Evolution of the fusogenic activity of the receptor FGFRL1

Zhuang, Lei; Trüeb, Beat

doi:10.1016/j.abb.2017.06.002

Cited by 5 publications

(7 citation statements)

References 27 publications

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“…Overexpression of FGFRL1 did not affect cell proliferation or ERK1/2 phosphorylation in response to FGF2 but did promote cell adhesion, suggesting that its primary function may not involve FGF signaling (X. Yang, Steinberg, et al, 2016). In vertebrates, the third immunoglobulin‐like domain of FGFRL1 is required for cell fusion activity (Zhuang & Trueb, 2017).…”

Section: Regulation Of Fgfr Signal Transduction By Extracellular and ...mentioning

confidence: 99%

“…When FGFRL1 is overexpressed in cultured cells, it forms a homodimer on the cell surface and promotes cell adhesion through binding to HS (Rieckmann et al, 2008). Additionally, FGFRL1 was shown to induce cell clustering, cell–cell fusion, and formation of large multinucleated syncytia (Rieckmann et al, 2008; Steinberg et al, 2010; X. Yang, Steinberg, et al, 2016; Zhuang et al, 2015; Zhuang & Trueb, 2017).…”

Section: Regulation Of Fgfr Signal Transduction By Extracellular and ...mentioning

confidence: 99%

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New developments in the biology of fibroblast growth factors

Ornitz

Itoh

2022

WIREs Mechanisms of Disease

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The fibroblast growth factor (FGF) family is composed of 18 secreted signaling proteins consisting of canonical FGFs and endocrine FGFs that activate four receptor tyrosine kinases (FGFRs 1-4) and four intracellular proteins (intracellular FGFs or iFGFs) that primarily function to regulate the activity of voltagegated sodium channels and other molecules. The canonical FGFs, endocrine FGFs, and iFGFs have been reviewed extensively by us and others. In this review, we briefly summarize past reviews and then focus on new developments in the FGF field since our last review in 2015. Some of the highlights in the past 6 years include the use of optogenetic tools, viral vectors, and inducible transgenes to experimentally modulate FGF signaling, the clinical use of small molecule FGFR inhibitors, an expanded understanding of endocrine FGF signaling, functions for FGF signaling in stem cell pluripotency and differentiation, roles for FGF signaling in tissue homeostasis and regeneration, a continuing elaboration of mechanisms of FGF signaling in development, and an expanding appreciation of roles for FGF signaling in neuropsychiatric diseases.

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Section: Regulation Of Fgfr Signal Transduction By Extracellular and ...mentioning

confidence: 99%

Section: Regulation Of Fgfr Signal Transduction By Extracellular and ...mentioning

confidence: 99%

New developments in the biology of fibroblast growth factors

Ornitz

Itoh

2022

WIREs Mechanisms of Disease

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“…Another protein implicated in myoblast fusion is fibroblast growth factor receptor-like 1 (FGFRL1), which can fuse CHO cells, although in knockout mice a defect is only observed in slow muscle fibers; premature death prevents evaluating a role for FGFRL1 at later stages of myogenic development (Steinberg et al, 2010a,b;Zhuang et al, 2015). Surprisingly, the TMD and specific hydrophobic amino acids in an Ig domain (Ig3) are essential for its fusogenic activity, although no receptor partners have been identified (Zhuang and Trueb, 2017). Additional experiments are thus needed to determine how the Myomaker-micropeptide system mediates fusion and whether it acts in conjunction with FGFRL1 or if they display non-overlapping functions in different myogenic tissues.…”

Section: Myomaker and Its Associated Micropeptide: The Machinery Of Mmentioning

confidence: 99%

The hallmarks of cell-cell fusion

2017

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Cell-cell fusion is essential for fertilization and organ development. Dedicated proteins known as fusogens are responsible for mediating membrane fusion. However, until recently, these proteins either remained unidentified or were poorly understood at the mechanistic level. Here, we review how fusogens surmount multiple energy barriers to mediate cell-cell fusion. We describe how early preparatory steps bring membranes to a distance of ∼10 nm, while fusogens act in the final approach between membranes. The mechanical force exerted by cell fusogens and the accompanying lipidic rearrangements constitute the hallmarks of cell-cell fusion. Finally, we discuss the relationship between viral and eukaryotic fusogens, highlight a classification scheme regrouping a superfamily of fusogens called Fusexins, and propose new questions and avenues of enquiry.

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“…These receptors are transmembrane proteins with their own well-defined structural characteristics [ 37 ]. Specifically, the extracellular portion consists of a hydrophobic signal sequence, e.g., IgG domains [ 38 ], and an acidic region (acid box) essential for binding to heparin [ 39 ], comprising four and eight acidic amino acids varying in the various FGFR receptors [ 40 ]. In the C-terminal portion of the receptor, on the other hand, there are transmembrane and intracellular regions; precisely, the latter includes a juxta-membrane region, two kinase domains, and a region between kinase domains (called kinase insert), as well as a carboxy-terminal region that contains the autophosphorylation sites, thus allowing interaction with specific substrates [ 41 ].…”

Section: Fibroblast Growth Factors (Fgfs) and Fibroblast Growth Famentioning

confidence: 99%

Role of Fibroblast Growth Factors Receptors (FGFRs) in Brain Tumors, Focus on Astrocytoma and Glioblastoma

Ardizzone

Scuderi

Giuffrida³

et al. 2020

Cancers

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Despite pharmacological treatments and surgical practice options, the mortality rate of astrocytomas and glioblastomas remains high, thus representing a medical emergency for which it is necessary to find new therapeutic strategies. Fibroblast growth factors (FGFs) act through their associated receptors (FGFRs), a family of tyrosine kinase receptors consisting of four members (FGFR1–4), regulators of tissue development and repair. In particular, FGFRs play an important role in cell proliferation, survival, and migration, as well as angiogenesis, thus their gene alteration is certainly related to the development of the most common diseases, including cancer. FGFRs are subjected to multiple somatic aberrations such as chromosomal amplification of FGFR1; mutations and multiple dysregulations of FGFR2; and mutations, translocations, and significant amplifications of FGFR3 and FGFR4 that correlate to oncogenesis process. Therefore, the in-depth study of these receptor systems could help to understand the etiology of both astrocytoma and glioblastoma so as to achieve notable advances in more effective target therapies. Furthermore, the discovery of FGFR inhibitors revealed how these biological compounds improve the neoplastic condition by demonstrating efficacy and safety. On this basis, this review focuses on the role and involvement of FGFRs in brain tumors such as astrocytoma and glioblastoma.

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Evolution of the fusogenic activity of the receptor FGFRL1

Cited by 5 publications

References 27 publications

New developments in the biology of fibroblast growth factors

New developments in the biology of fibroblast growth factors

The hallmarks of cell-cell fusion

Role of Fibroblast Growth Factors Receptors (FGFRs) in Brain Tumors, Focus on Astrocytoma and Glioblastoma

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