Basic FGF Antibody [L15D6] | Primary Antibodies

Application: Reactivity: Human, Mouse

Usage Information

Dilution
WB1:1000 IHC1:125 - 1:500 IF1:200 - 1:800

Application
WB, IHC, IF

Reactivity
Human, Mouse

Source
Rabbit 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
18-24 kDa

Positive Control	Human prostate adenocarcinoma;Human papillary thyroid carcinoma; Human esophageal adenocarcinoma; Human prostate; Human colon; Human kidney; 4T1 syngeneic tumor; Renca syngeneic tumor; Mouse pancreas; Mouse liver; Mouse heart; Human small intestine; Mouse colon; MC/9 cells; A-172 cells; NCI-H522 cells
Negative Control	Capan-1 cells; Neuro-2a cells

Datasheet & SDS

Biological Description

Specificity
Basic FGF Antibody [L15D6] detects endogenous levels of total Basic FGF protein.

Clone
L15D6

Synonym(s)
Fibroblast growth factor 2; FGF-2; Basic fibroblast growth factor (bFGF); Heparin-binding growth factor 2 (HBGF-2); Fgf2; Fgf-2

Background
Basic FGF (FGF2, basic fibroblast growth factor) is a member of the fibroblast growth factor family, a group of 22 heparin-binding polypeptides in mammals that signal through tyrosine kinase FGF receptors (FGFR1-4) and heparan sulfate proteoglycans (HSPGs) to regulate proliferation, differentiation, migration, and survival in mesenchymal, epithelial, and neuroectoderm-derived tissues. The predominant 18 kDa isoform of FGF2 features a compact β-trefoil fold comprising 12 antiparallel β-strands (β1–β12) that form a β-barrel structure approximately 3–4 nm in diameter, with a hydrophobic core and surface-exposed basic residues located mainly in the β1–β2 loop and β11/β12 strands for HSPG interaction. FGF2 lacks a classical signal peptide and is secreted via an unconventional, ER/Golgi-independent pathway involving PI(4,5)P2, Tec kinase, and ATP1A1-mediated plasma membrane translocation. FGF2 forms a HSPG-stabilized ternary complex with FGFRs, inducing receptor dimerization and autophosphorylation that activates downstream pathways such as FRS2/PLCγ/Crk for RAS/MAPK/ERK-mediated proliferation and angiogenesis, PI3K/AKT for cell survival, and PLC/IP3 for Ca²⁺ mobilization. FGF2 promotes cortical neurogenesis by amplifying neural progenitors, enhances axon branching through upregulation of L-type Ca²⁺ channels, and confers neuroprotection against excitotoxicity and reactive oxygen species by modulating NMDA receptors, inducing calbindin, and activating anti-apoptotic signaling. FGF2 is essential for vascular remodeling, wound healing, bone and cartilage maintenance, and adult hippocampal neurogenesis, with its high-affinity HSPG binding generating extracellular reservoirs that modulate its bioavailability. FGF2 overexpression drives tumor angiogenesis and progression in cancers such as gliomas and melanomas, contributes to atherosclerosis, retinopathy, and osteoarthritis, while deficiency impairs fracture healing.

Background

Basic FGF (FGF2, basic fibroblast growth factor) is a member of the fibroblast growth factor family, a group of 22 heparin-binding polypeptides in mammals that signal through tyrosine kinase FGF receptors (FGFR1-4) and heparan sulfate proteoglycans (HSPGs) to regulate proliferation, differentiation, migration, and survival in mesenchymal, epithelial, and neuroectoderm-derived tissues. The predominant 18 kDa isoform of FGF2 features a compact β-trefoil fold comprising 12 antiparallel β-strands (β1–β12) that form a β-barrel structure approximately 3–4 nm in diameter, with a hydrophobic core and surface-exposed basic residues located mainly in the β1–β2 loop and β11/β12 strands for HSPG interaction. FGF2 lacks a classical signal peptide and is secreted via an unconventional, ER/Golgi-independent pathway involving PI(4,5)P2, Tec kinase, and ATP1A1-mediated plasma membrane translocation. FGF2 forms a HSPG-stabilized ternary complex with FGFRs, inducing receptor dimerization and autophosphorylation that activates downstream pathways such as FRS2/PLCγ/Crk for RAS/MAPK/ERK-mediated proliferation and angiogenesis, PI3K/AKT for cell survival, and PLC/IP3 for Ca²⁺ mobilization. FGF2 promotes cortical neurogenesis by amplifying neural progenitors, enhances axon branching through upregulation of L-type Ca²⁺ channels, and confers neuroprotection against excitotoxicity and reactive oxygen species by modulating NMDA receptors, inducing calbindin, and activating anti-apoptotic signaling. FGF2 is essential for vascular remodeling, wound healing, bone and cartilage maintenance, and adult hippocampal neurogenesis, with its high-affinity HSPG binding generating extracellular reservoirs that modulate its bioavailability. FGF2 overexpression drives tumor angiogenesis and progression in cancers such as gliomas and melanomas, contributes to atherosclerosis, retinopathy, and osteoarthritis, while deficiency impairs fracture healing.

References
https://pubmed.ncbi.nlm.nih.gov/32498439/ https://pubmed.ncbi.nlm.nih.gov/37858405/

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%