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Protein Page:
FGF8 (human)

FGF8 Plays an important role in the regulation of embryonic development, cell proliferation, cell differentiation and cell migration. Required for normal brain, eye, ear and limb development during embryogenesis. Required for normal development of the gonadotropin-releasing hormone (GnRH) neuronal system. Defects in FGF8 are the cause of Kallmann syndrome type 6 (KAL6). Kallmann syndrome is a disorder that associates hypogonadotropic hypogonadism and anosmia. Anosmia or hyposmia is related to the absence or hypoplasia of the olfactory bulbs and tracts. Hypogonadism is due to deficiency in gonadotropin-releasing hormone and probably results from a failure of embryonic migration of gonadotropin-releasing hormone- synthesizing neurons. In some patients other developmental anomalies can be present, which include renal agenesis, cleft lip and/or palate, selective tooth agenesis, and bimanual synkinesis. In some cases anosmia may be absent or inconspicuous. Defects in FGF8 are a cause of idiopathic hypogonadotropic hypogonadism (IHH). IHH is defined as a deficiency of the pituitary secretion of follicle-stimulating hormone and luteinizing hormone, which results in the impairment of pubertal maturation and of reproductive function. Belongs to the heparin-binding growth factors family. 4 isoforms of the human protein are produced by alternative splicing. Note: This description may include information from UniProtKB.
Protein type: Secreted; Cytokine; Secreted, signal peptide
Chromosomal Location of Human Ortholog: 10q24
Cellular Component: external side of plasma membrane; extracellular region; extracellular space; intracellular
Molecular Function: chemoattractant activity; fibroblast growth factor receptor binding; growth factor activity; type 1 fibroblast growth factor receptor binding; type 2 fibroblast growth factor receptor binding
Biological Process: activation of MAPKK activity; adrenocorticotropin hormone secreting cell differentiation; anatomical structure morphogenesis; apoptosis; axon guidance; blood vessel remodeling; BMP signaling pathway; cell fate commitment; cell proliferation in forebrain; dorsal/ventral axon guidance; embryonic hindlimb morphogenesis; epidermal growth factor receptor signaling pathway; fibroblast growth factor receptor signaling pathway; forebrain dorsal/ventral pattern formation; forebrain morphogenesis; forebrain neuron development; gastrulation; gonad development; heart looping; induction of an organ; innate immune response; insulin receptor signaling pathway; male genitalia development; MAPKKK cascade; mesodermal cell migration; mesonephros development; metanephros development; midbrain-hindbrain boundary development; motor axon guidance; negative regulation of cardiac muscle development; negative regulation of neuron apoptosis; nerve growth factor receptor signaling pathway; neural plate morphogenesis; odontogenesis; otic vesicle formation; pallium development; patterning of blood vessels; pharyngeal system development; phosphoinositide-mediated signaling; positive chemotaxis; positive regulation of cell proliferation; positive regulation of mitosis; positive regulation of organ growth; Ras protein signal transduction; regulation of odontogenesis of dentine-containing teeth; response to drug; response to organic cyclic substance; response to oxidative stress; small GTPase mediated signal transduction; subpallium development; thyroid gland development; thyroid stimulating hormone secreting cell differentiation; ureteric bud branching; vascular endothelial growth factor receptor signaling pathway; Wnt receptor signaling pathway through beta-catenin
Disease: Hypogonadotropic Hypogonadism 6 With Or Without Anosmia
Reference #:  P55075 (UniProtKB)
Alt. Names/Synonyms: AIGF; Androgen-induced growth factor; FGF-8; FGF8; Fibroblast growth factor 8; fibroblast growth factor 8 (androgen-induced); HBGF-8; Heparin-binding growth factor 8; KAL6; MGC149376
Gene Symbols: FGF8
Molecular weight: 26,525 Da
Basal Isoelectric point: 10.44  Predict pI for various phosphorylation states
Select Structure to View Below


Protein Structure Not Found.

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Modification Sites and Domains  

Modification Sites in Parent Protein, Orthologs, and Isoforms  

Show Multiple Sequence Alignment


LTP: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.


HTP: The number of records in which this modification site was assigned using ONLY proteomic discovery-mode mass spectrometry.


► Hide Isoforms
  FGF8 iso3  
  FGF8 iso4  

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