| 2001 |
Purified recombinant FGFBP1 directly binds FGF-2 without additional cofactors, releases FGF-2 from the extracellular matrix, and stimulates tumor cell and endothelial cell proliferation/chemotaxis in a manner fully blocked by anti-FGF-2 antibodies, demonstrating that its paracrine growth-supporting effect is dependent on endogenously expressed FGF-2. |
In vitro binding assay with recombinant purified FGF-BP, cell proliferation and chemotaxis assays, antibody neutralization, immunoreactive complex analysis |
International journal of cancer |
High |
11304685
|
| 1998 |
Peptide mapping of FGFBP1 (HBp17) identified residues 110–143 as the principal heparin-binding site, with a basic amino acid cluster contributing to binding to heparin and heparan sulfate proteoglycans of the ECM. |
V8 protease and chymotrypsin digestion of purified HBp17 followed by heparin-Sepharose affinity isolation of binding fragments |
Biochemistry and molecular biology international |
Medium |
9784842
|
| 2001 |
Serum induction of FGF-BP transcription requires PKC, MEK/ERK, and p38 MAP kinase activation, and is mediated through C/EBP promoter elements rather than AP-1 or E-box sites, as distinct from EGF-mediated induction. |
Promoter deletion analysis, kinase inhibitors, transcription rate assay, serum stimulation of ME-180 cells |
Oncogene |
Medium |
11313920
|
| 2005 |
Bovine milk FGFBP1 (p37) binds bFGF with higher affinity than lactoferrin, serves as a phosphate acceptor for PKA, CK1, and CK2, and full PKA-mediated phosphorylation abolishes its binding to lactoferrin; sulfatide-induced conformational changes enable CK1 phosphorylation and also reduce lactoferrin binding. |
HPLC purification, in vitro kinase assay, FGF binding assay, phosphorylation/binding competition experiments |
Biochimica et biophysica acta |
Medium |
16412577
|
| 2001 |
FGFBP1 (HBp17) exerts a biphasic dose-dependent effect on DNA synthesis: stimulatory at low concentrations (~8 ng/ml) and inhibitory at high concentrations (~500 ng/ml); the inhibitory effect is reversed by addition of aFGF or bFGF but not EGF, indicating functional interdependence with FGFs. |
DNA synthesis assay in 3T3 cells and HUVECs with recombinant HBp17, FGF rescue experiments |
Cell biology international |
Medium |
11407864
|
| 2012 |
1α,25(OH)2D3 down-regulates FGFBP1 (HBp17) expression via the NF-κB pathway: treatment upregulates IκBα, and promoter luciferase assays map the responsive region to -217/+61; VDR siRNA silencing abrogates the effect, confirming VDR dependence. |
Luciferase reporter assay, NF-κB pathway analysis (IκBα Western blot), VDR siRNA knockdown |
The Journal of steroid biochemistry and molecular biology |
Medium |
23104116
|
| 2014 |
1α,25(OH)2D3 suppresses FGFBP1 expression in both nucleus and cytosol of OSCC cells, leading to reduced FGF-2 release into conditioned medium, directly linking FGFBP1 levels to extracellular FGF-2 availability. |
Immunofluorescence localization, ELISA measurement of FGF-2 in conditioned medium, 1α,25(OH)2D3 treatment |
In vitro cellular & developmental biology. Animal |
Medium |
24938357
|
| 2016 |
miR-146a promotes angiogenesis in endothelial cells via the CREB3L1-FGFBP1 axis: miR-146a directly targets CREB3L1, which normally represses FGFBP1 transcription by binding two CRE-like sites at −1780 and −868 bp relative to the FGFBP1 TSS; loss of CREB3L1 increases FGFBP1 expression and FGF2 secretion. |
Luciferase reporter assay, ChIP of CREB3L1 on FGFBP1 promoter, lentiviral miR-146a overexpression, FGF2 ELISA |
Scientific reports |
Medium |
27121396
|
| 2017 |
Muscle fiber-secreted FGFBP1 is concentrated at neuromuscular junctions (NMJs); its expression decreases during aging and in SOD1G93A ALS mice before NMJ degeneration. FGFBP1 knockout mice develop structural NMJ abnormalities; knockout in SOD1G93A mice accelerates NMJ degeneration and death. TGF-β1 accumulation in skeletal muscle inhibits FGFBP1 expression. |
FGFBP1 knockout mouse model, SOD1G93A double mutant, immunofluorescence localization at NMJs, TGF-β1 treatment |
The Journal of neuroscience |
High |
28053031
|
| 2017 |
Inducible transgenic expression of FGFBP1 in adult mice elevates mean arterial pressure by >30 mmHg. This hypertensive effect is prevented by angiotensin II receptor antagonist candesartan or ROS inhibitor tempol. FGFBP1 sensitizes peripheral resistance vessels and renal afferent arterioles to AngII constriction ~20-fold via FGF receptor kinase-dependent signaling. In FGF2−/− mice, AngII-mediated arteriolar constriction is abolished but restored by FGF2 plus FGFBP1 add-back. Proteomics identifies downstream MAPK signaling via MKK4, p38, and JNK as integrators of FGFR and AngII crosstalk. |
Inducible transgenic mouse model, pharmacological inhibition (candesartan, tempol, FGFR kinase inhibitor), isolated arteriole constriction assay, FGF2−/− mice with protein add-back, kidney proteomics/gene expression |
Hypertension |
High |
29158353
|
| 2020 |
Endothelial-specific ablation of Fgfbp1 in mice delays BBB maturation with upregulation of Plvap and increased tracer leakage, reduces Wnt/β-catenin activity, and decreases collagen IV deposition in the vascular basement membrane, impairing endothelial cell-pericyte interactions. Fgfbp1 acts cell-autonomously in brain endothelial cells to concentrate Wnt ligands near cell junctions. |
Conditional endothelial knockout mouse, tracer leakage assay, immunofluorescence, collagen IV staining, in vitro Wnt reporter in mBECs |
Development |
High |
32747434
|
| 2020 |
FGFBP1-mediated signaling sensitizes brain microvessels and macrovessels to AngII constriction after acute kidney injury (AKI); administration of recombinant FGF2 plus FGFBP1 proteins to healthy isolated brain vessels mimics AKI-induced sensitization, and Fgfbp1−/− AKI mice fail to develop this sensitization. FGFR kinase inhibition with BGJ398 reverses the effect. |
Bilateral renal ischemia-reperfusion AKI model, Fgfbp1−/− mice, ex vivo vessel constriction assay, recombinant protein add-back, pharmacological FGFR inhibition |
Hypertension |
High |
33040621
|
| 2020 |
HSD11B2 promotes colorectal cancer cell migration and invasion by upregulating FGFBP1 expression, which subsequently increases AKT phosphorylation. Knockdown of FGFBP1 or AKT impairs the pro-invasive effect of HSD11B2 overexpression, placing FGFBP1 downstream of HSD11B2 in the HSD11B2-FGFBP1-AKT axis. |
mRNA transcriptome array, overexpression and knockdown in CRC cells, in vitro migration/invasion assays, in vivo xenograft, AKT phosphorylation Western blot |
American journal of cancer research |
Medium |
32195034
|
| 2021 |
FGFBP1 promotes pancreatic cancer invasion/metastasis through a paracrine mechanism involving cancer-associated fibroblasts (CAFs): FGFBP1 regulates FGF22 secretion from CAFs, and FGF22 signals through FGFR2 on pancreatic cancer cells to facilitate their migration and invasion. |
Co-culture of CAFs and pancreatic cancer cells with FGFBP1/FGF22/FGFR2 knockdown, ELISA for FGF22 in conditioned medium, invasion assay |
Acta biochimica et biophysica Sinica |
Medium |
34117747
|
| 2021 |
Poly-L-arginine (mimic of eosinophil MBP) induces FGFBP1 expression in airway epithelial cells via the mTORC1-STAT3 pathway; STAT3 directly binds the FGFBP1 promoter to transactivate it; secreted FGFBP1 acts as a proangiogenic factor, and rapamycin treatment reduces FGFBP1 expression and angiogenesis in OVA-induced asthma mice. |
ChIP of STAT3 on FGFBP1 promoter, mTORC1/STAT3 inhibitors, OVA mouse model, rapamycin treatment |
Cell death & disease |
Medium |
34341336
|
| 2015 |
FGFBP1 is a direct transcriptional target of Sox12: serial deletion, site-directed mutagenesis, and ChIP assays confirm Sox12 binding to the FGFBP1 promoter. FGFBP1 knockdown decreases Sox12-mediated HCC invasion and metastasis, whereas FGFBP1 overexpression rescues the reduced metastasis caused by Sox12 knockdown. |
Serial deletion and mutagenesis of FGFBP1 promoter, ChIP, siRNA knockdown and rescue overexpression, in vitro invasion and in vivo metastasis assays |
Hepatology |
Medium |
25704764
|
| 2023 |
SGCE interacts with the Sp1 transcription factor and translocates to the nucleus, increasing FGF-BP1 transcription; secreted FGF-BP1 then activates FGF-FGFR signaling to promote cancer cell stemness in triple-negative breast cancer. |
Co-immunoprecipitation of SGCE-Sp1, nuclear fractionation, transcriptional reporter assay, FGFBP1 knockdown/overexpression, stem cell 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 of human keratinocytes independently of FGF interactions. This novel function requires HAI-1; recombinant FGFBP1 at 1 ng/ml reverts morphological and F-actin defects caused by HAI-1 knockout. |
HAI-1 KO HaCaT cells, conditioned medium rescue, tandem mass spectrometry identification of FGFBP1, recombinant FGFBP1 add-back, F-actin staining |
Human cell |
Medium |
37076641
|
| 2010 |
Morpholino knockdown of fgfbp1 in zebrafish embryos causes massive cell death predominantly in the brain and neural tube and structural abnormalities, indicating an essential role in cellular survival during embryogenesis that can be exerted in an FGF2-independent manner. |
Morpholino antisense knockdown in zebrafish, phenotypic analysis of cell death and structural defects |
Molecules and cells |
Medium |
20396962
|
| 2025 |
FGF6 from skeletal muscle regulates FGFBP1 expression through ERK-ATF3 signaling, and FGF6 also perturbs heparin-dependent release kinetics of FGFBP1 by disrupting its liquid-liquid phase separation (LLPS)-driven condensates at the plasma membrane. Circulating FGFBP1 then interacts with hepatic FGF5 via LLPS mechanisms to regulate liver regeneration. |
RNA-seq, ATAC-seq, ChIP, luciferase assay, muscle-specific GR/FGF6 knockout mice, FGF6 neutralizing antibody, phase separation assay, ELISA |
Military Medical Research |
Medium |
40685360
|
| 2026 |
FGFBP1 is a STAT3-dependent effector of pathological cardiac remodeling: AngII activates STAT3 in cardiomyocytes, which induces FGFBP1 transcription and promotes profibrotic signaling. FGFBP1 KO mice show significantly attenuated cardiac hypertrophy and fibrosis after AngII/TAC, and STAT3 inhibitor S3I-201 reduces FGFBP1 expression and recapitulates the KO phenotype. |
FGFBP1 KO mouse model, AngII and TAC cardiac stress models, RNA sequencing, STAT3 pharmacological inhibition, cardiac function and fibrosis assessment |
Biochimica et biophysica acta. Molecular basis of disease |
High |
42013958
|
| 2026 |
HMGA1 directly binds the FGFBP1 promoter to induce its expression, increasing secretion of FGF2 and promoting tumor progression and angiogenesis in head and neck squamous cell carcinoma via FGFR1 signaling. FGFBP1 silencing or FGFR1 inhibitor PD166866 recapitulates HMGA1 silencing phenotypes. |
ChIP of HMGA1 on FGFBP1 promoter, RNA sequencing, FGFBP1 siRNA, FGFR1 inhibitor, xenograft mouse model |
International journal of biological sciences |
Medium |
41943828
|
| 2025 |
FGFBP1 promotes TNBC cell proliferation, migration, and invasion through the KLK10-AKT axis: FGFBP1 overexpression upregulates KLK10 expression, activating AKT; KLK10 knockdown or AKT inhibition impairs the pro-tumorigenic effects of FGFBP1 overexpression. |
Overexpression and knockdown in TNBC cell lines, in vivo xenograft, Western blot for KLK10/AKT, rescue epistasis experiments |
Biochemical and biophysical research communications |
Medium |
40233428
|