Expression of a Dominant Negative FGF Receptor Inhibits Axonal Growth and FGF Receptor Phosphorylation Stimulated by CAMs

Saffell, Jane L.; Williams, Emma J.; Mason, Ivor; Walsh, Frank S.; Doherty, Patrick

doi:10.1016/s0896-6273(00)80264-0

Cited by 315 publications

(256 citation statements)

References 52 publications

(37 reference statements)

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“…For example, differential signaling between NCAM and c-Ret may regulate the balance between stem cell self-renewal and differentiation. Interestingly, it has been reported that NCAM-mediated cell-cell adhesion leads to activation of FGF-receptor tyrosine kinase, which is required for NCAM-induced neurogenesis (27). These studies indicate cross-talk occurs between NCAM binding and the FGF signaling pathway.…”

Section: Discussionmentioning

confidence: 93%

Conservation of spermatogonial stem cell self-renewal signaling between mouse and rat

Ryu

Kubota

Avarbock

et al. 2005

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

252

236

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Self-renewal of spermatogonial stem cells (SSCs) is the foundation for maintenance of spermatogenesis throughout life in males and for continuation of a species. The molecular mechanism underlying stem cell self-renewal is a fundamental question in stem cell biology. Recently, we identified growth factors necessary for self-renewal of mouse SSCs and established a serum-free culture system for their proliferation in vitro. To determine whether the stimulatory signals for SSC replication are conserved among different species, we extended the culture system to rat SSCs. Initially, a method to assess in vitro expansion of SSCs was developed by using flow cytometric analysis, and, subsequently, we found that a combination of glial cell line-derived neurotrophic factor, soluble glial cell line-derived neurotrophic factor-family receptor ␣-1 and basic fibroblast growth factor supports proliferation of rat SSCs. When cultured with the three factors, stem cells proliferated continuously for >7 months, and transplantation of the cultured SSCs to recipient rats generated donor stem cell-derived progeny, demonstrating that the cultured stem cells are normal. The growth factor requirement for replication of rat SSCs is identical to that of mouse; therefore, the signaling factors for SSC self-renewal are conserved in these two species. Because SSCs from many mammals, including human, can replicate in mouse seminiferous tubules after transplantation, the growth factors required for SSC self-renewal may be conserved among many different species. Furthermore, development of a long-term culture system for rat SSCs has established a foundation for germ-line modification of the rat by gene targeting technology.germ-line stem cell ͉ spermatogenesis ͉ testis ͉ glial cell line-derived neurotrophic factor

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Section: Discussionmentioning

confidence: 93%

Conservation of spermatogonial stem cell self-renewal signaling between mouse and rat

Ryu

Kubota

Avarbock

et al. 2005

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

252

236

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“…Recently, basic studies have shown the presence of the interactions between N-cadherin and fibroblast growth factor (FGF) receptor (Doherty and Walsh, 1996;Saffell et al, 1997). Hazan et al (2000) demonstrated that treatment with FGF-2 induced N-cadherin-expressing breast carcinoma cells into a more invasive phenotype, with upregulation of matrix metalloproteinase MMP-9.…”

Section: Discussionmentioning

confidence: 99%

Neural-cadherin expression associated with angiogenesis in non-small-cell lung cancer patients

et al. 2003

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An immunohistochemical analysis for E(epithelial)-cadherin and N(neural)-cadherin expression in relation to tumour angiogenesis was performed in 150 patients with non-small-cell lung cancer (NSCLC). In all, 71 carcinomas (47.3%) were E-cadherin-negative. Epithelial-cadherin-negative tumours had lymph node metastases significantly more frequently than E-cadherin-positive tumours (P ¼ 0.0100). On the other hand, 46 carcinomas (30.7%) were N-cadherin-positive. Regarding tumour vascularity, there was no significant correlation between E-cadherin expression and tumour vascular. In contrast, the frequency of hypervascular tumours was significantly higher for N-cadherin-positive carcinomas than for N-cadherin-negative carcinomas (P ¼ 0.0373). Regarding prognosis, the 5-year survival rate of patients with E-cadherin-negative NSCLCs was significantly lower than that of patients with E-cadherinpositive NSCLCs (P ¼ 0.0146). In contrast, of the patients with large cell carcinomas, the 5-year survival rate of patients with N-cadherin-positive tumours was significantly lower than that of patients with N-cadherin-negative tumours (P ¼ 0.0013). A multivariate analysis demonstrated that E-cadherin status (P ¼ 0.0339) and tumour vascularity (P ¼ 0.0295) were significant indicators for survival. In conclusion, E-cadherin expression and tumour vascularity are significant prognostic factors of NSCLC patients. Furthermore, N-cadherin expression is associated with tumour angiogenesis, and its expression is one of prognostic factors of patients with large cell carcinomas. Thus, N-cadherin also might play a specific role in undifferentiated large cell carcinomas.

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“…NCAM has been demonstrated to induce neurite outgrowth by activation of the Ras-MAP kinase cascade and a pathway involving the fibroblast growth factor receptor, PLC␥ and PKC (Williams et al, 1994;Saffell et al, 1997;Schmid et al, 1999;Kolkova et al, 2000). To clarify whether cytNCAM-140 is involved in NCAM-dependent activation of the Ras-MAP kinase pathway, constitutively active MEK2 was expressed in PC12-E2 cells transfected with cytNCAM-140.…”

Section: Discussionmentioning

confidence: 99%

Identification of an Amino Acid Sequence Motif in the Cytoplasmic Domain of the NCAM‐140 kDa Isoform Essential for Its Neuritogenic Activity

Kolkova

Pedersen

Berezin

et al. 2000

Journal of Neurochemistry

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Abstract:The functions of the extracellular domains of neural cell adhesion molecule (NCAM) have been studied extensively, whereas the roles of the cytoplasmic domains of the transmembrane forms of NCAM are less elucidated. We investigated the importance of the cytoplasmic domain of the 140-kDa NCAM isoform (cyt-NCAM-140) and of the 180-kDa NCAM isoform (cyt-NCAM-180) in NCAM-induced neurite extension by estimating NCAM-dependent neurite outgrowth from PC12-E2 cells grown in coculture with NCAM-negative or NCAM-positive fibroblasts. PC12-E2 cells were transiently transfected with expression plasmids encoding cytNCAM-140, cytNCAM-180, the constitutively active form of the mitogen-activated protein (MAP) kinase/extracellular signal-regulated kinase kinase (MEK2), and the enhanced variant of the green fluorescent protein (EGFP). EGFP expression was used for identification of transfected cells. We found that expression of cytNCAM-180 had no effect on NCAM-stimulated neuritogenesis, whereas expression of cytNCAM-140 strongly inhibited this process. However, if MEK2 was expressed concomitantly with cytNCAM-140, neurite outgrowth was rescued, indicating that cytNCAM-140 is involved in signaling via the Ras-MAP kinase pathway. PC12-E2 cells were subsequently transiently transfected with constructs encoding a series of fragments of cytNCAM-140 and various full-length cytNCAM-140 mutants, and the residues Thr-Glu-Val-Lys-Thr (839 -843) were identified as essential in NCAM-stimulated neuritogenesis. The combined substitution of Glu 840 and Lys 842 with Ala abrogated the effect of the construct, assigning a critical role to these two residues. Key Words: NCAM-Cytoplasmic domain-Fibroblasts-Neurite outgrowth.

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Expression of a Dominant Negative FGF Receptor Inhibits Axonal Growth and FGF Receptor Phosphorylation Stimulated by CAMs

Cited by 315 publications

References 52 publications

Conservation of spermatogonial stem cell self-renewal signaling between mouse and rat

Conservation of spermatogonial stem cell self-renewal signaling between mouse and rat

Neural-cadherin expression associated with angiogenesis in non-small-cell lung cancer patients

Identification of an Amino Acid Sequence Motif in the Cytoplasmic Domain of the NCAM‐140 kDa Isoform Essential for Its Neuritogenic Activity

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