FRS3 Antibody

Introduction to FRS3 Antibody

FRS3 (also known as FRS2B or SNT-2) is a 492-amino-acid protein that modulates signaling downstream of fibroblast growth factor receptors (FGFRs) and neurotrophin receptors . It acts as a feedback inhibitor of epidermal growth factor receptor (EGFR) family members by preventing heterodimerization and regulating extracellular signal-regulated kinase (ERK) pathways . The FRS3 antibody enables detection of endogenous FRS3 protein in research settings, facilitating studies on its role in neural development, cancer, and signaling regulation.

Neural Development

• Microtubule Binding: FRS3 exhibits microtubule-binding properties distinct from FRS2, as shown in radial processes of developing cortical neurons. This interaction resembles MAP2, a known microtubule-associated protein .

• Subcellular Localization: Endogenous FRS3 is both soluble and plasma membrane-associated in neurons, contrasting with lipid raft localization in transfected 293T cells .

Cancer Signaling

• Functional Redundancy: FRS3 compensates for FRS2 loss in prostate cancer cells, enhancing FGF-induced proliferation and ERK activation. Dual suppression of both proteins inhibits cell growth and invasion more effectively than targeting either alone .

• Therapeutic Implications: Co-inhibition of FRS2/FRS3 synergizes with irradiation to reduce prostate cancer cell survival, suggesting a potential clinical strategy .

Techniques

Experimental Challenges

• Antibody Specificity: Early studies lacked effective FRS3-specific antibodies, hindering functional analysis. Recent antibodies (e.g., HPA030174) address this gap with stringent validation .

• Storage and Handling: Sodium azide-containing antibodies require caution; avoid repeated freeze-thaw cycles .

Key Research Findings

1. Neural Tissue Expression:

   • FRS3 is expressed in the ventricular zone of developing cortex (E12–E15) and colocalizes with nestin (progenitor cells) and βIII-tubulin (differentiated neurons) .

2. Cancer Biology:

   • FRS3 overexpression in DU145 prostate cancer cells enhances FGF1-induced proliferation and ERK phosphorylation .

   • Dual FRS2/FRS3 knockdown reduces ERK activation, migration, and invasion in prostate cancer cells .