| 2001 |
Purified recombinant FGF-BP (FGFBP1) directly binds FGF-2 without additional cofactors, releases FGF-2 from the extracellular matrix, and stimulates tumor cell and endothelial cell proliferation and chemotaxis in a manner completely blocked by anti-FGF-2 antibodies, demonstrating that its paracrine growth-supporting effects are dependent on endogenously expressed FGF-2. |
In vitro binding assay with recombinant purified FGF-BP; cell proliferation and chemotaxis assays; antibody neutralization; immunodetection of high-molecular-weight FGF-BP complexes in xenografts |
International journal of cancer |
High |
11304685
|
| 1998 |
The heparin-binding site of FGFBP1 (HBp17) was mapped to residues 110–143 using protease digestion (V8 and chymotrypsin) followed by heparin-Sepharose isolation of binding fragments; a basic amino acid cluster in this region mediates binding to heparin/heparan sulfate proteoglycan. |
Protease peptide mapping; heparin-Sepharose affinity chromatography of peptide fragments |
Biochemistry and molecular biology international |
Medium |
9784842
|
| 2001 |
Serum induction of FGF-BP mRNA in squamous cell carcinoma cells is dependent on PKC, ERK kinase (MEK), and p38 MAP kinase activation, and the C/EBP promoter element is the main element required for this serum response; the mechanism differs from EGF-mediated induction (which uses AP-1 and E-box sites). |
Promoter analysis; kinase inhibitors; transcription run-on assay; site-directed mutagenesis of promoter elements |
Oncogene |
Medium |
11313920
|
| 2001 |
HBp17 (FGFBP1) exhibits a biphasic dose-dependent effect on DNA synthesis: low concentrations (8 ng/ml) maximally stimulate DNA synthesis while high concentrations (~500 ng/ml) cause half-maximal inhibition, and this inhibition is reversed by addition of aFGF or bFGF but not EGF. |
DNA synthesis assay in 3T3 cells and HUVECs at varying HBp17 concentrations; FGF rescue experiment |
Cell biology international |
Medium |
11407864
|
| 2005 |
Bovine FGF-BP (FGFBP1 ortholog, p37) purified from milk has higher binding affinity for bFGF than lactoferrin, serves as a phosphate acceptor for PKA, CK1, and CK2, and full phosphorylation by PKA abolishes its binding to lactoferrin in vitro; sulfatide-induced conformational changes enable CK1-mediated phosphorylation and also reduce lactoferrin binding. |
Heparin-HPLC purification; in vitro kinase assays (PKA, CK1, CK2); binding affinity assay; N-terminal sequencing |
Biochimica et biophysica acta |
Medium |
16412577
|
| 2007 |
N-terminal fragment p5 (residues 24–51) cleaved from FGF-BP in bovine milk is phosphorylated by PKA and CK1δ; CK1δ phosphorylation requires sulfated lipids (sulfatide or cholesterol-3-sulfate); a novel CK1δ phosphorylation site (RNRRGS) and SCS-binding site (RNRR) were identified; p5 (but not phosphorylated p5) directly binds aFGF. |
Gel filtration purification; in vitro kinase assays; immunoprecipitation; synthetic peptide analysis |
Biochimica et biophysica acta |
Medium |
17560725
|
| 2010 |
Morpholino-mediated knockdown of Fgfbp1 in zebrafish causes massive cell death prominently in brain and neural tube, indicating that Fgfbp1 is essential for cellular survival during embryogenesis; this function appears to be at least partly FGF2-independent, as fgf2 morphants show a more severe and earlier phenotype. |
Morpholino knockdown in zebrafish embryos; cell death assay; comparison with fgf2 morphants |
Molecules and cells |
Medium |
20396962
|
| 2012 |
1α,25(OH)2D3 downregulates HBp17/FGFBP1 mRNA and protein in oral squamous cell carcinoma cells via the NF-κB pathway (upregulating IκBα), and this effect requires vitamin D receptor (VDR); luciferase assay identified the responsive promoter region between −217 and +61. |
RT-PCR; Western blotting; luciferase reporter assay; VDR siRNA knockdown |
The Journal of steroid biochemistry and molecular biology |
Medium |
23104116
|
| 2014 |
1α,25(OH)2D3 suppresses HBp17/FGFBP1 expression in both nucleus and cytosol of OSCC cells via NF-κB/VDR pathway, and this suppression results in reduced FGF-2 release into culture medium, establishing FGFBP1 as a chaperone required for FGF-2 secretion. |
Immunofluorescence; ELISA for FGF-2 in conditioned medium; pharmacological treatment |
In vitro cellular & developmental biology. Animal |
Medium |
24938357
|
| 2016 |
CREB3L1 suppresses FGFBP1 expression by binding to two CRE-like sites at approximately −1780 and −868 bp in the FGFBP1 promoter; miR-146a targets CREB3L1, thereby de-repressing FGFBP1 expression and increasing FGF2 secretion to promote angiogenesis in HUVECs. |
Luciferase reporter assay with FGFBP1 promoter; ChIP; CREB3L1 overexpression; FGF2 ELISA; lentiviral miR-146a overexpression |
Scientific reports |
Medium |
27121396
|
| 2017 |
Muscle fibers secrete and concentrate FGFBP1 at neuromuscular junctions (NMJs); FGFBP1 expression decreases before NMJ degeneration during aging and in SOD1G93A ALS mice; genetic deletion of FGFBP1 causes NMJ structural abnormalities and accelerates NMJ degeneration and death in SOD1G93A mice; TGF-β1 accumulation in stressed muscles inhibits FGFBP1 expression. |
FGFBP1 knockout mice; SOD1G93A mouse model; NMJ structural analysis; survival assay; TGF-β1 treatment |
The Journal of neuroscience |
High |
28053031
|
| 2017 |
Inducible transgenic expression of FGFBP1 (BP1) in adult mice causes a sustained >30 mmHg rise in mean arterial blood pressure; this hypertensive effect is prevented by the AngII receptor antagonist candesartan or by the ROS inhibitor tempol; BP1 expression sensitizes peripheral resistance vessels and renal afferent arterioles to AngII constriction by ~20-fold via FGF receptor kinase-dependent signaling; AngII-mediated constriction is abolished in FGF2−/− mice but restored by FGF2 + BP1 add-back; MAPK signaling via MKK4, p38, and JNK integrates FGF receptor and AngII pathway crosstalk. |
Inducible transgenic mouse model; blood pressure telemetry; pharmacological inhibition (candesartan, tempol, FGFR kinase inhibitor); isolated vessel constriction assay; FGF2−/− mice with protein add-back; proteomics and gene expression analysis of kidney |
Hypertension |
High |
29158353
|
| 2019 |
FGFBP1 is regulated by the FBW7/c-Myc axis in pancreatic cancer: FBW7 reduces FGFBP1 expression in a c-Myc-dependent manner; FGFBP1 silencing inhibits pancreatic cancer cell proliferation and metastasis, and FBW7 silencing partially reverses the effects of FGFBP1 silencing. |
siRNA knockdown; overexpression; co-expression correlation in patient tissue; epistasis rescue experiments in cell lines |
American journal of cancer research |
Medium |
31911852
|
| 2020 |
Endothelial genetic ablation of Fgfbp1 in mice causes transient hypervascularization, delays blood-brain barrier maturation (increased Plvap, increased tracer leakage) due to reduced Wnt/β-catenin activity, and reduces collagen IV deposition in the vascular basement membrane leading to defective pericyte interactions; Fgfbp1 acts cell-autonomously in brain endothelial cells to concentrate Wnt ligands near cell junctions. |
Endothelial-specific Fgfbp1 knockout mice; tracer leakage assay; immunostaining for Plvap and collagen IV; in vitro barrier assay with Wnt ligand localization |
Development (Cambridge, England) |
High |
32747434
|
| 2020 |
FGFBP1 mediates AKI-induced brain vascular sensitization to AngII: after bilateral renal ischemia-reperfusion injury, FGF2 and FGFBP1 are upregulated in serum and kidney; exogenous FGF2 + FGFBP1 proteins applied to healthy brain vessels mimic AKI-induced AngII sensitization; Fgfbp1−/− AKI mice fail to develop brain vascular AngII sensitization; FGFR kinase inhibition (BGJ398) reverses sensitization. |
Bilateral renal ischemia-reperfusion mouse model; Fgfbp1 knockout mice; isolated vessel constriction assay; protein add-back; FGFR inhibitor treatment |
Hypertension |
High |
33040621
|
| 2020 |
HSD11B2 promotes colorectal cancer cell migration and invasion by upregulating FGFBP1 expression, which subsequently increases AKT phosphorylation; knockdown of either FGFBP1 or AKT impairs the migration/invasion promoted by HSD11B2 overexpression, placing FGFBP1 downstream of HSD11B2 in the HSD11B2-FGFBP1-AKT pathway. |
mRNA transcriptome array; overexpression and knockdown in CRC cell lines; in vitro migration/invasion assay; in vivo metastasis model; AKT phosphorylation Western blot |
American journal of cancer research |
Medium |
32195034
|
| 2021 |
In pancreatic cancer, FGFBP1 expressed in cancer-associated fibroblasts (CAFs) promotes FGF22 release; FGF22 activates FGFR2 on pancreatic cancer cells to facilitate their invasion and metastasis; silencing FGFR2 in cancer cells blocks FGF22-driven invasion even with FGF22 treatment. |
Co-culture of CAFs with pancreatic cancer cells; FGFBP1 knockdown; ELISA for FGF22 in conditioned medium; siRNA knockdown of FGF22 and FGFR2; invasion assay |
Acta biochimica et biophysica Sinica |
Medium |
34117747
|
| 2021 |
Poly-L-arginine (mimic of eosinophil major basic protein) induces FGFBP1 expression in airway epithelial cells via activation of the mTORC1-STAT3 signaling pathway; STAT3 directly binds to the FGFBP1 promoter and transactivates its expression; FGFBP1 secreted by PLA-treated cells promotes angiogenesis. |
ChIP for STAT3 on FGFBP1 promoter; mTOR inhibitor (rapamycin); STAT3 pathway assays; angiogenesis assay; OVA asthma mouse model |
Cell death & disease |
Medium |
34341336
|
| 2023 |
SGCE interacts with the Sp1 transcription factor and translocates to the nucleus, leading to transcriptional activation of FGF-BP1; secreted FGF-BP1 then activates FGF-FGFR signaling to promote breast cancer cell stemness. |
Co-immunoprecipitation of SGCE and Sp1; nuclear fractionation; SGCE overexpression/depletion; FGF-BP1 promoter reporter assay; stemness functional assays |
The Journal of biological chemistry |
Medium |
37838174
|
| 2023 |
FGFBP1 acts as an extracellular ligand that rapidly elicits F-actin rearrangement and maintains cobblestone morphology in human keratinocytes; this function depends on HAI-1, as HAI-1 KO cells lose normal morphology and F-actin organization, which is restored by conditioned medium containing FGFBP1 or by recombinant FGFBP1 at ≥1 ng/ml; FGFBP1 was identified as the active factor in conditioned medium by tandem mass spectrometry. |
HAI-1 knockout in HaCaT cells; conditioned medium rescue; tandem mass spectrometry identification; recombinant FGFBP1 add-back; F-actin imaging |
Human cell |
Medium |
37076641
|
| 2023 |
KLF5 transcription factor binds to the FGF-BP1 promoter and transcriptionally activates its expression in esophageal squamous cell carcinoma, contributing to tumor proliferation, migration, and invasion via FGF-BP1/SNAIL2 signaling. |
ChIP for KLF5 on FGFBP1 promoter; luciferase reporter assay; KLF5 overexpression/knockdown; cell proliferation and invasion assays |
Medical oncology |
Medium |
38087142
|
| 2025 |
FGFBP1 overexpression in sheep adipocytes inhibits proliferation by causing G2/M cell cycle arrest and promotes adipocyte differentiation by upregulating PPARγ, Adiponectin, C/EBPα, and FABP4; knockdown has the opposite effects, establishing FGFBP1 as a regulator of adipogenesis. |
Overexpression and siRNA knockdown in ovine preadipocytes; cell cycle analysis; lipid droplet staining; RT-qPCR for adipogenic markers |
Animals |
Low |
40427333
|
| 2025 |
During acute liver injury, FGF6 (induced by glucocorticoid signaling in skeletal muscle) regulates FGFBP1 expression through an ERK-ATF3 signaling pathway and perturbs FGFBP1 heparin-dependent release kinetics by disrupting FGFBP1 liquid-liquid phase separation (LLPS)-driven condensate dynamics at the plasma membrane; circulating FGFBP1 subsequently interacts with hepatic FGF5 via LLPS to regulate liver regeneration. |
RNA-seq; ATAC-seq; ChIP; luciferase assay; muscle-specific GR knockdown mice; Fgf6 knockout mice; FGF6 neutralizing antibody; LLPS/phase separation assay; ELISA for serum FGFBP1 in ALI patients |
Military Medical Research |
Medium |
40685360
|
| 2025 |
FGFBP1 promotes TNBC cell proliferation, migration, and invasion by upregulating KLK10 expression, which activates AKT; knockdown of KLK10 or AKT inhibition impairs FGFBP1 overexpression-driven tumor cell phenotypes. |
FGFBP1 overexpression/knockdown in TNBC cell lines; KLK10 knockdown; AKT inhibitor; proliferation and invasion assays in vitro and in vivo (xenograft) |
Biochemical and biophysical research communications |
Low |
40233428
|
| 2026 |
Angiotensin II activates STAT3 in cardiomyocytes, which directly induces FGFBP1 transcription; FGFBP1 KO mice show significantly attenuated Ang II- and TAC-induced cardiac hypertrophy, dysfunction, and interstitial fibrosis; pharmacological STAT3 inhibition (S3I-201) reduces FGFBP1 expression and recapitulates the protective KO phenotype. |
FGFBP1 knockout mice; Ang II infusion and TAC models; RNA sequencing; STAT3 inhibitor (S3I-201); cardiac function and histology |
Biochimica et biophysica acta. Molecular basis of disease |
Medium |
42013958
|