical and genetic relationship is Kitlga→Kita. (yao2013spatialdistributionand pages 1-2, yao2013spatialdistributionand pages 13-14)
Upon Kita activation, the receptor initiates intracellular signaling that includes RAS–RAF–MEK–ERK/MAPK. In adult melanocyte regeneration, live ERK-reporter imaging showed that injury normally increases ERK activity in progenitors; this response failed in kita loss-of-function animals. Expression of constitutively active BRAFV600E downstream of Kita restored regeneration toward wild-type levels, supplying both necessity and downstream-sufficiency evidence for the KIT–RAS/MAPK model. (frantz2023pigmentcellprogenitor pages 11-13)
Sequence and splice-form evidence indicates that Kitlga is initially a membrane-associated cytokine and can be proteolytically released as a soluble extracellular ligand. kitlga transcripts include forms differing around exon 6 and predicted cleavage-associated sequences. Recombinant soluble extracellular Kitlga is biologically active in receptor and marrow-culture assays. Thus, its functional compartment is the producing-cell surface and adjacent extracellular space, where it acts through juxtacrine or paracrine signaling. Direct endogenous-protein imaging and zebrafish cleavage-site mutagenesis remain limited, so exact topology and the relative physiological contributions of soluble versus membrane-bound forms are less firmly established than receptor activity. (hultman2007geneduplicationof pages 10-11, oltova2020zebrafishkitligands pages 9-12, oltova2020zebrafishkitligands pages 4-7)
The supplied InterPro/Pfam annotations—4_helix_cytokine-like_core, SCF, and PF02404—are therefore coherent with the experimentally established signaling role. The domain assignment itself is principally sequence/structure inference; the ligand function is supported directly by genetics and receptor-activation assays.
The strongest classical evidence assigns Kitlga a central role in melanocyte/melanophore development. During embryogenesis, kitlga RNA is present along the medial trunk melanocyte-migration route at approximately 18–30 hpf and later in skin at 4–5 dpf. Other complementary Kitlga/Kita expression domains include the tail bud, ear, and pineal region. (hultman2007geneduplicationof pages 1-2, hultman2007geneduplicationof pages 2-3)
Paralog-specific morpholino knockdown showed that loss of kitlga, but not kitlgb, phenocopied kita deficiency, causing defects in melanocyte migration and later survival. Low-dose kitlga knockdown genetically enhanced a sensitized kita allele, whereas kitlga overexpression caused Kita-dependent hyperpigmentation by increasing melanocyte number and size. Temperature-shift experiments placed the principal Kita requirement before 2 dpf for migration and after 2 dpf for survival. These complementary loss-of-function, interaction, expression, and gain-of-function results make melanocyte regulation the most secure primary annotation for Q56JH6. (hultman2007geneduplicationof pages 1-2, hultman2007geneduplicationof pages 2-3, hultman2007geneduplicationof pages 10-11)
The most important recent exact-gene study located was Frantz et al., published in eLife in April 2023 (DOI and article URL). It combined single-cell RNA sequencing, ligand–receptor inference, qRT-PCR, longitudinal single-cell imaging, mutants, an in-vivo ERK activity reporter, and downstream BRAF activation. No comparably substantive 2024 exact-kitlga study was identified in the retrieved literature. (frantz2023pigmentcellprogenitor pages 11-13, frantz2023pigmentcellprogenitor pages 9-11, frantz2023pigmentcellprogenitor pages 7-9)
Following neocuproine-mediated melanocyte destruction, skin kitlga expression rose transiently and then declined as regeneration progressed. Single-cell data localized ligand expression mainly to fibroblasts and keratinocytes, while kita was expressed in melanocyte progenitors and differentiating intermediates. Wild-type fish restored their full stripe melanocyte complement within two weeks, whereas kita mutants regenerated a mean of only 51.4%; the preceding report gave 65.2% for kitlga mutants. (frantz2022stemcellheterogeneity pages 14-20, frantz2023pigmentcellprogenitor pages 7-9)
Serial imaging found that Kita loss produced more than an eightfold reduction in direct progenitor differentiation and approximately a twofold reduction in asymmetric divisions; kitlga loss caused similar defects. Cohorts comprised wild type n=10, kita(lf) n=9, and kitlga(lf) n=11, analyzed by ANOVA with Dunnett correction. The strongest dependence was in the direct-differentiation route; some cycling progenitor populations were less affected, demonstrating progenitor heterogeneity rather than a universal requirement at every melanocyte-lineage stage. (frantz2023pigmentcellprogenitor pages 17-19, frantz2023pigmentcellprogenitor pages 9-11)
Mechanistically, progenitors had relatively low basal ERK activity, but injury induced Kita-dependent ERK activation. BRAFV600E bypassed receptor loss and increased melanocyte density toward wild-type levels. The current model is therefore that injury induces Kitlga in the skin niche, Kitlga activates Kita on melanocyte progenitors, and Kita–RAS/MAPK signaling biases these cells toward direct differentiation and contributes to asymmetric regenerative divisions. (frantz2023pigmentcellprogenitor pages 11-13, frantz2023pigmentcellprogenitor pages 17-19)
In the zebrafish ovary, kitlga is expressed by somatic follicle cells, while Kita is localized to the oocyte, creating a paracrine follicle-cell-to-oocyte pathway. Expression rises markedly during the transition from primary to rapid secondary growth, peaks in early vitellogenesis, then declines; it is marginal in ovulated oocytes from which follicle cells are absent. Broader RT-PCR detected transcripts in brain, gill, kidney, liver, muscle, ovary, and testis, although transcript detection does not by itself demonstrate active protein signaling in every tissue. (yao2010kitsystemin pages 2-3, yao2013spatialdistributionand pages 13-14)
Recombinant Kitlga preferentially activated Kita and MAPK in denuded oocytes. In vitro, it suppressed spontaneous germinal-vesicle breakdown, but unlike Kitlgb it did not significantly enhance DHP-induced maturation. These findings support a role in folliculogenesis and restraint of premature spontaneous maturation while also demonstrating specialization between the duplicated ligand systems. The evidence for localization and acute in-vitro signaling is strong; whole-animal evidence defining its indispensability at each ovarian stage is less complete. (yao2013spatialdistributionand pages 1-2, yao2013spatialdistributionand pages 13-14)
A 2020 study tested recombinant Kitlga in adult zebrafish whole-kidney-marrow cultures (bioRxiv DOI). Cultures were initiated at 3×10⁶ cells/ml, maintained at 2×10⁶ cells/ml, and treated with Epo and/or Kitlga at 100 ng/ml. Kitlga alone produced a mild, reproducible but nonsignificant effect. Kitlga plus Epo significantly increased day-7 cell numbers over Epo alone, while addition of dexamethasone further promoted erythroid-progenitor expansion and colony formation. RNA sequencing associated the response with erythroid, translation, and cell-cycle programs. (oltova2020zebrafishkitligands pages 7-9, oltova2020zebrafishkitligands pages 4-7, oltova2020zebrafishkitligands pages 9-12)
In embryos, full-length kitlga mRNA cooperated with epo to increase erythroid readouts at 72 hpf, including lcr:EGFP-positive cells, hemoglobinization, and erythroid-gene expression. This cooperation disappeared in kita/sparse mutants, as did induction of gata1a and β-globin hbbe1, indicating receptor dependence. Soluble and full-length ligand forms were not equivalent, and Kitlgb also contributed in vivo. These results support annotation as an erythroid growth/survival co-signal, especially under expansion or stress conditions, rather than as a uniquely lineage-determining factor. Because this source is a preprint and exact effect sizes were unavailable in the retrieved text, confidence is moderate rather than equivalent to the pigmentation evidence. (oltova2020zebrafishkitligands pages 12-15, oltova2020zebrafishkitligands pages 9-12)
A crucial qualification is that Kitlga is not the principal demonstrated embryonic HSC-specification ligand. Injected kitlga did not alter cmyb expression at 4 dpf, whereas Kitlgb–Kitb controlled HSC/HSPC markers. Combined subthreshold kitlgb and osm increased cmyb with p=0.0001, and combined kitb/osmr inhibition reduced HSC markers with p=9×10⁻⁷. Low Kita expression and possible receptor cross-activation leave room for minor context-dependent effects, but the authoritative interpretation is functional partitioning: Kitlga–Kita dominates pigmentation and contributes to erythropoiesis; Kitlgb–Kitb is more central to embryonic HSC control. (mahony2018oncostatinmand pages 1-2, mahony2018oncostatinmand pages 8-11)
Kitlga currently has value primarily as a research tool and model-system pathway, rather than as a deployed clinical or aquaculture product:
A defensible concise annotation is:
Kit ligand a is a membrane-associated and releasable extracellular SCF-family cytokine that preferentially activates the Kita receptor tyrosine kinase. In zebrafish, Kitlga–Kita signaling controls embryonic melanocyte migration and survival and is reactivated after pigment-cell injury to stimulate RAS/MAPK-dependent melanocyte-progenitor differentiation. It also functions as a somatic-follicle-cell signal to the oocyte and cooperates with erythropoietin in erythroid-progenitor expansion.
The pigmentation and regeneration assignments have the strongest direct support. Ovarian receptor specificity is also well demonstrated biochemically. Erythroid activity is supported by ex-vivo and embryonic experiments but rests partly on preprint evidence. Membrane attachment, proteolytic release, and the four-helix cytokine fold are consistent with sequence and soluble-protein activity, but endogenous zebrafish protein-topology data remain comparatively limited. Finally, embryonic HSC findings must not be imported from the separate Kitlgb–Kitb pathway.
References
(yao2010kitsystemin pages 2-3): Kai Yao and Wei Ge. Kit system in the zebrafish ovary: evidence for functional divergence of two isoforms of kit (kita and kitb) and kit ligand (kitlga and kitlgb) during folliculogenesis1. Jun 2010. URL: https://doi.org/10.1095/biolreprod.109.082644, doi:10.1095/biolreprod.109.082644. This article has 23 citations and is from a peer-reviewed journal.
(hultman2007geneduplicationof pages 2-3): Keith A Hultman, Nathan Bahary, Leonard I Zon, and Stephen L Johnson. Gene duplication of the zebrafish kit ligand and partitioning of melanocyte development functions to kit ligand a. PLoS Genetics, 3:e17, Jan 2007. URL: https://doi.org/10.1371/journal.pgen.0030017, doi:10.1371/journal.pgen.0030017. This article has 125 citations and is from a domain leading peer-reviewed journal.
(hultman2007geneduplicationof pages 1-2): Keith A Hultman, Nathan Bahary, Leonard I Zon, and Stephen L Johnson. Gene duplication of the zebrafish kit ligand and partitioning of melanocyte development functions to kit ligand a. PLoS Genetics, 3:e17, Jan 2007. URL: https://doi.org/10.1371/journal.pgen.0030017, doi:10.1371/journal.pgen.0030017. This article has 125 citations and is from a domain leading peer-reviewed journal.
(yao2013spatialdistributionand pages 1-2): Kai Yao and Wei Ge. Spatial distribution and receptor specificity of zebrafish kit system - evidence for a kit-mediated bi-directional communication system in the preovulatory ovarian follicle. PLoS ONE, 8:e56192, Feb 2013. URL: https://doi.org/10.1371/journal.pone.0056192, doi:10.1371/journal.pone.0056192. This article has 18 citations and is from a peer-reviewed journal.
(frantz2023pigmentcellprogenitor pages 11-13): William Tyler Frantz, Sharanya Iyengar, James Neiswender, Alyssa Cousineau, René Maehr, and Craig J Ceol. Pigment cell progenitor heterogeneity and reiteration of developmental signaling underlie melanocyte regeneration in zebrafish. eLife, Apr 2023. URL: https://doi.org/10.7554/elife.78942, doi:10.7554/elife.78942. This article has 12 citations and is from a domain leading peer-reviewed journal.
(oltova2020zebrafishkitligands pages 4-7): Jana Oltova, Ondrej Svoboda, Olga Machonova, Petra Svatonova, David Traver, Michal Kolar, and Petr Bartunek. Zebrafish kit ligands cooperate with erythropoietin to promote erythroid cell expansion. bioRxiv, Feb 2020. URL: https://doi.org/10.1101/2020.02.03.931634, doi:10.1101/2020.02.03.931634. This article has 9 citations.
(hultman2007geneduplicationof pages 10-11): Keith A Hultman, Nathan Bahary, Leonard I Zon, and Stephen L Johnson. Gene duplication of the zebrafish kit ligand and partitioning of melanocyte development functions to kit ligand a. PLoS Genetics, 3:e17, Jan 2007. URL: https://doi.org/10.1371/journal.pgen.0030017, doi:10.1371/journal.pgen.0030017. This article has 125 citations and is from a domain leading peer-reviewed journal.
(yao2013spatialdistributionand pages 13-14): Kai Yao and Wei Ge. Spatial distribution and receptor specificity of zebrafish kit system - evidence for a kit-mediated bi-directional communication system in the preovulatory ovarian follicle. PLoS ONE, 8:e56192, Feb 2013. URL: https://doi.org/10.1371/journal.pone.0056192, doi:10.1371/journal.pone.0056192. This article has 18 citations and is from a peer-reviewed journal.
(frantz2023pigmentcellprogenitor pages 17-19): William Tyler Frantz, Sharanya Iyengar, James Neiswender, Alyssa Cousineau, René Maehr, and Craig J Ceol. Pigment cell progenitor heterogeneity and reiteration of developmental signaling underlie melanocyte regeneration in zebrafish. eLife, Apr 2023. URL: https://doi.org/10.7554/elife.78942, doi:10.7554/elife.78942. This article has 12 citations and is from a domain leading peer-reviewed journal.
(frantz2023pigmentcellprogenitor pages 9-11): William Tyler Frantz, Sharanya Iyengar, James Neiswender, Alyssa Cousineau, René Maehr, and Craig J Ceol. Pigment cell progenitor heterogeneity and reiteration of developmental signaling underlie melanocyte regeneration in zebrafish. eLife, Apr 2023. URL: https://doi.org/10.7554/elife.78942, doi:10.7554/elife.78942. This article has 12 citations and is from a domain leading peer-reviewed journal.
(frantz2023pigmentcellprogenitor pages 7-9): William Tyler Frantz, Sharanya Iyengar, James Neiswender, Alyssa Cousineau, René Maehr, and Craig J Ceol. Pigment cell progenitor heterogeneity and reiteration of developmental signaling underlie melanocyte regeneration in zebrafish. eLife, Apr 2023. URL: https://doi.org/10.7554/elife.78942, doi:10.7554/elife.78942. This article has 12 citations and is from a domain leading peer-reviewed journal.
(frantz2022stemcellheterogeneity pages 14-20): William Tyler Frantz, Sharanya Iyengar, James Neiswender, Alyssa Cousineau, Rene Maehr, and Craig J. Ceol. Stem cell heterogeneity and reiteration of developmental signaling underlie melanocyte regeneration in zebrafish. BioRxiv, Apr 2022. URL: https://doi.org/10.1101/2022.04.27.489712, doi:10.1101/2022.04.27.489712. This article has 2 citations.
(oltova2020zebrafishkitligands pages 12-15): Jana Oltova, Ondrej Svoboda, Olga Machonova, Petra Svatonova, David Traver, Michal Kolar, and Petr Bartunek. Zebrafish kit ligands cooperate with erythropoietin to promote erythroid cell expansion. bioRxiv, Feb 2020. URL: https://doi.org/10.1101/2020.02.03.931634, doi:10.1101/2020.02.03.931634. This article has 9 citations.
(oltova2020zebrafishkitligands pages 9-12): Jana Oltova, Ondrej Svoboda, Olga Machonova, Petra Svatonova, David Traver, Michal Kolar, and Petr Bartunek. Zebrafish kit ligands cooperate with erythropoietin to promote erythroid cell expansion. bioRxiv, Feb 2020. URL: https://doi.org/10.1101/2020.02.03.931634, doi:10.1101/2020.02.03.931634. This article has 9 citations.
(oltova2020zebrafishkitligands pages 7-9): Jana Oltova, Ondrej Svoboda, Olga Machonova, Petra Svatonova, David Traver, Michal Kolar, and Petr Bartunek. Zebrafish kit ligands cooperate with erythropoietin to promote erythroid cell expansion. bioRxiv, Feb 2020. URL: https://doi.org/10.1101/2020.02.03.931634, doi:10.1101/2020.02.03.931634. This article has 9 citations.
(mahony2018oncostatinmand pages 1-2): Christopher B. Mahony, Corentin Pasche, and Julien Y. Bertrand. Oncostatin m and kit-ligand control hematopoietic stem cell fate during zebrafish embryogenesis. Stem Cell Reports, 10:1920-1934, Jun 2018. URL: https://doi.org/10.1016/j.stemcr.2018.04.016, doi:10.1016/j.stemcr.2018.04.016. This article has 42 citations and is from a domain leading peer-reviewed journal.
(mahony2018oncostatinmand pages 8-11): Christopher B. Mahony, Corentin Pasche, and Julien Y. Bertrand. Oncostatin m and kit-ligand control hematopoietic stem cell fate during zebrafish embryogenesis. Stem Cell Reports, 10:1920-1934, Jun 2018. URL: https://doi.org/10.1016/j.stemcr.2018.04.016, doi:10.1016/j.stemcr.2018.04.016. This article has 42 citations and is from a domain leading peer-reviewed journal.