FGR Antibody (YA3732)
(Synonyms: SRC2; c-fgr; c-src2; p55c-fgr; p58c-fgr)FGR Antibody (YA3732) is a Mouse-derived and non-conjugated IgG1 monoclonal antibody, targeting to FGR.
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Host:
Mouse
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Isotype:
IgG
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Application:
WB, IHC-P, ELISA
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Reactivity :
Human, Mouse
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Formulation:
Supplied in PBS with 0.05% sodium azide.
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Conjugation:
Non-conjugated
Applications
| Application |
WB
WB: Western Blot
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IHC-P
IHC-P: Immunohistochemistry-Paraffin
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ELISA
ELISA: Enzyme Linked Immunosorbent Assay
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|---|---|---|---|
| Dilution Ratio | 1:500-1:2000 | 1:200-1:1000 | 1:10000 |
Product Details
FGR Antibody (YA3732) is a Mouse-derived and non-conjugated IgG1 monoclonal antibody, targeting to FGR.
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Host Mouse
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Clonality Monoclonal
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Species ReactivityHuman, Mouse
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Observed Molecular WeightObserved band size: 56 kDaNote: 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: 59 kDa
Purified recombinant fragment of human FGR aa 2-100.
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
Fgr is a Src family tyrosine kinase activated during β2 integrin-dependent signaling in human neutrophils, linking adhesion to protein tyrosine phosphorylation[1]. Mechanistically, Fgr and Hck support adhesion-dependent neutrophil respiratory burst, spreading, and degranulation, showing that Fgr participates in integrin-driven inflammatory effector functions[2][3]. Fgr also acts with Hck to negatively regulate neutrophil and dendritic-cell chemokine signaling through PIR-B, indicating a context-dependent role in myeloid signal control[4]. In disease models, hematopoietic loss of Hck, Fgr, and Lyn protected mice from autoantibody-induced arthritis, blistering skin inflammation, and reverse passive Arthus reaction by impairing inflammatory-environment generation rather than intrinsic leukocyte recruitment[5]. Compared with related Src family isoforms, Fgr shows substantial functional overlap with Hck and Lyn, because single Fgr deficiency did not block arthritis development, whereas combined Hck/Fgr/Lyn loss produced complete protection[5]. For experimental applications, an Fgr kinase inhibitor attenuated sepsis-associated encephalopathy by reducing mitochondrial dysfunction, oxidative stress, and neuroinflammation through the SIRT1/PGC-1α pathway[6].
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Subcellular Localization
Cell membrane; Lipid-anchor; Cytoplasmic side; Cell membrane; Peripheral membrane protein; Cytoplasmic side; Cell projection, ruffle membrane; Cytoplasm, cytosol; Cytoplasm, cytoskeleton; Mitochondrion inner membrane; Mitochondrion intermembrane space
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Expression
Tissue_specificity:Detected (protein levels) in neutrophils, monocytes, and natural killer cells. Detected in monocytes and large lymphocytes. -
Subunit
Interacts with ITGB1, ITGB2, MS4A2/FCER1B, FCER1G, FCGR2A and/or FCGR2B. Interacts (via SH2 domain) with SYK (tyrosine phosphorylated). Interacts (via SH2 domain) with FLT3 (tyrosine phosphorylated).
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SwissProt ID
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Synonyms
SRC2; c-fgr; c-src2; p55c-fgr; p58c-fgr
Documentation
[1]. Berton G, et al. Beta 2 integrin-dependent protein tyrosine phosphorylation and activation of the FGR protein tyrosine kinase in human neutrophils. J Cell Biol. 1994 Aug;126(4):1111-21. [Content Brief]
[2]. Lowell CA, et al. Deficiency of Src family kinases p59/61hck and p58c-fgr results in defective adhesion-dependent neutrophil functions. J Cell Biol. 1996 May;133(4):895-910. [Content Brief]
[3]. Sibley CD, et al. Discovery of a Small Side Cavity in Sphingosine Kinase 2 that Enhances Inhibitor Potency and Selectivity. J Med Chem. 2020 Feb 13;63(3):1178-1198. [Content Brief]
[4]. Zhang H, et al. The Src family kinases Hck and Fgr negatively regulate neutrophil and dendritic cell chemokine signaling via PIR-B. Immunity. 2005 Feb;22(2):235-46. [Content Brief]
[5]. Kovács M, et al. The Src family kinases Hck, Fgr, and Lyn are critical for the generation of the in vivo inflammatory environment without a direct role in leukocyte recruitment. J Exp Med. 2014 Sep 22;211(10):1993-2011. [Content Brief]
[6]. Liu Y, et al. An Fgr kinase inhibitor attenuates sepsis-associated encephalopathy by ameliorating mitochondrial dysfunction, oxidative stress, and neuroinflammation via the SIRT1/PGC-1α signaling pathway. J Transl Med. 2023 Jul 20;21(1):486. [Content Brief]