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Fibroblast Growth Factor (FGF) 13. | LitMetric

Fibroblast Growth Factor (FGF) 13.

Differentiation

Department of Biosciences, Rice University, Houston, TX, United States; Biochemistry and Cell Biology Graduate Program, Rice University, Houston, TX, United States. Electronic address:

Published: December 2024

AI Article Synopsis

  • FGF 13, or FGF homologous factor 2, is part of the FGF11 subfamily, distinguished by its lack of binding to classical FGF receptors despite having similar sequences.
  • It is predominantly expressed in neurons and the heart, remains present in adult tissues, and has a unique localization within both the cytoplasm and nucleus.
  • FGF13 plays a versatile role by interacting with various proteins and stabilizing microtubules, and mutations in the Fgf13 gene are linked to several X-linked neurological diseases.

Article Abstract

Fibroblast Growth Factor (FGF) 13, also referred to as FGF homologous factor (FHF) 2, is a member of the FGF11 subfamily that is characterized as having sequence similarities to classical FGF receptor (FGFR)-binding FGFs, but functionally do not bind FGFRs. In this primer mini-review, we summarize current knowledge regarding FGF13 expression, mutant analyses, and gene and protein structure. Similar to other FHFs, FGF13 has been considered a non-secreted protein that lacks an amino signal and is prominently expressed in developing and mature neurons of the central and peripheral nervous systems, as well as the heart. The expression of FGF13 is not limited to early embryonic stages and has been shown to persist in adult tissues. As well, FGF13 is known to localize subcellularly, both within the cytoplasm and the nucleus. FGF13 is extremely adaptable, as it interacts with MAPK scaffolding protein islet brain 2 (IB2), stabilizes microtubules, or binds to voltage-gated sodium channels. Fgf13 mutant mouse lines display various neurological pathologies. Through sequence mapping, FGF13 is considered a candidate causative gene that is mutated in multiple human X-linked neurological diseases.

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Source
http://dx.doi.org/10.1016/j.diff.2024.100814DOI Listing

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