Purification of recombinant human fibroblast growth factor 13 in E. coli and its molecular mechanism of mitogenesis

Lin, Haipeng; Lu, Panyu; Zhou, Mi; Wu, Fenfang; Weng, Lei; Meng, Kuikui; Yang, Dan; Li, Shijun; Jiang, Chao; Tian, Haishan

doi:10.1007/s00253-019-09973-y

Cited by 19 publications

(13 citation statements)

References 32 publications

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“…Globally, cell cycle-related genes, such as CDK1 and AURKB , are downregulated in the adult, while structural and metabolic genes, such as MYOM2 and CD36 , are upregulated in the adult compared with fetal and in vitro CMs ( Figure 1 E). Similarly, several MAPK genes, such as MAP2K6 and MAP3K1 , or upstream activators of the pathway, such as FGF13 ( Lin et al., 2019 ) and IGF2BP3 ( Suvasini et al., 2011 ), show significant downregulation postnatally. Meanwhile, negative regulators, such as the dual-specificity phosphatases DUSP1 and DUSP6 ( Owens and Keyse, 2007 ), are significantly upregulated in the adult compared with fetal and in vitro CMs ( Figure 1 E).…”

Section: Resultsmentioning

confidence: 99%

Dual inhibition of MAPK and PI3K/AKT pathways enhances maturation of human iPSC-derived cardiomyocytes

et al. 2022

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Section: Resultsmentioning

confidence: 99%

Dual inhibition of MAPK and PI3K/AKT pathways enhances maturation of human iPSC-derived cardiomyocytes

et al. 2022

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“…Structural studies suggested that differences in two conserved amino acid residues would greatly reduce the ability of iFGFs to interact with FGFRs (Olsen et al, 2003). However, a recent study demonstrated that recombinant FGF13 (FHF2) can induce proliferation of NIH3T3 cells in a heparin and FGFR-dependent manner (H. Lin, Lu, et al, 2019). Another study showed that FGF12 (FHF1) internalization is protective against radiation injury, but independent of FGFRs (Nakayama et al, 2014).…”

Section: Intracellular Fgfsmentioning

confidence: 99%

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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“…However, recent studies have shown that exogenous iFGFs can activate signaling. Treatment of cells with FGF11 and FGF13 can activate signaling cascades [ 174 , 175 ] and, in the case of FGF11, can initiate antiapoptotic processes and bind all four FGFRs to activate signaling when ectopically expressed [ 174 ]. Given that a mechanism of iFGF secretion has not been described, the physiological role of iFGFs in activating FGFR remains to be elucidated.…”

Section: Fgf Signaling Diversity In Cancermentioning

confidence: 99%

Fibroblast Growth Factor Receptors (FGFRs) and Noncanonical Partners in Cancer Signaling

Ferguson

Smith

Francavilla

2021

Cells

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Increasing evidence indicates that success of targeted therapies in the treatment of cancer is context-dependent and is influenced by a complex crosstalk between signaling pathways and between cell types in the tumor. The Fibroblast Growth Factor (FGF)/FGF receptor (FGFR) signaling axis highlights the importance of such context-dependent signaling in cancer. Aberrant FGFR signaling has been characterized in almost all cancer types, most commonly non-small cell lung cancer (NSCLC), breast cancer, glioblastoma, prostate cancer and gastrointestinal cancer. This occurs primarily through amplification and over-expression of FGFR1 and FGFR2 resulting in ligand-independent activation. Mutations and translocations of FGFR1-4 are also identified in cancer. Canonical FGF-FGFR signaling is tightly regulated by ligand-receptor combinations as well as direct interactions with the FGFR coreceptors heparan sulfate proteoglycans (HSPGs) and Klotho. Noncanonical FGFR signaling partners have been implicated in differential regulation of FGFR signaling. FGFR directly interacts with cell adhesion molecules (CAMs) and extracellular matrix (ECM) proteins, contributing to invasive and migratory properties of cancer cells, whereas interactions with other receptor tyrosine kinases (RTKs) regulate angiogenic, resistance to therapy, and metastatic potential of cancer cells. The diversity in FGFR signaling partners supports a role for FGFR signaling in cancer, independent of genetic aberration.

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Purification of recombinant human fibroblast growth factor 13 in E. coli and its molecular mechanism of mitogenesis

Cited by 19 publications

References 32 publications

Dual inhibition of MAPK and PI3K/AKT pathways enhances maturation of human iPSC-derived cardiomyocytes

Dual inhibition of MAPK and PI3K/AKT pathways enhances maturation of human iPSC-derived cardiomyocytes

New developments in the biology of fibroblast growth factors

Fibroblast Growth Factor Receptors (FGFRs) and Noncanonical Partners in Cancer Signaling

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