Affinage

FGF8

Fibroblast growth factor 8 · UniProt P55075

Length
233 aa
Mass
26.5 kDa
Annotated
2026-04-28
100 papers in source corpus 51 papers cited in narrative 51 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

FGF8 is a secreted fibroblast growth factor that functions as a dose-dependent morphogen and organizer signal essential for gastrulation, midbrain-hindbrain boundary maintenance, limb outgrowth, cardiac development, otic placode induction, kidney nephrogenesis, and neural crest specification. FGF8 isoforms exhibit differential receptor specificity—FGF8b and FGF8c activate FGFR2c, FGFR3c, and FGFR4, while FGF8b signals through FGFR1 at the midbrain-hindbrain boundary to drive Ras-ERK pathway activation and cerebellar differentiation, and through PI3K/Akt in limb mesenchyme to promote cell survival via MKP3 induction (PMID:8582274, PMID:15294862, PMID:12766772, PMID:15221377). Its extracellular signaling range is controlled by target-cell endocytosis and lysosomal degradation, and its transcription is directly repressed by retinoic acid through RAR-mediated recruitment of PRC2 and NCOR1/2 corepressors to a conserved RARE, while being positively regulated by Pax2, Six1/Eya1, Tbx1, Jagged1/Notch, and the androgen receptor (PMID:15498491, PMID:25053430, PMID:27506116, PMID:11704761, PMID:21364285, PMID:12140757). Null or hypomorphic Fgf8 mutations cause gastrulation failure due to blocked cell migration, loss of midbrain and cerebellum through ectopic apoptosis, limb skeletal defects, absent nephrogenesis, and cardiac outflow tract malformations, with non-linear dose-response relationships in which both excess and deficiency of FGF8 increase cell death (PMID:10421635, PMID:12736208, PMID:11101845, PMID:16049111, PMID:12574514).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 1995 High

    Establishing that FGF8 signals through specific FGFR isoforms resolved the receptor selectivity question: FGF8b/c activate 'c' splice forms of FGFR2-4 but not 'b' splice forms, while FGF8a lacks detectable activity, defining isoform-specific receptor engagement.

    Evidence In vitro receptor activation assays with recombinant FGF8 isoforms against panels of FGFR splice variants

    PMID:8582274

    Open questions at the time
    • FGF8 binding to FGFR1c was not detected here but later implicated genetically
    • structural basis for isoform-specific receptor selectivity unknown
    • heparan sulfate cofactor requirements not addressed
  2. 1996 High

    FGF8 was established as a sufficient and necessary endogenous limb inducer, resolving whether any single FGF could initiate and maintain limb outgrowth: FGF8 bead application induced ectopic limbs, maintained Shh expression, and replaced AER function.

    Evidence FGF8 bead implantation in chick embryo flank and AER-removed limb buds with molecular readouts

    PMID:8548816 PMID:8674413

    Open questions at the time
    • whether FGF8 is the sole endogenous AER-FGF or acts redundantly with FGF4 was not resolved
    • downstream intracellular pathway not yet identified
  3. 1998 High

    Genetic studies placed FGF8 as a maintenance factor (not initiator) of the midbrain-hindbrain organizer and defined its epistatic relationship with Pax2.1: zebrafish ace mutants lose MHB marker expression during somitogenesis while Fgf8 is activated independently of Pax2.1.

    Evidence Zebrafish ace (fgf8) mutant phenotyping and genetic epistasis with no isthmus (pax2.1) mutants

    PMID:9609821

    Open questions at the time
    • how FGF8 maintains MHB gene expression mechanistically was not known
    • whether FGF8 acts cell-autonomously at MHB not resolved
  4. 1999 High

    FGF8 was shown to be essential for gastrulation cell migration: null embryos undergo EMT but mesoderm cells fail to migrate from the primitive streak, establishing FGF8 as a motility factor rather than an EMT inducer.

    Evidence Mouse Fgf8-/- knockout with cellular and molecular phenotype analysis

    PMID:10421635

    Open questions at the time
    • mechanism by which FGF8 promotes migration (chemotaxis vs. chemokinesis) unresolved
    • whether FGF4 loss contributes to the phenotype was addressed later
  5. 1999 High

    Gain-of-function experiments established that FGF8 patterns the midbrain-hindbrain by repressing Otx2 and inducing Gbx2/En1, creating a negative feedback that positions the isthmic organizer.

    Evidence FGF8 bead implantation in chick and mouse brain explants; Wnt1-Fgf8b transgenic mice; in situ hybridization for multiple markers

    PMID:10021338 PMID:10518499

    Open questions at the time
    • direct vs. indirect regulation of Otx2 repression unclear
    • whether concentration thresholds determine different gene responses not tested quantitatively
  6. 2000 High

    Conditional Fgf8 knockout in the AER demonstrated that FGF8 is required for specific proximal and distal limb skeletal elements, while zebrafish studies showed FGF8 is required for earliest cardiac gene expression (nkx2.5, gata4), broadening its organogenesis roles.

    Evidence Mouse conditional AER-Fgf8 knockout with skeletal analysis; zebrafish ace mutant with FGF8 RNA/bead rescue of cardiac markers

    PMID:10603341 PMID:11101845

    Open questions at the time
    • compensation by other AER-FGFs not fully delineated
    • cardiac mechanism downstream of FGF8 not resolved
  7. 2001 High

    FGF8 was shown to generate nested target gene expression domains (pea3 close, erm broad), providing molecular evidence for morphogen gradient readout, and Pax2 was identified as necessary and sufficient for MHB Fgf8 induction.

    Evidence Zebrafish ace mutant and ectopic Fgf8 expression for target gene analysis; mouse gain/loss-of-function for Pax2-Fgf8 regulation

    PMID:11413000 PMID:11704761

    Open questions at the time
    • whether graded target gene response reflects graded FGF8 protein or differential pathway sensitivity unknown
    • direct Pax2 binding to Fgf8 regulatory elements not shown
  8. 2002 High

    Multiple transcriptional inputs to Fgf8 were defined: the androgen receptor directly activates Fgf8 via promoter AREs in prostate cancer cells, while unliganded and liganded RARα bind distinct elements to drive different Fgf8 isoforms, and BMP2 cooperates with FGF8 in cardiac induction.

    Evidence ChIP for AR at FGF8 promoter in LNCaP cells; RAR binding/mutagenesis of Fgf8 promoter; chick endoderm ablation/FGF8 rescue with BMP2 co-application

    PMID:11934859 PMID:12054865 PMID:12140757

    Open questions at the time
    • whether AR-driven FGF8 contributes to tumor progression in vivo unresolved
    • interplay between RA repression and AR activation on the same promoter not tested
  9. 2003 High

    The downstream signaling logic was clarified: FGF8 from the AER activates PI3K/Akt (not ERK) in limb mesenchyme to induce MKP3, which in turn dephosphorylates ERK to promote cell survival; separately, allelic series showed non-linear dose-response where both excess and deficiency of FGF8 increase apoptosis.

    Evidence Pathway inhibitors, siRNA, and constitutively active Mek1 in chick/mouse/zebrafish limbs; multiple Fgf8 alleles in mouse forebrain with cell death quantification

    PMID:12574514 PMID:12766772

    Open questions at the time
    • identity of the concentration-proportionate intracellular inhibitor unknown
    • how PI3K/Akt vs. Ras-ERK pathway choice is made in different tissues not resolved
  10. 2004 High

    FGF8 morphogen range was shown to be controlled by receptor-mediated endocytosis: blocking internalization extended extracellular FGF8 spread and expanded target gene domains, establishing restrictive clearance as the range-limiting mechanism.

    Evidence Live imaging of epitope-tagged Fgf8 in zebrafish embryos with pharmacological endocytosis inhibition

    PMID:15498491

    Open questions at the time
    • relative contribution of diffusion rate vs. clearance rate to gradient shape not quantified
    • whether HSPG binding modulates clearance not tested
  11. 2004 High

    Isoform-specific signaling was resolved at the MHB: FGF8b activates Ras-ERK to specify cerebellar fate, while FGF8a does not activate ERK, and dominant-negative Ras converts cerebellar to tectal fate, defining the critical downstream pathway for brain patterning.

    Evidence In ovo electroporation of dominant-negative Ras and isoform-specific siRNA in chick; ERK phosphorylation analysis

    PMID:15294862

    Open questions at the time
    • structural basis for differential ERK activation by FGF8a vs. FGF8b unknown
    • downstream ERK targets in cerebellar specification not identified
  12. 2005 High

    Tissue-specific conditional knockouts revealed FGF8's essential roles in kidney nephrogenesis (cooperating with WNT4 to induce Lim1 for mesenchyme survival), olfactory neurogenesis, otic induction (as upstream element in an FGF cascade), and neural crest specification (converging with WNT on Pax3).

    Evidence Mouse conditional Fgf8 knockouts in metanephric mesenchyme, anterior neural structures; chick/mouse compound Fgf3/Fgf8 mutants for otic studies; Xenopus epistasis for neural crest

    PMID:15691759 PMID:15741321 PMID:16049111 PMID:16267092

    Open questions at the time
    • direct FGF8 targets in nephron progenitors not identified
    • whether FGF8 acts as morphogen gradient or binary signal in kidney unclear
  13. 2006 High

    Tissue-specific Fgf8 inactivation dissected mesodermal vs. endodermal FGF8 roles in heart development: mesodermal FGF8 provides autocrine signaling for outflow tract alignment and Isl1/Mef2c regulation, while endodermal FGF8 is required for outflow tract septation.

    Evidence Multiple tissue-specific Cre conditional Fgf8 knockouts in mouse with cardiac morphology and marker gene analysis

    PMID:16720879

    Open questions at the time
    • which FGF receptors mediate autocrine signaling in anterior heart field not identified
    • whether FGF8 acts directly on neural crest or indirectly through cardiac mesoderm unclear
  14. 2011 High

    FGF8 was placed in a Tbx1-Six1/Eya1-Fgf8 genetic pathway for cardiocraniofacial morphogenesis, and shown to maintain MHB lineage restriction through cell-autonomous effects on cell sorting after initial Gbx2-dependent boundary establishment.

    Evidence Mouse Six1/Eya1 compound knockout with ChIP for direct Fgf8 regulation; Gbx2CreER fate mapping with conditional Fgf8 deletion

    PMID:21266408 PMID:21364285

    Open questions at the time
    • Six1/Eya1 binding site in Fgf8 regulatory region not mapped at base-pair resolution
    • mechanism by which FGF8 controls cell sorting/adhesion properties unknown
  15. 2014 High

    The mechanism of RA-mediated Fgf8 repression was resolved: RA promotes RAR binding to a conserved RARE upstream of Fgf8, recruits PRC2 and H3K27me3, and releases the co-activator RERE, establishing a direct epigenetic silencing mechanism.

    Evidence ChIP for H3K27me3, PRC2, and RERE at Fgf8 RARE in mouse embryo trunk; transgenic Fgf8-lacZ reporter with RARE deletion

    PMID:25053430

    Open questions at the time
    • whether PRC2 recruitment is sufficient or only contributory to repression not tested
    • kinetics of chromatin remodeling at Fgf8 locus unknown
  16. 2016 High

    NCOR1 and NCOR2 were identified as redundant corepressors mediating RA-dependent Fgf8 silencing, recruited specifically to the Fgf8 RARE in an RA-dependent manner, completing the corepressor arm of the RA-Fgf8 regulatory circuit.

    Evidence CRISPR/Cas9 Ncor1/Ncor2 double knockout; ChIP for NCOR1/2 at Fgf8 RARE; CRISPR deletion of Fgf8 RARE; embryo phenotyping

    PMID:27506116

    Open questions at the time
    • whether additional corepressors contribute beyond NCOR1/2 unknown
    • interplay between PRC2 and NCOR1/2 at the Fgf8 locus not dissected

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the structural basis for FGF8 isoform-specific receptor activation, the identity of concentration-dependent intracellular inhibitors that generate the non-linear apoptotic dose-response, and how tissue-specific transcriptional inputs (AR, RAR, Pax2, Six1/Eya1, Notch) are integrated at the Fgf8 locus in different developmental contexts.
  • no crystal structure of FGF8b-FGFR complex explaining isoform specificity
  • identity of concentration-proportionate apoptosis inhibitor unknown
  • integrated cis-regulatory logic of the Fgf8 locus not mapped comprehensively

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0048018 receptor ligand activity 5 GO:0060089 molecular transducer activity 3
Localization
GO:0005576 extracellular region 3
Pathway
R-HSA-1266738 Developmental Biology 8 R-HSA-162582 Signal Transduction 4 R-HSA-74160 Gene expression (Transcription) 4
Partners
FGF3FGF4FGFR1FGFR2FGFR3FGFR4PAX2SHH

Evidence

Reading pass · 51 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1995 FGF8 isoforms b and c activate the 'c' splice forms of FGFR2, FGFR3, and FGFR4, but not the 'b' splice forms of FGFR1-3 or the 'c' splice form of FGFR1. FGF8a shows no detectable receptor activation activity, indicating isoform-specific receptor binding. In vitro receptor activation assay with recombinant FGF8 protein isoforms Development (Cambridge, England) High 8582274
1996 FGF8 functions as an endogenous inducer of chick limb formation, expressed in intermediate mesoderm to trigger forelimb development, then initiates Fgf8 expression in the overlying ectoderm, promotes outgrowth and Sonic hedgehog expression in lateral plate mesoderm, and maintains mesoderm outgrowth and Shh expression in the established limb bud. Bead implantation of recombinant FGF8 protein in chick embryos; expression analysis Cell High 8548816
1996 FGF8 application to the flank induces additional limbs in chick embryos, can replace the apical ectodermal ridge to maintain Shh expression and outgrowth, and continuous misexpression causes limb truncations and skeletal alterations. FGF8 protein bead application to chick embryo flank; AER replacement assay Development (Cambridge, England) High 8674413
1998 Fgf8 is required to maintain (but not initiate) expression of Pax2.1 and other marker genes at the midbrain-hindbrain boundary organizer during somitogenesis. Fgf8 is activated independently of Pax2.1 in adjacent domains. Fgf8 also polarizes the midbrain. Zebrafish acerebellar (ace) loss-of-function mutant analysis; genetic epistasis with no isthmus (Pax2.1) mutants Development (Cambridge, England) High 9609821
1998 FGFR2 signaling is essential for a reciprocal regulation loop between FGF8 and FGF10 during limb induction: in Fgfr2 mutants, Fgf8 expression is absent in presumptive limb ectoderm and Fgf10 is downregulated in underlying mesoderm, preventing limb bud formation. Conditional mouse knockout of Fgfr2 (deletion of immunoglobulin-like domain III); expression analysis of Fgf8 and Fgf10 Development (Cambridge, England) High 9435295
1999 FGF8 bead implantation in chick prospective caudal diencephalon or midbrain induces ectopic isthmic organizers by repressing Otx2 and inducing En1, Fgf8, and Wnt1 expression. This suggests a negative feedback loop between Fgf8 and Otx2 in patterning the midbrain and anterior hindbrain. FGF8-bead implantation in chick embryo neural tube; in situ hybridization for marker genes Development (Cambridge, England) High 10021338
1999 In the mouse embryo, Fgf8 null embryos fail to express Fgf4 in the primitive streak. In the absence of FGF8 and FGF4, epiblast cells undergo epithelial-to-mesenchymal transition but fail to migrate away from the streak, resulting in absence of embryonic mesoderm and endoderm. Fgf8 is thus essential for cell migration during gastrulation. Mouse Fgf8 knockout (Fgf8-/-) phenotypic analysis; expression analysis of Fgf4 and neuroectoderm markers Genes & development High 10421635
1999 In mouse embryos, FGF8 functions as a left determinant for left-right axis specification, contrasting with its role as a right determinant reported in chick, demonstrating species-specific pathway differences. Genetic analysis of Fgf8 mutant mouse embryos; comparison with chick pathway Science (New York, N.Y.) High 10411502
1999 En1 expression in the avian neural plate is induced by FGF4 (from notochord), and subsequently En1 induces Fgf8 expression in the isthmus. FGF8 then maintains patterns of gene expression including En1 and Pax2 in posterior midbrain and provides mitogenic stimulation. Tissue recombination explants; retroviral ectopic expression of En1; FGF8 protein bead implantation in avian embryo Development (Cambridge, England) High 9927596
1999 FGF8b-soaked beads in mouse embryo forebrain/midbrain explants induce hindbrain gene Gbx2, repress Otx2, and alter Wnt1 expression. Wnt1-Fgf8b transgenic mice show ectopic transformation of midbrain and caudal forebrain to anterior hindbrain fate through Gbx2 expansion and Otx2 repression. FGF8b bead treatment of mouse brain explants; Wnt1-Fgf8b transgenic mice; in situ hybridization Development (Cambridge, England) High 10518499
2000 Conditional disruption of Fgf8 in the mouse forelimb AER reveals that Fgf8 is required for formation of the stylopod, anterior zeugopod and autopod, and that its loss alters expression of other Fgf genes, Shh, and Bmp2. Conditional mouse Fgf8 knockout in forelimb AER; skeletal analysis and marker gene expression Nature genetics High 11101845
2000 Fgf8 is expressed in zebrafish cardiac precursors and is required for the earliest stages of nkx2.5 and gata4 (but not gata6) expression. Injection of fgf8 RNA or implantation of FGF8-coated beads into the heart primordium restores cardiac gene expression in ace mutants. Zebrafish ace/fgf8 mutant analysis; fgf8 RNA rescue; FGF8 bead implantation; pharmacological FGF inhibition Development (Cambridge, England) High 10603341
2001 Zebrafish pea3 and erm (ETS transcription factors) are direct transcriptional targets of FGF8 signaling: their expression is abolished in fgf8 mutants in all FGF8-dependent tissues, is abolished by pharmacological FGF pathway inhibition, and is induced by ectopic Fgf8 expression. FGF8 induces a nested expression pattern with pea3 close to the source and erm in a broader domain. Zebrafish fgf8 (ace) mutant analysis; pharmacological inhibition; ectopic Fgf8 expression; in situ hybridization Current biology : CB High 11413000
2001 Pax2 is necessary and sufficient for induction of FGF8 at the mid/hindbrain boundary, partly by regulating Pax5/8 expression. A network including En1, Otx2, Gbx2, Grg4, Wnt1 and Wnt4 further refines FGF8 expression domain and level through opposing effects on Pax2 activity. Gain- and loss-of-function experiments in mouse; in situ hybridization; genetic epistasis Nature neuroscience High 11704761
2001 En2 and Gbx2 are the first genes induced by FGF8 in mouse diencephalic and midbrain explants. EN transcription factors are required for FGF8-mediated induction of Pax5 but not Pax6 repression. GBX2 acts upstream of FGF8 in repressing Otx2 and downstream of FGF8 in repression of Wnt1. FGF8 bead treatment of mouse brain explants from wild-type and En1/2 double mutants and Gbx2 mutants; epistasis analysis Development (Cambridge, England) High 11124114
2001 Zebrafish fgf3 and fgf8 are co-expressed in hindbrain rhombomere 4 and together are required for otic placode induction: disruption of either alone causes moderate reduction in otic vesicle size, but combined fgf3 morpholino knockdown in fgf8 (ace) mutants causes severe reduction or complete loss of otic tissue and failure of pax8 and pax2.1 expression. Zebrafish fgf8 ace mutant combined with fgf3 antisense morpholino knockdown; in situ hybridization for otic markers Developmental biology High 11437442
2002 In avian cardiogenesis, Fgf8 is expressed in endoderm adjacent to precardiac mesoderm and can rescue Nkx2.5 and Mef2c expression after endoderm removal. Ectopic FGF8 induces ectopic cardiac markers only where BMP signaling is also present, demonstrating cooperativity between FGF8 and BMP signaling in cardiogenesis. Fgf8 expression is regulated by BMP2 levels. Endoderm ablation and FGF8 rescue assay in chick; ectopic FGF8 bead application; BMP2 application Development (Cambridge, England) High 11934859
2002 Fgf8 conditional knockout in mouse mes/met results in failure to maintain Wnt1, Fgf17, Fgf18, and Gbx2 expression, followed by ectopic cell death in the mes/met between 7 and 30 somite stages, and subsequent deletion of midbrain and cerebellum. FGF8 is part of a gene regulatory network essential for cell survival in the mes/met. Conditional Fgf8 knockout in mouse mes/met; molecular marker analysis; cell death assays; comparison with Wnt1-null and En1-null phenotypes Development (Cambridge, England) High 12736208
2002 FGF3 and FGF8, co-expressed in zebrafish rhombomere 4, are together required for the development of adjacent rhombomeres (r5 and r6). Transplantation of r4 cells or misexpression of either FGF3 or FGF8 can induce r5/r6 markers, demonstrating FGF-mediated inter-rhombomere signaling. Zebrafish fgf8 (ace) mutant; fgf3 morpholino knockdown; r4 cell transplantation; FGF misexpression Development (Cambridge, England) High 12135921
2003 MKP3 (MAPK phosphatase-3) is induced in limb mesenchyme by FGF8 signaling from the AER through the PI3K/Akt pathway (not MAPK/ERK). High phospho-ERK is found in the AER where Mkp3 is excluded, while phospho-Akt is detected only in the mesenchyme. MKP3 mediates the anti-apoptotic, proliferative effect of AER-derived FGF8; constitutively active Mek1 or Mkp3 siRNA knockdown induces mesenchymal apoptosis. In situ hybridization; FGF8 signaling pathway inhibitors; siRNA knockdown of Mkp3; constitutively active Mek1 misexpression; phospho-protein immunostaining in chick, mouse, and zebrafish Nature cell biology High 12766772
2003 Fgf8 conditional knockout in mouse midbrain/hindbrain using different Cre drivers reveals that either eliminating or increasing Fgf8 expression increases apoptosis, whereas reducing expression has the opposite effect, suggesting an FGF8-dependent cell-survival pathway is negatively regulated by concentration-proportionate intracellular inhibitors. Multiple Fgf8 alleles (null, hypomorphic, conditional) in mouse; cell death quantification in forebrain Proceedings of the National Academy of Sciences of the United States of America High 12574514
2004 FGF8 spreading through zebrafish neuroectoderm is controlled by endocytosis and lysosomal degradation ('restrictive clearance'). Inhibition of internalization causes FGF8 protein to accumulate extracellularly, spread further, and activate target gene expression over greater distance; enhanced internalization shortens signaling range. FGF8 spreads extracellularly by diffusion. Live imaging of epitope-tagged Fgf8 in living zebrafish embryos; pharmacological inhibition of endocytosis; target gene expression analysis Current biology : CB High 15498491
2004 The Fgf8 signal causes cerebellar differentiation through activation of the Ras-ERK signaling pathway. Fgf8b (stronger signal) activates ERK while Fgf8a does not. Dominant-negative Ras (RasS17N) converts metencephalic alar plate fate from cerebellum to tectum and cancels Fgf8b effects. Disruption of Fgf8b (but not Fgf8a) by siRNA leads to posterior extension of Otx2 expression domain. In ovo electroporation of dominant-negative Ras and siRNA in chick; ERK phosphorylation analysis; isoform-specific siRNA knockdown Development (Cambridge, England) High 15294862
2004 When both Fgf4 and Fgf8 are inactivated in the mouse AER, limb bud mesenchyme fails to survive, leading to a prolonged period of increased apoptosis and failure to form distal limb structures. Shh and Fgf10 expression is nearly abolished in double mutants. Fgf4 is responsible for partial compensation of distal limb development when Fgf8 alone is absent. Conditional mouse double knockout of Fgf4 and Fgf8 in AER; skeletal analysis; apoptosis assays; marker gene expression Developmental biology High 15328019
2005 FGF8 from hindbrain rhombomere 4 region is required for zebrafish otic placode induction, maintenance, and inner ear patterning. FGF8-coated beads implanted near the otic placode can increase ear size, but competence to respond is restricted. Joint inactivation of fgf3 and fgf8 (by mutation or morpholino) causes ear-less embryos, mimicking pharmacological FGF inhibition. Zebrafish ace/fgf8 mutant; antisense morpholino; FGF8 bead implantation; cell transplantation; pharmacological FGF inhibition Mechanisms of development High 12385757
2005 Pan-mesodermal conditional Fgf8 knockout in mouse reveals that FGF8 is not required for somitogenesis but is essential for kidney development: loss of Fgf8 in metanephric mesenchyme causes aberrant cell death, absence of Wnt4 and Lim1 expression, and failure of nephrogenesis. FGF8 and WNT4 function together to induce Lim1 expression for mesenchyme survival and tubulogenesis. T-Cre conditional mouse Fgf8 knockout; renal histology; marker gene expression; comparison with Wnt4 null mutants Development (Cambridge, England) High 16049111
2005 In chick and mouse, endodermal FGF8 acts upstream in an FGF signaling cascade for otic induction: FGF8 in chick endoderm is sufficient and necessary for expression of mesodermal FGF19, which then induces neural ectoderm to express WNT8c and FGF3. In mouse, otic induction fails in Fgf3 null/Fgf8 hypomorphic embryos with reduced mesodermal Fgf10. FGF8 bead application and morpholino knockdown in chick; mouse Fgf3/Fgf8 compound mutant analysis Genes & development High 15741321
2005 Fgf8 expression at the nasal pit rim is required for olfactory epithelium neurogenesis and nasal cavity development. Loss of Fgf8 in anterior neural structures causes high apoptosis in the Fgf8-expressing domain, cessation of nasal cavity invagination, and loss of virtually all olfactory neuronal cell types. Conditional Fgf8 knockout in anterior neural structures in mouse; apoptosis analysis; cell type marker expression Development (Cambridge, England) High 16267092
2005 FGF8 from inner hair cells signals through FGFR3 to induce pillar cell fate in the organ of Corti and simultaneously inhibit outer hair cell development. Deletion of Fgf8 or inhibition of Fgf8-Fgfr3 binding causes pillar cell defects; overexpression induces ectopic pillar cells and inhibits outer hair cell fate. Some effects are reversible, suggesting PC differentiation requires constant Fgfr3 activation by Fgf8. Conditional Fgf8 knockout; in vitro organ of Corti culture; Fgf8 overexpression; Fgfr3 inhibition assays; in vivo analysis Development (Cambridge, England) High 17634195
2005 Increasing Fgf4 expression in place of Fgf8 in the limb bud (using conditional Fgf4 gain-of-function simultaneously with Fgf8 inactivation) rescues all skeletal defects caused by Fgf8 loss, demonstrating that FGF4 can functionally replace FGF8 in limb skeletal development. Conditional mouse Fgf4 gain-of-function/Fgf8 loss-of-function; skeletal analysis Development (Cambridge, England) High 16308330
2005 In Xenopus, FGF8 induces neural crest through both Msx1 and Pax3 activities. WNT and FGF8 signals act in parallel at the neural border and converge on Pax3 activity during neural crest induction. Msx1 acts upstream of Pax3, and Pax3 combined with ZicR1 activates Slug in a WNT-dependent manner. Xenopus overexpression and morpholino-mediated knockdown of Msx1, Pax3, ZicR1; epistasis analysis with FGF8 and WNT pathways Developmental cell High 15691759
2005 Retinoic acid activates myogenesis in zebrafish through Fgf8 signaling: RA regulates fgf8 expression in somites and anterior presomitic mesoderm, and in the absence of Fgf8 signaling (ace mutant), RA fails to promote myoD expression. Zebrafish pharmacological RA pathway manipulation; ace/fgf8 mutant analysis; myogenic marker gene expression Developmental biology High 16316642
2006 Fgf8 in the anterior heart field (AHF) mesoderm provides autocrine signaling required for formation of the primary heart tube and addition of right ventricular/outflow tract myocardium. Loss of Fgf8 in cardiac crescent mesoderm decreases expression of target gene Erm and aberrantly affects Isl1 and Mef2c in AHF. Mesodermal and endodermal FGF8 perform distinct roles: mesodermal Fgf8 is required for outflow tract alignment, endodermal Fgf8 for outflow tract septation. Conditional Fgf8 mutagenesis using tissue-specific Cre drivers; cardiac morphology analysis; marker gene expression (Erm, Isl1, Mef2c) Development (Cambridge, England) High 16720879
2006 Fgf8 dose-dependently regulates telencephalic patterning centers: hypomorphic and conditional null mutations cause reduced Foxg1 expression, decreased cell proliferation, increased cell death, and alterations in Bmp4, Wnt8b, Nkx2.1, and Shh expression. Nonlinear Fgf8 dosage effects on Bmp4 and Msx1 correlate with holoprosencephaly phenotype. Mouse hypomorphic and conditional null Fgf8 alleles; cell proliferation and death assays; marker gene expression analysis Development (Cambridge, England) High 16613831
2009 In zebrafish, Fgf8 is required for asymmetric migration of the parapineal nucleus to the left side of the brain. Local provision of Fgf8 restores asymmetric parapineal migration irrespective of source location. Left-sided Nodal signaling biases migration toward the left in combination with Fgf8. When Nodal bias is removed, parapineal cells migrate toward the Fgf8 source. Zebrafish fgf8 mutant analysis; local Fgf8 protein provision; Nodal signaling manipulation; live imaging of parapineal migration Neuron High 19146810
2009 Jagged1/Notch signaling in second heart field tissues controls Fgf8 expression: loss of Jagged1 or Notch inhibition in second heart field causes decreased Fgf8 and Bmp4 expression, faulty neural crest migration, and defective endothelial-mesenchymal transition in outflow tract cushions. Exogenous Fgf8 rescues the endothelial-mesenchymal transition defect in explant assays. Conditional Jagged1 mouse knockout; Notch inhibition; FGF8 rescue in endocardial cushion explants; neural crest migration analysis The Journal of clinical investigation High 19509466
2011 Six1 and Eya1 transcription complex directly regulates Fgf8 as a downstream effector. Combined Six1/Eya1 mouse mutation recapitulates del22q11 syndrome features. Six1 and Eya1 genetically interact with Fgf8 and Tbx1. This defines a Tbx1-Six1/Eya1-Fgf8 genetic pathway for cardiocraniofacial morphogenesis. Mouse compound Six1/Eya1 knockout; ChIP/direct transcriptional target analysis; genetic interaction with Fgf8 and Tbx1 mutants The Journal of clinical investigation High 21364285
2011 Gbx2 and Fgf8 act sequentially to establish the midbrain-hindbrain compartment boundary: Gbx2 specifies hindbrain fate and prevents Gbx2+ cells from crossing the MHB, and subsequently Fgf8 from the MHB maintains the lineage-restricted boundary through cell-autonomous effects on cell sorting in midbrain progenitors. Gbx2CreER knock-in genetic fate mapping; partial Fgf8 deletion; cell clonal analysis blocking FGF signaling Development (Cambridge, England) High 21266408
2012 FGF4 and FGF8 are together required for axial elongation of the mouse embryo after gastrulation. Double loss of Fgf8 and Fgf4 during late gastrulation severely reduces paraxial mesoderm, disrupts NOTCH pathway segmentation genes, reduces Wnt3a expression in the tail, and causes failure of somite formation after ~15-20 somites. The defect reflects failure to maintain a mesodermal progenitor cell population. Conditional mouse double knockout of Fgf4 and Fgf8 during late gastrulation; skeletal analysis; gene expression analysis; cell proliferation/apoptosis assays Developmental biology High 22954964
2014 Retinoic acid directly represses Fgf8 transcription through a conserved RARE upstream of Fgf8 that binds RAR isoforms. RA recruits repressive histone marker H3K27me3 and polycomb repressive complex 2 (PRC2) near the Fgf8 RARE. The co-regulator RERE is released from the Fgf8 RARE by RA, promoting repressive chromatin. Transgenic Fgf8-lacZ reporter with RARE deletion; chromatin immunoprecipitation (ChIP) for H3K27me3, PRC2, and RERE in mouse embryo trunk tissues; comparison of wild-type and Raldh2-/- embryos Development (Cambridge, England) High 25053430
2002 The androgen receptor (AR) directly regulates FGF8 transcription in human prostate cancer cells. AR binds androgen response elements in the FGF8 promoter (confirmed by ChIP), and AR activation increases FGF8 promoter-driven luciferase activity 2.5-fold; the anti-androgen bicalutamide abolishes this induction. ChIP assay for AR binding at FGF8 promoter; luciferase reporter assays in LNCaP, SC3, and DU145 cells; androgen treatment and bicalutamide inhibition Oncogene High 12140757
2002 Unliganded RARα homodimer (phosphorylated on Ser77) binds a novel response element composed of two half-sites separated by 87 nucleotides in the Fgf8 promoter, while liganded RARα-RXRα heterodimer binds a canonical DR2 RARE. These two distinct modes of RAR binding drive expression of different Fgf8 isoforms. Biochemical and cellular experiments with Fgf8 promoter constructs; mutagenesis of response elements; gel shift and reporter assays Journal of molecular biology High 12054865
2015 FGF8 promotes colorectal cancer cell growth and metastasis by activating YAP1: FGF8 induces nuclear localization of YAP1 and enhances CTGF and CYR61 transcription. YAP1 knockdown impedes FGF8-induced cell growth, EMT, migration, and invasion. FGF8 overexpression and knockdown in CRC cells; YAP1 localization by immunofluorescence; YAP1 siRNA knockdown; mouse tumor growth/metastasis models Oncotarget Medium 25473897
2015 FGF8 acts as a chemoattractant on leader cells of the elongating Wolffian duct and prevents them from epithelialization, functioning as a binary switch that distinguishes tubular elongation from lumen formation during early kidney tubulogenesis. Chick embryo Wolffian duct analysis; FGF8 expression correlation with elongation vs. epithelialization; functional assays Development (Cambridge, England) Medium 26130757
2016 Nuclear receptor corepressors NCOR1 and NCOR2 (SMRT) redundantly mediate RA-dependent repression of Fgf8. NCOR1/2 are recruited to the Fgf8 RARE in an RA-dependent manner (not to RA-activated RAREs). Ncor1;Ncor2 double mutants (generated by CRISPR/Cas9) show increased Fgf8 expression and FGF signaling in caudal and heart progenitors. CRISPR/Cas9 double knockout of Ncor1/Ncor2; ChIP for NCOR1/2 and coactivators at Fgf8 RARE; CRISPR deletion of Fgf8 RARE; embryo phenotype analysis Developmental biology High 27506116
2007 Fgfr1 in zebrafish is a member of the fgf8 synexpression group (co-expressed with fgf8 at the MHB and other sites), and knockdown of fgfr1 phenocopies many aspects of the fgf8 (ace) mutant, indicating that Fgf8 exerts its MHB function primarily by binding to FgfR1. Zebrafish fgfr1 expression analysis; morpholino knockdown phenotype compared to ace/fgf8 mutant Development genes and evolution Medium 15221377
2009 In the chick embryo proepicardium, FGF8 and Snai1 form a right-sided pathway that controls asymmetric PE development. Inhibition of FGF8 prevents PE formation; ectopic left-sided FGF8 expression results in bilateral PE development. FGF8 inhibition and ectopic FGF8 expression in chick embryo; analysis of PE formation and sidedness Proceedings of the National Academy of Sciences of the United States of America Medium 19365073
2010 Setdb2 (a SET domain protein with H3K9 methyltransferase activity) restricts dorsal organizer territory by suppressing fgf8 expression in zebrafish. Setdb2 knockdown causes expansion of dorsal organizer markers and increased fgf8 mRNA; these defects are corrected by dominant-negative FGF receptor or fgf8 knockdown, placing Setdb2 upstream of Fgf8 in organizer restriction. Zebrafish Setdb2 morpholino knockdown; dominant-negative FGFR rescue; fgf8 morpholino epistasis; in situ hybridization Proceedings of the National Academy of Sciences of the United States of America Medium 20133783
2013 FGF8 and FGF18 signal through divergent intracellular pathways in bovine ovarian granulosa cells despite activating the same receptors: FGF8 increases ERK1/2 phosphorylation and induces SPRY1/2/4, NR4A1/3, and FOS expression, while FGF18 does not activate ERK1/2 and does not induce those targets. FGF8 and FGF18 treatment of bovine granulosa cells; ERK1/2 phosphorylation assay; mRNA expression; microarray analysis Molecular and cellular endocrinology Medium 23707615
2007 Fgf8b splice-form-specific mouse knockout reveals that Fgf8b is required before gastrulation for Brachyury induction in the pregastrular embryo and for proper anteroposterior axis alignment with uterine axes. During gastrulation, Fgf8a can partially compensate for loss of Fgf8b. Increased Fgf8a expression can promote mesoderm migration by inducing Fgf4 expression in the primitive streak. Splice-site mouse mutation abolishing Fgf8b; comparison with Fgf8-null embryos; marker gene expression Development (Cambridge, England) High 17507393
1996 Human FGF8b induces marked morphological transformation and strong tumorigenicity in NIH3T3 cells; FGF8a and FGF8e are moderately transforming. Three alternatively spliced FGF8 mRNA isoforms (a, b, e) with different N-terminal sequences are expressed in human prostate cancer cells. NIH3T3 transfection with FGF8 isoform expression vectors; nude mouse tumorigenicity assay; Northern blot and RT-PCR Cell growth & differentiation Medium 8891346

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1998 Fgf8 is mutated in zebrafish acerebellar (ace) mutants and is required for maintenance of midbrain-hindbrain boundary development and somitogenesis. Development (Cambridge, England) 598 9609821
1999 Targeted disruption of Fgf8 causes failure of cell migration in the gastrulating mouse embryo. Genes & development 513 10421635
1996 Roles for FGF8 in the induction, initiation, and maintenance of chick limb development. Cell 507 8548816
1998 Fibroblast growth factor receptor 2 (FGFR2)-mediated reciprocal regulation loop between FGF8 and FGF10 is essential for limb induction. Development (Cambridge, England) 458 9435295
2002 Fgf8 is required for pharyngeal arch and cardiovascular development in the mouse. Development (Cambridge, England) 360 12223417
1999 FGF8 induces formation of an ectopic isthmic organizer and isthmocerebellar development via a repressive effect on Otx2 expression. Development (Cambridge, England) 325 10021338
2006 Dose-dependent functions of Fgf8 in regulating telencephalic patterning centers. Development (Cambridge, England) 304 16613831
1996 Involvement of FGF-8 in initiation, outgrowth and patterning of the vertebrate limb. Development (Cambridge, England) 302 8674413
2005 Inactivation of FGF8 in early mesoderm reveals an essential role in kidney development. Development (Cambridge, England) 276 16049111
2005 Msx1 and Pax3 cooperate to mediate FGF8 and WNT signals during Xenopus neural crest induction. Developmental cell 266 15691759
2000 Fgf8 is required for outgrowth and patterning of the limbs. Nature genetics 263 11101845
2003 The isthmic organizer signal FGF8 is required for cell survival in the prospective midbrain and cerebellum. Development (Cambridge, England) 255 12736208
1999 Differences in left-right axis pathways in mouse and chick: functions of FGF8 and SHH. Science (New York, N.Y.) 249 10411502
2003 MKP3 mediates the cellular response to FGF8 signalling in the vertebrate limb. Nature cell biology 225 12766772
2001 Zebrafish pea3 and erm are general targets of FGF8 signaling. Current biology : CB 222 11413000
2001 Local retinoid signaling coordinates forebrain and facial morphogenesis by maintaining FGF8 and SHH. Development (Cambridge, England) 221 11526081
2000 Induction and differentiation of the zebrafish heart requires fibroblast growth factor 8 (fgf8/acerebellar). Development (Cambridge, England) 215 10603341
2001 Zebrafish fgf3 and fgf8 encode redundant functions required for otic placode induction. Developmental biology 211 11437442
2002 Fgf3 and Fgf8 are required together for formation of the otic placode and vesicle. Development (Cambridge, England) 202 11959820
2006 Required, tissue-specific roles for Fgf8 in outflow tract formation and remodeling. Development (Cambridge, England) 198 16720879
1995 FGF-8 isoforms activate receptor splice forms that are expressed in mesenchymal regions of mouse development. Development (Cambridge, England) 196 8582274
2002 Fgf8 and Fgf3 are required for zebrafish ear placode induction, maintenance and inner ear patterning. Mechanisms of development 187 12385757
2002 FGF3 and FGF8 mediate a rhombomere 4 signaling activity in the zebrafish hindbrain. Development (Cambridge, England) 186 12135921
1999 Sequential roles for Fgf4, En1 and Fgf8 in specification and regionalisation of the midbrain. Development (Cambridge, England) 181 9927596
1999 FGF8 can activate Gbx2 and transform regions of the rostral mouse brain into a hindbrain fate. Development (Cambridge, England) 175 10518499
2003 Zebrafish fgf24 functions with fgf8 to promote posterior mesodermal development. Development (Cambridge, England) 170 12925590
1998 Comparison of the expression of three highly related genes, Fgf8, Fgf17 and Fgf18, in the mouse embryo. Mechanisms of development 169 9651520
2005 FGF8 initiates inner ear induction in chick and mouse. Genes & development 164 15741321
2002 Regulation of avian cardiogenesis by Fgf8 signaling. Development (Cambridge, England) 164 11934859
2009 Murine Jagged1/Notch signaling in the second heart field orchestrates Fgf8 expression and tissue-tissue interactions during outflow tract development. The Journal of clinical investigation 159 19509466
1994 Involvement of androgen-induced growth factor (FGF-8) gene in mouse embryogenesis and morphogenesis. Biochemical and biophysical research communications 159 7980556
2004 The roles of Fgf4 and Fgf8 in limb bud initiation and outgrowth. Developmental biology 158 15328019
2003 Dosage of Fgf8 determines whether cell survival is positively or negatively regulated in the developing forebrain. Proceedings of the National Academy of Sciences of the United States of America 152 12574514
2003 Loss of Bmp7 and Fgf8 signaling in Hoxa13-mutant mice causes hypospadia. Development (Cambridge, England) 145 12783783
2004 Reciprocal relationships between Fgf8 and neural crest cells in facial and forebrain development. Proceedings of the National Academy of Sciences of the United States of America 133 15041748
2001 EN and GBX2 play essential roles downstream of FGF8 in patterning the mouse mid/hindbrain region. Development (Cambridge, England) 133 11124114
2005 Fgf8 expression defines a morphogenetic center required for olfactory neurogenesis and nasal cavity development in the mouse. Development (Cambridge, England) 130 16267092
1995 Expression of bone morphogenetic protein-4 (BMP-4), bone morphogenetic protein-7 (BMP-7), fibroblast growth factor-8 (FGF-8) and sonic hedgehog (SHH) during branchial arch development in the chick. Mechanisms of development 130 8645604
2007 Fgf8 induces pillar cell fate and regulates cellular patterning in the mammalian cochlea. Development (Cambridge, England) 124 17634195
2001 Expression patterns of Fgf-8 during development and limb regeneration of the axolotl. Developmental dynamics : an official publication of the American Association of Anatomists 123 11146506
2003 Fgf3 and Fgf8 dependent and independent transcription factors are required for otic placode specification. Development (Cambridge, England) 122 12668634
2013 An integrated holo-enhancer unit defines tissue and gene specificity of the Fgf8 regulatory landscape. Developmental cell 121 23453598
1999 FGF8 over-expression in prostate cancer is associated with decreased patient survival and persists in androgen independent disease. Oncogene 121 10348350
2008 The complex genetics of Kallmann syndrome: KAL1, FGFR1, FGF8, PROKR2, PROK2, et al. Sexual development : genetics, molecular biology, evolution, endocrinology, embryology, and pathology of sex determination and differentiation 118 18987492
2011 A Tbx1-Six1/Eya1-Fgf8 genetic pathway controls mammalian cardiovascular and craniofacial morphogenesis. The Journal of clinical investigation 112 21364285
2008 FGF15 promotes neurogenesis and opposes FGF8 function during neocortical development. Neural development 110 18625063
2008 Frontal cortex subdivision patterning is coordinately regulated by Fgf8, Fgf17, and Emx2. The Journal of comparative neurology 107 18459137
1999 Expression of chick Barx-1 and its differential regulation by FGF-8 and BMP signaling in the maxillary primordia. Developmental dynamics : an official publication of the American Association of Anatomists 107 10213385
2003 Unique and combinatorial functions of Fgf3 and Fgf8 during zebrafish forebrain development. Development (Cambridge, England) 106 12900450
2014 Retinoic acid controls body axis extension by directly repressing Fgf8 transcription. Development (Cambridge, England) 103 25053430
2007 Sp8 exhibits reciprocal induction with Fgf8 but has an opposing effect on anterior-posterior cortical area patterning. Neural development 98 17509151
2001 Distinct regulators control the expression of the mid-hindbrain organizer signal FGF8. Nature neuroscience 98 11704761
2004 Endocytosis controls spreading and effective signaling range of Fgf8 protein. Current biology : CB 97 15498491
2011 Novel FGF8 mutations associated with recessive holoprosencephaly, craniofacial defects, and hypothalamo-pituitary dysfunction. The Journal of clinical endocrinology and metabolism 96 21832120
2012 Signaling by FGF4 and FGF8 is required for axial elongation of the mouse embryo. Developmental biology 95 22954964
2009 Role of mesodermal FGF8 and FGF10 overlaps in the development of the arterial pole of the heart and pharyngeal arch arteries. Circulation research 93 20035084
1999 Shh, Bmp-2, Bmp-4 and Fgf-8 are associated with initiation and patterning of mouse tongue papillae. Mechanisms of development 84 10330496
2007 Differential requirements for FGF3, FGF8 and FGF10 during inner ear development. Developmental biology 82 17601531
2005 Increasing Fgf4 expression in the mouse limb bud causes polysyndactyly and rescues the skeletal defects that result from loss of Fgf8 function. Development (Cambridge, England) 80 16308330
2005 Retinoic acid activates myogenesis in vivo through Fgf8 signalling. Developmental biology 79 16316642
2002 Regulation of FGF8 expression by the androgen receptor in human prostate cancer. Oncogene 73 12140757
2000 Involvement of fibroblast growth factor (FGF)18-FGF8 signaling in specification of left-right asymmetry and brain and limb development of the chick embryo. Mechanisms of development 72 10906450
2009 An Fgf8-dependent bistable cell migratory event establishes CNS asymmetry. Neuron 70 19146810
2003 FGF8 isoform b expression in human prostate cancer. British journal of cancer 66 12778074
2004 Induction and specification of midbrain dopaminergic cells: focus on SHH, FGF8, and TGF-beta. Cell and tissue research 64 15322912
2004 The Fgf8 signal causes cerebellar differentiation by activating the Ras-ERK signaling pathway. Development (Cambridge, England) 63 15294862
2000 Pax2, Otx2, Gbx2 and Fgf8 expression in early otic vesicle development. Mechanisms of development 63 10906468
2003 Engrailed and Fgf8 act synergistically to maintain the boundary between diencephalon and mesencephalon. Development (Cambridge, England) 60 12917294
2007 FGFR2, FGF8, FGF10 and BMP7 as candidate genes for hypospadias. European journal of human genetics : EJHG 59 17264867
2003 Sonic hedgehog and FGF8 collaborate to induce dopaminergic phenotypes in the Nurr1-overexpressing neural stem cell. Biochemical and biophysical research communications 59 12767935
1998 MMTV-Fgf8 transgenic mice develop mammary and salivary gland neoplasia and ovarian stromal hyperplasia. Oncogene 59 9840935
2001 Increased expression of FGF-8 isoforms and FGF receptors in human premalignant prostatic intraepithelial neoplasia lesions and prostate cancer. Laboratory investigation; a journal of technical methods and pathology 58 11406643
1996 Molecular cloning and characterization of human FGF8 alternative messenger RNA forms. Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research 58 8891346
2004 Zebrafish fgfr1 is a member of the fgf8 synexpression group and is required for fgf8 signalling at the midbrain-hindbrain boundary. Development genes and evolution 57 15221377
2015 FGF8 promotes colorectal cancer growth and metastasis by activating YAP1. Oncotarget 55 25473897
2010 Nonsense mutations in FGF8 gene causing different degrees of human gonadotropin-releasing deficiency. The Journal of clinical endocrinology and metabolism 55 20463092
2005 Mkp3 is a negative feedback modulator of Fgf8 signaling in the mammalian isthmic organizer. Developmental biology 55 15572144
2016 Fgf8 signaling for development of the midbrain and hindbrain. Development, growth & differentiation 53 27273073
2009 The duration of Fgf8 isthmic organizer expression is key to patterning different tectal-isthmo-cerebellum structures. Development (Cambridge, England) 51 19793884
2013 Interaction between Foxc1 and Fgf8 during mammalian jaw patterning and in the pathogenesis of syngnathia. PLoS genetics 49 24385915
2009 Functional and phylogenetic analysis shows that Fgf8 is a marker of genital induction in mammals but is not required for external genital development. Development (Cambridge, England) 49 19592577
1999 aFGF immunoreactivity in prostate cancer and its co-localization with bFGF and FGF8. The Journal of pathology 49 10629559
2014 The oncoprotein HBXIP enhances angiogenesis and growth of breast cancer through modulating FGF8 and VEGF. Carcinogenesis 48 24464787
2011 Gbx2 and Fgf8 are sequentially required for formation of the midbrain-hindbrain compartment boundary. Development (Cambridge, England) 47 21266408
2007 Distinct functions of the major Fgf8 spliceform, Fgf8b, before and during mouse gastrulation. Development (Cambridge, England) 47 17507393
2003 Ventral axial organs regulate expression of myotomal Fgf-8 that influences rib development. Developmental biology 45 12618132
2002 Promoter of FGF8 reveals a unique regulation by unliganded RARalpha. Journal of molecular biology 45 12054865
2016 Nuclear receptor corepressors Ncor1 and Ncor2 (Smrt) are required for retinoic acid-dependent repression of Fgf8 during somitogenesis. Developmental biology 44 27506116
2010 Setdb2 restricts dorsal organizer territory and regulates left-right asymmetry through suppressing fgf8 activity. Proceedings of the National Academy of Sciences of the United States of America 44 20133783
2006 Fgf8 expression in the Tbx1 domain causes skeletal abnormalities and modifies the aortic arch but not the outflow tract phenotype of Tbx1 mutants. Developmental biology 41 16696966
2013 Divergence of intracellular signaling pathways and early response genes of two closely related fibroblast growth factors, FGF8 and FGF18, in bovine ovarian granulosa cells. Molecular and cellular endocrinology 40 23707615
2006 Cell aggregation-induced FGF8 elevation is essential for P19 cell neural differentiation. Molecular biology of the cell 40 16641368
2002 Spatial and temporal pattern of Fgf-8 expression during chicken development. Anatomy and embryology 38 11875659
1996 The human FGF-8 gene localizes on chromosome 10q24 and is subjected to induction by androgen in breast cancer cells. Oncogene 38 8700553
2010 Role of Fgf8 signalling in the specification of rostral Cajal-Retzius cells. Development (Cambridge, England) 37 20040495
2009 Zebrafish Hagoromo mutants up-regulate fgf8 postembryonically and develop neuroblastoma. Molecular cancer research : MCR 36 19531571
2015 FGF8 coordinates tissue elongation and cell epithelialization during early kidney tubulogenesis. Development (Cambridge, England) 35 26130757
2009 A right-sided pathway involving FGF8/Snai1 controls asymmetric development of the proepicardium in the chick embryo. Proceedings of the National Academy of Sciences of the United States of America 35 19365073
2018 FGF8 Signaling Alters the Osteogenic Cell Fate in the Hard Palate. Journal of dental research 34 29342370
2001 Sonic hedgehog and FGF8: inadequate signals for the differentiation of a dopamine phenotype in mouse and human neurons in culture. Experimental neurology 34 11312556