FGF-19 Antibody [L9N16] | Primary Antibodies

Application: Reactivity: Human

Usage Information

Dilution
WB1:1000 IHC1:40-1:125

Application
WB, IHC

Reactivity
Human

Source
Mouse Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW
24 kDa

Datasheet & SDS

Biological Description

Specificity
FGF-19 Antibody [L9N16] detects endogenous levels of total FGF-19 protein.

Clone
L9N16

Synonym(s)
Fibroblast growth factor 19, FGF-19, FGF19

Background
FGF‑19 is an endocrine member of the fibroblast growth factor family that links bile acid sensing in the distal intestine to metabolic and proliferative signaling in the liver through selective activation of FGFR4–β‑Klotho receptor complexes. The protein shares the conserved FGF core fold that supports heparin binding and receptor engagement but displays distinctive sequence features that confer high affinity and functional specificity for FGFR4, positioning it as a ligand with restricted receptor usage compared with many paracrine FGFs. FGF‑19 expression in ileal enterocytes is induced by bile acid–activated farnesoid X receptor, and the secreted hormone enters the portal circulation to engage FGFR4–β‑Klotho on hepatocytes, where receptor autophosphorylation triggers downstream kinase cascades including ERK and other MAPK branches that repress transcription of the bile acid synthesis enzyme CYP7A1 and adjust bile acid transport and conjugation pathways. Through these mechanisms, FGF‑19 establishes a negative feedback loop that stabilizes bile acid pool size and composition after feeding and coordinates intestinal uptake with hepatic synthesis to maintain bile acid homeostasis. FGF‑19 also signals through FGFR4–β‑Klotho and, in some contexts, through β‑Klotho complexes with other FGFRs in metabolic tissues to influence glucose utilization, lipid handling, and energy expenditure, integrating nutrient status with transcriptional programs that regulate gluconeogenesis, glycogen storage, and lipid metabolism. Persistent or ectopic FGF‑19–FGFR4 activation in the liver engages mitogenic signaling outputs of FGFR4, including sustained ERK pathway activity and associated transcriptional responses, and this mode of signaling is linked to hepatocyte hyperproliferation and hepatocellular carcinoma in experimental models where FGF‑19 acts as an oncogenic driver. In tumor such as liver and lung squamous cell carcinoma, FGF‑19 expression and amplification create an autocrine loop with FGFR4 that supports cell-cycle progression, survival, and invasiveness, aligning receptor phosphorylation and downstream pathway activation with aggressive growth behavior.

Background

FGF‑19 is an endocrine member of the fibroblast growth factor family that links bile acid sensing in the distal intestine to metabolic and proliferative signaling in the liver through selective activation of FGFR4–β‑Klotho receptor complexes. The protein shares the conserved FGF core fold that supports heparin binding and receptor engagement but displays distinctive sequence features that confer high affinity and functional specificity for FGFR4, positioning it as a ligand with restricted receptor usage compared with many paracrine FGFs. FGF‑19 expression in ileal enterocytes is induced by bile acid–activated farnesoid X receptor, and the secreted hormone enters the portal circulation to engage FGFR4–β‑Klotho on hepatocytes, where receptor autophosphorylation triggers downstream kinase cascades including ERK and other MAPK branches that repress transcription of the bile acid synthesis enzyme CYP7A1 and adjust bile acid transport and conjugation pathways. Through these mechanisms, FGF‑19 establishes a negative feedback loop that stabilizes bile acid pool size and composition after feeding and coordinates intestinal uptake with hepatic synthesis to maintain bile acid homeostasis. FGF‑19 also signals through FGFR4–β‑Klotho and, in some contexts, through β‑Klotho complexes with other FGFRs in metabolic tissues to influence glucose utilization, lipid handling, and energy expenditure, integrating nutrient status with transcriptional programs that regulate gluconeogenesis, glycogen storage, and lipid metabolism. Persistent or ectopic FGF‑19–FGFR4 activation in the liver engages mitogenic signaling outputs of FGFR4, including sustained ERK pathway activity and associated transcriptional responses, and this mode of signaling is linked to hepatocyte hyperproliferation and hepatocellular carcinoma in experimental models where FGF‑19 acts as an oncogenic driver. In tumor such as liver and lung squamous cell carcinoma, FGF‑19 expression and amplification create an autocrine loop with FGFR4 that supports cell-cycle progression, survival, and invasiveness, aligning receptor phosphorylation and downstream pathway activation with aggressive growth behavior.

References
https://pubmed.ncbi.nlm.nih.gov/10525310/ https://pubmed.ncbi.nlm.nih.gov/35301051/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%