FRK Antibody (YA4017)
(Synonyms: GTK; RAK; PTK5)FRK Antibody (YA4017) is a Mouse-derived and non-conjugated IgG1 monoclonal antibody, targeting to FRK.
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Host:
Mouse
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Isotype:
IgG
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Application:
WB, ELISA
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Reactivity :
Human
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Formulation:
Supplied in PBS with 0.05% sodium azide.
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Conjugation:
Non-conjugated
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
Applications
| Application |
WB
WB: Western Blot
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ELISA
ELISA: Enzyme Linked Immunosorbent Assay
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|---|---|---|
| Dilution Ratio | 1:500-1:2000 | 1:10000 |
Product Details
FRK Antibody (YA4017) is a Mouse-derived and non-conjugated IgG1 monoclonal antibody, targeting to FRK.
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Host Mouse
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Clonality Monoclonal
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Species ReactivityHuman
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Observed Molecular WeightObserved band size: 58 kDa
Note: Due to possible protein modifications or aggregation, the molecular weight should be confirmed by actual measurement, and the predicted value is for reference only.
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Calculated Molecular Weight Predicted band size: 58 kDa
Purified recombinant fragment of human FRK aa 1-107.
affinity purified.
Non-conjugated
Unmodified
IgG
Product Properties
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Appearance
Solution
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Formulation
Supplied in PBS with 0.05% sodium azide.
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Storage & Stability
Stored at -20°C for 1 year. Avoid repeated freeze / thaw cycles.
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Shipping
Shipping with blue ice.
Background
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Function
FRK is a non-receptor tyrosine kinase in the BRK family kinases, distantly related to Src family kinases, and its biology centers on phosphorylation-dependent control of growth and signaling[1][2]. Mechanistically, FRK has been linked to PTEN stability, EGFR internalization, cyclin D1 nuclear accumulation, ITGB1/FAK signaling, and YAP ubiquitylation, placing it in cell-cycle, receptor-trafficking, adhesion, and Hippo-pathway research[3][4][5][6][7]. In disease models, FRK suppressed breast cancer cell proliferation and invasion, inhibited glioma growth or progression in several studies, but recurrent FRK-activating mutations drove STAT3 activation and proliferation in hepatocellular adenoma[3][5][6][7][8]. Compared with related isoforms, FRK/Rak/Gtk/Iyk/Bsk belongs to a conserved Brk/Srm/Frk/Src42A group that remains structurally distinct from c-Src and Fyn[2]. For experimental applications, FRK fusions in ALK-negative anaplastic large-cell lymphoma showed kinase targetability, and FRK-activating hepatocellular adenoma mutations showed sensitivity to Src inhibitors[8][9].
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Subcellular Localization
Cytoplasm; Nucleus
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Expression
Tissue_specificity:It is primarily expressed in epithelial cell lines and tissues, particularly in normal liver, kidney, mammary gland, and colon. -
Subunit
Interacts (via the SH3-domain) with PTEN. Interacts with RB1
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SwissProt ID
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Synonyms
GTK; RAK; PTK5
Documentation
[1]. Goel RK, et al. Understanding the cellular roles of Fyn-related kinase (FRK): implications in cancer biology. Cancer Metastasis Rev. 2016 Jun;35(2):179-99. [Content Brief]
[2]. Serfas MS, et al. Brk, Srm, Frk, and Src42A form a distinct family of intracellular Src-like tyrosine kinases. Oncol Res. 2003;13(6-10):409-19. [Content Brief]
[3]. Yim EK, et al. Rak functions as a tumor suppressor by regulating PTEN protein stability and function. Cancer Cell. 2009 Apr 7;15(4):304-14. [Content Brief]
[4]. Jin L, et al. The Rak/Frk tyrosine kinase associates with and internalizes the epidermal growth factor receptor. Oncogene. 2014 Jan 16;33(3):326-35. [Content Brief]
[5]. Hua L, et al. FRK suppresses the proliferation of human glioma cells by inhibiting cyclin D1 nuclear accumulation. J Neurooncol. 2014 Aug;119(1):49-58. [Content Brief]
[6]. Wang J, et al. FRK suppresses human glioma growth by inhibiting ITGB1/FAK signaling. Biochem Biophys Res Commun. 2019 Oct 1;517(4):588-595. [Content Brief]
[7]. Wang Y, et al. FRK inhibits glioblastoma progression via phosphorylating YAP and inducing its ubiquitylation and degradation by Siah1. Neuro Oncol. 2022 Dec 1;24(12):2107-2120. [Content Brief]
[8]. Pilati C, et al. Genomic profiling of hepatocellular adenomas reveals recurrent FRK-activating mutations and the mechanisms of malignant transformation. Cancer Cell. 2014 Apr 14;25(4):428-41. [Content Brief]
[9]. Hu G, et al. Targetable fusions of the FRK tyrosine kinase in ALK-negative anaplastic large cell lymphoma. Leukemia. 2018 Feb;32(2):565-569. [Content Brief]
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