描述：
FGF-17 is a member of the fibroblast growth factor (FGF) family. FGFs play multiple roles in
biological functions, including angiogenesis, mitogenesis, cell differentiation and wound
repair. FGFs share 30-70% amino acid (aa) identity in a conserved, approximately 120 amino
acid core domain. The human or mouse FGF-17 cDNA encodes a cleavable 22 aa signal
sequence and a 194 secreted mature protein (1). Mature human FGF-17 shares 99% aa
identity with mouse, rat, porcine and canine FGF-17. The FGF domain of FGF-17 shares the
most aa identity with FGF-8 (75%) and FGF-18 (~64%). These three FGFs constitute a subfamily
that overlaps in some areas of expression and function. All are reported to bind and signal
through FGF R4 the “c” splice forms of FGF R1-3. During embryogenesis, FGF-17 plays an
organizing and inducing role in the patterning at the midbrain/hindbrain junction, and is also
expressed in hindgut, parts of the developing skeleton, tail bud, major arteries, and heart.
In many of these areas, it is expressed along with FGF-8, but slightly later. Unlike FGF-8 and
FGF-18, deletion of FGF-17 produces viable mice. However, FGF-17/mice show abnormalities
in the dorsal frontal cortex, midbrain and cerebellum, manifested in some cases by ataxia,
auditory defects, and abnormal social behavior. In humans, down-regulation of FGF-17
expression has been associated with Dandy-Walker cerebellar malformation. FGF-17 is also
expressed in adult bovine ovarian follicles and the human prostate, and its expression is
increased by both benign hypertrophy and cancer of the prostate. FGF-8, FGF-17, and FGF-18
are also abnormally expressed in many human leukemic cell lines and can enhance growth of
cancer cells.
原厂资料：
FGF-17 is a member of the fibroblast growth factor (FGF) family. FGFs play multiple roles in
biological functions, including angiogenesis, mitogenesis, cell differentiation and wound
repair. FGFs share 30-70% amino acid (aa) identity in a conserved, approximately 120 amino
acid core domain. The human or mouse FGF-17 cDNA encodes a cleavable 22 aa signal
sequence and a 194 secreted mature protein (1). Mature human FGF-17 shares 99% aa
identity with mouse, rat, porcine and canine FGF-17. The FGF domain of FGF-17 shares the
most aa identity with FGF-8 (75%) and FGF-18 (~64%). These three FGFs constitute a subfamily
that overlaps in some areas of expression and function. All are reported to bind and signal
through FGF R4 the “c” splice forms of FGF R1-3. During embryogenesis, FGF-17 plays an
organizing and inducing role in the patterning at the midbrain/hindbrain junction, and is also
expressed in hindgut, parts of the developing skeleton, tail bud, major arteries, and heart.
In many of these areas, it is expressed along with FGF-8, but slightly later. Unlike FGF-8 and
FGF-18, deletion of FGF-17 produces viable mice. However, FGF-17/mice show abnormalities
in the dorsal frontal cortex, midbrain and cerebellum, manifested in some cases by ataxia,
auditory defects, and abnormal social behavior. In humans, down-regulation of FGF-17
expression has been associated with Dandy-Walker cerebellar malformation. FGF-17 is also
expressed in adult bovine ovarian follicles and the human prostate, and its expression is
increased by both benign hypertrophy and cancer of the prostate. FGF-8, FGF-17, and FGF-18
are also abnormally expressed in many human leukemic cell lines and can enhance growth of
cancer cells.
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