Fibroblast growth factor homologous factors: Evolution, structure, and function

Goldfarb, Mitchell

doi:10.1016/j.cytogfr.2005.02.002

Cited by 186 publications

(179 citation statements)

References 39 publications

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“…Taken together, these findings suggest roles for FGFs in ENS development, which remain to be explored. One of the genes identified in our screen, Fgf13, shares strong sequence and structural similarity to FGFs but is not secreted and does not activate FGF receptors (40). Therefore, FGF13 is unlikely to mediate the FGF responses we propose.…”

Section: Sox2 As a Potential Marker Of Proliferative And Stem Cell Pomentioning

confidence: 85%

Expression profiling the developing mammalian enteric nervous system identifies marker and candidate Hirschsprung disease genes

Heanue

Pachnis

2006

Proc. Natl. Acad. Sci. U.S.A.

106

121

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The enteric nervous system (ENS) is composed of neurons and glial cells, organized as interconnected ganglia within the gut wall, which controls persistalsis of the gut wall and secretions from its glands. The Ret receptor tyrosine kinase is expressed throughout enteric neurogenesis and is required for normal ENS development; humans with mutations in the RET locus have Hirschsprung disease (HSCR, an absence of ganglia in the colon), and mice lacking Ret have total intestinal aganglionosis. The Ret mutant mouse provides a tool for identifying genes implicated in development of the ENS. By using RNA from WT and Ret mutant (aganglionic) gut tissue and DNA microarrays, we have conducted a differential screen for ENS-expressed genes and have identified hundreds of candidate ENS-expressed genes. Forty-seven genes were selected for further analysis, representing diverse functional classes. We show that all of the analyzed genes are expressed in the ENS and that the screen was sensitive enough to identify genes marking only subpopulations of ENS cells. Our screen, therefore, was reliable and sensitive and has identified many previously undescribed genes for studying ENS development. Moreover, two of the genes identified in our screen Arhgef3 and Ctnnal1, have human homologues that map to previously identified HSCR susceptibility loci, thus representing excellent candidates for HSCR genes. This comprehensive profile of ENS gene expression refines our understanding of ENS development and serves as a resource for future developmental, biochemical, and human genetic studies.T he enteric nervous system (ENS) is composed of a vast number of neurons and glial cells, which form interconnected ganglia that control the contractility of the smooth muscle of the gut wall and the secretory activity of its glands (1). The ENS is derived from vagal and sacral enteric neural crest cells (ENCs), which invade the foregut and hindgut, respectively (2, 3). Once situated within the gut, ENCs migrate along the developing bowel, proliferate, and differentiate to form many different neuronal subtypes and make synaptic connections (4, 5). Migration of ENCs within the gut requires signaling between these cells and the gut environment and depends on dynamic changes in cell shape and adhesive properties. How cell shape and adhesion are controlled to allow regulated and directed migration of ENCs currently is unknown. Furthermore, how cell fate decisions are controlled to specify the correct number and subtypes of neurons and glial cells within ENS ganglia or how correct synaptic circuits are established also is unknown.Genetic studies in mouse and human have identified several genes whose function is required for normal ENS development (6, 7). For example, the Ret receptor tyrosine kinase is expressed in ENCs during migration into the gut and persists during later ENS development (8). Humans carrying mutations in RET develop congenital megacolon [Hirschsprung disease (HSCR) OMIM 142623; ref. 7], which is characterized by the absence of enteric ga...

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Section: Sox2 As a Potential Marker Of Proliferative And Stem Cell Pomentioning

confidence: 85%

Expression profiling the developing mammalian enteric nervous system identifies marker and candidate Hirschsprung disease genes

Heanue

Pachnis

2006

Proc. Natl. Acad. Sci. U.S.A.

106

121

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“…Current data suggest that iFGFs act in an FGFR-independent manner. They have been shown to interact with intracellular domains of voltage-gate sodium channels and with the neuronal mitogen-activated protein kinase scaffold protein, islet-brain-2 (reviewed in Goldfarb, 2005).…”

Section: Identification Of the Mouse Fgf Gene Familymentioning

confidence: 99%

“…However, their roles and mechanisms of action are highly diverse. FGF11-FGF14 (iFGFs) function as intracellular proteins in an FGFR-independent manner (Wang et al, 2000;Goldfarb, 2005). In contrast, canonical FGFs function as extracellular proteins in an FGFR-dependent manner.…”

Section: Perspectivesmentioning

confidence: 99%

“…Most FGFs mediate their biological responses as extracellular proteins by binding to and activating cell surface tyrosine kinase FGF receptors (FGFRs) (Ornitz and Itoh, 2001;Itoh and Ornitz, 2004;Thisse and Thisse, 2005). However, FGFs 11-14 function as intracellular proteins, hereafter referred to as iFGFs, and act in an FGF Receptor (FGFR)-independent manner (Goldfarb, 2005).…”

Section: Introductionmentioning

confidence: 99%

“…Alternative spliced variants of Fgf8 and Fgf17 are generated from distinct splice sites that divide the "first" exon into four (in humans) sub-exons (MacArthur et al, 1995;Gemel et al, 1996;Xu et al, 1999;Olsen et al, 2006). Similarly, the iFgfs have acquired alternatively spliced amino terminal variants that are generated by alternative utilization of distinct first exons (reviewed in Goldfarb, 2005). Importantly, none of these alternative splicing events affects the sequences of the conserved FGF core domain.…”

Section: Exon/intron Organizations Of Mouse Fgf Genesmentioning

confidence: 99%

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Functional evolutionary history of the mouse Fgf gene family

Itoh

Ornitz

2007

Developmental Dynamics

346

313

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FGF11 induced by hypoxia interacts with HIF‐1α and enhances its stability

et al. 2017

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Fibroblast growth factor 11 (FGF11) is an intracellular FGF. Although induction of FGF11 by hypoxia has been observed in several cell types, the molecular function of FGF11 is not clearly understood yet. Here, we investigated the role of FGF11 under hypoxia. We identified hypoxia-inducible factor-1α (HIF-1α) as an interacting protein of FGF11 using immunoprecipitation and mass spectrometry. FGF11 knockdown decreased HIF-1α protein, while FGF11 overexpression increased it, without affecting HIF-1α mRNA. Protein stability test and ubiquitination assay showed that FGF11 increased HIF-1α stability by acting upstream of proteasomal degradation. Altogether, these results suggest a cross-regulation between HIF-1α and FGF11, through which hypoxia-induced FGF11 reinforces hypoxia responses by enhancing the stability of HIF-1α.

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Fibroblast growth factor homologous factors: Evolution, structure, and function

Cited by 186 publications

References 39 publications

Expression profiling the developing mammalian enteric nervous system identifies marker and candidate Hirschsprung disease genes

Expression profiling the developing mammalian enteric nervous system identifies marker and candidate Hirschsprung disease genes

Functional evolutionary history of the mouse Fgf gene family

FGF11 induced by hypoxia interacts with HIF‐1α and enhances its stability

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