FRK Antibodies
Background
FRK tyrosine protein kinase gene encoding a kind of the size, are mainly distributed in multiple tissues of vertebrates, especially in the nervous system and immune system plays an important role. This protein participates in cell signal transduction through phosphorylated substrate proteins and regulates key physiological processes such as cell proliferation, differentiation and migration. Studies have shown that FRK plays a dual role in tumorigenesis and development. It can not only inhibit the growth of certain cancer cells but also promote the metastasis of specific tumors. This gene was first identified by Semba and other scholars in 1990. Its unique SH2 and SH3 domains provide an important model for studying the tyrosine kinase signaling network. The in-depth study of the structure and function of the FRK protein has greatly promoted our understanding of the mechanism of cell signal regulation, especially in the application of targeted cancer therapy, which is of great value.
Structure of FRK
FRK is a non-receptor tyrosine protein kinase with a molecular weight of approximately 58-60 kDa. There are subtle differences in its molecular weight among different species, mainly due to structural changes in the regulatory domain and catalytic domain.
Species | Human | Mouse | Rat | Bovine |
Molecular Weight (kDa) | 58-60 | 59 | 58 | 60 |
Primary Structural Differences | Contains SH2 and SH3 domains that regulate signal transduction | Highly conserved, with a homology of over 90% to humans | The catalytic domain is slightly different | Similar to the function, but phosphorylation sites have subtle differences |
FRK is composed of approximately 540 amino acids and features typical Src homologous 2 (SH2) and Src homologous 3 (SH3) domains, which mediate protein-protein interactions and regulate kinase activity. Its tertiary structure presents a typical kinase folding pattern, and the N-terminal regulatory region affects the activity of the C-terminal catalytic domain through its own inhibitory mechanism. The phosphorylation state of key tyrosine residues (such as Tyr395) in the activation loop of FRK determines its enzymatic activity and downstream signal transduction efficiency. This protein is distributed in both the cytoplasm and the nucleus, and is involved in regulating important biological processes such as cell proliferation, differentiation, and tumor suppression.
Fig. 1 FRK kinase domains and key regulatory sites: Functional characteristics of phosphorylation sites SH3, SH2 and Y387/Y497.1
Key structural properties of FRK:
- Modular domain composition
- Self-inhibitory conformation
- Core characteristics of catalysis
- Regulatory key sites
Functions of FRK
FRK gene encoding of tyrosine kinase regulation, mainly involved in signal transduction in cell growth, differentiation, and play a key role in tumor suppressor. Its functional diversity is reflected in multiple important physiological processes:
Function | Description |
Regulation of cell proliferation | Regulate the cell cycle process by phosphorylating downstream target proteins (such as p130Cas and paxillin) to inhibit abnormal proliferation. |
Immune regulation | In the T cell and B cell receptor signaling pathways play a role, affect the immune cell activation and differentiation. |
Tumor suppressive effect | By inhibiting pro-cancer signaling pathways such as EGFR/STAT3, it exerts anti-cancer functions in various cancers including breast cancer and liver cancer. |
Nervous system development | Participate in neuronal migration and synaptic plasticity regulation, development affects the brain cortex. |
Metabolic regulation | Regulate the insulin signaling pathway, influencing glucose metabolism and adipocyte differentiation. |
The enzymatic activity of FRK exhibits typical substrate-specific phosphorylation characteristics. Unlike Src family kinases, it is more inclined to regulate growth-inhibitory signaling pathways. In the tumor microenvironment, the changes in FRK expression levels are significantly correlated with cancer progression and prognosis, especially showing a definite tumor suppressor effect in triple-negative breast cancer. The functional research of this gene provides an important theoretical basis for the development of new targeted anti-cancer drugs.
Applications of FRK and FRK Antibody in Literature
1. Wang, Xinyue, et al. "A novel rabbit anti-myoglobin monoclonal antibody's potential application in rhabdomyolysis associated acute kidney injury." International Journal of Molecular Sciences 24.9 (2023): 7822. https://doi.org/10.18632/oncotarget.22958
This study demonstrates that FRK (FYN-related kinase) is a non-receptor tyrosine kinase that has a tumor suppressor effect in breast cancer. Research has found that overexpression of FRK can inhibit the proliferation, migration and invasion of breast cancer cells, and suppress epithelial-mesenchymal transition (EMT) by down-regulating signaling pathways such as STAT3 and MAPK. In addition, the expression of FRK is negatively correlated with interstitial markers, suggesting that it may inhibit tumor metastasis by regulating EMT.
2. Mayumi, Azusa, et al. "Leukaemic cells expressing ETV6:: FRK are sensitive to dasatinib in vivo." EJHaem 4.3 (2023): 751-755. https://doi.org/10.1002/jha2.701
This study discovered the ETV6::FRK fusion gene for the first time in high-risk B-cell precursor acute lymphoblastic leukemia (B-ALL) in children, confirming that this fusion gene drives leukemia occurrence by activating the FRK-STAT3/STAT5 pathway. Experiments have shown that dasatinib can effectively inhibit the proliferative activity of ETV6::FRK and significantly prolong the survival period of mice with transplanted tumors (p<0.01), providing a new targeted treatment option for patients with FRK rearrangement B-ALL.
3. Ogunbolude, Yetunde, et al. "FRK inhibits breast cancer cell migration and invasion by suppressing epithelial-mesenchymal transition." Oncotarget 8.68 (2017): 113034. https://doi.org/10.18632/oncotarget.22958
This study demonstrates that FRK (FYN-related kinase) is a non-receptor tyrosine kinase that has a tumor suppressor effect in breast cancer. Research has found that overexpression of FRK can inhibit the proliferation, migration and invasion of breast cancer cells, and suppress epithelial-mesenchymal transition (EMT) by down-regulating signaling pathways such as STAT3 and MAPK. In addition, the expression of FRK is negatively correlated with interstitial markers, suggesting that it may inhibit tumor metastasis by regulating EMT.
4. Zang, Qiwei, et al. "GATA6 activated long non-coding RNA PCAT1 maintains stemness of non-small cell lung cancer by mediating FRK." J BUON 25.5 (2020): 2371-81. https://europepmc.org/article/med/33277858
Research has found that long non-coding RNA PCAT1 promotes the maintenance of stemness in non-small cell lung cancer (NSCLC) by down-regulating FYN-related kinase (FRK). PCAT1 is highly expressed in advanced NSCLC tissues, positively correlated with FRK levels, and enhances the characteristics of tumor stem cells through the GATA6/PCAT1/FRK axis, leading to a poor prognosis for patients.
5. He, anwei, et al. "LncRNA HOTTIP leads to osteoarthritis progression via regulating miR-663a/Fyn-related kinase axis." BMC Musculoskeletal Disorders 22.1 (2021): 67. https://doi.org/10.1186/s12891-020-03861-7
Studies have found that lncRNA HOTTIP regulates the proliferation and apoptosis of chondrocytes in osteoarthritis through the miR-663a/FRK axis. HOTTIP is highly expressed in OA tissues. As a competitive endogenous RNA, it binds to miR-663a, relieving its inhibitory effect on FRK, thereby promoting chondrocyte proliferation and inhibiting apoptosis. This suggests that the HOTTIP/miR-663a/FRK pathway may be a potential target for the treatment of OA.
Creative Biolabs: FRK Antibodies for Research
Creative Biolabs specializes in the production of high-quality FRK antibodies for research and industrial applications. Our portfolio includes monoclonal antibodies tailored for ELISA, Flow Cytometry, Western blot, immunohistochemistry, and other diagnostic methodologies.
- Custom FRK Antibody Development: Tailor-made solutions to meet specific research requirements.
- Bulk Production: Large-scale antibody manufacturing for industry partners.
- Technical Support: Expert consultation for protocol optimization and troubleshooting.
- Aliquoting Services: Conveniently sized aliquots for long-term storage and consistent experimental outcomes.
For more details on our FRK antibodies, custom preparations, or technical support, contact us at email.
Reference
- Ogunbolude, Yetunde, et al. "FRK inhibits breast cancer cell migration and invasion by suppressing epithelial-mesenchymal transition." Oncotarget 8.68 (2017): 113034. https://doi.org/10.18632/oncotarget.22958
Anti-FRK antibodies

Hot products 
- AActivation
- AGAgonist
- APApoptosis
- BBlocking
- BABioassay
- BIBioimaging
- CImmunohistochemistry-Frozen Sections
- CIChromatin Immunoprecipitation
- CTCytotoxicity
- CSCostimulation
- DDepletion
- DBDot Blot
- EELISA
- ECELISA(Cap)
- EDELISA(Det)
- ESELISpot
- EMElectron Microscopy
- FFlow Cytometry
- FNFunction Assay
- GSGel Supershift
- IInhibition
- IAEnzyme Immunoassay
- ICImmunocytochemistry
- IDImmunodiffusion
- IEImmunoelectrophoresis
- IFImmunofluorescence
- IHImmunohistochemistry
- IMImmunomicroscopy
- IOImmunoassay
- IPImmunoprecipitation
- ISIntracellular Staining for Flow Cytometry
- LALuminex Assay
- LFLateral Flow Immunoassay
- MMicroarray
- MCMass Cytometry/CyTOF
- MDMeDIP
- MSElectrophoretic Mobility Shift Assay
- NNeutralization
- PImmunohistologyp-Paraffin Sections
- PAPeptide Array
- PEPeptide ELISA
- PLProximity Ligation Assay
- RRadioimmunoassay
- SStimulation
- SESandwich ELISA
- SHIn situ hybridization
- TCTissue Culture
- WBWestern Blot
