Recombinant
RabMAb

Recombinant Anti-FGFR3 (phospho Y724) antibody [EPR2281(3)] (Alexa Fluor® 488) (ab237164)

Overview

  • Product name

    Anti-FGFR3 (phospho Y724) antibody [EPR2281(3)] (Alexa Fluor® 488)
    See all FGFR3 primary antibodies
  • Description

    Rabbit monoclonal [EPR2281(3)] to FGFR3 (phospho Y724) (Alexa Fluor® 488)
  • Host species

    Rabbit
  • Conjugation

    Alexa Fluor® 488. Ex: 495nm, Em: 519nm
  • Specificity

    This antibody only detects FGFR3 when phosphorylated at tyrosine 724.
  • Tested applications

    Suitable for: Flow Cyt, ICC/IFmore details
  • Species reactivity

    Reacts with: Human
    Predicted to work with: Mouse
  • Immunogen

    Synthetic peptide within Human FGFR3 (phospho Y724). The exact sequence is proprietary.
    Database link: P22607

  • Positive control

    • Flow Cyt: MCF7 cells treated with Pervandate (1mM, 30 min). ICC/IF: MCF7 cells treated with Pervandate (1mM, 30 min)
  • General notes

    Our RabMAb® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMab® patents.

    Alexa Fluor® is a registered trademark of Molecular Probes, Inc, a Thermo Fisher Scientific Company. The Alexa Fluor® dye included in this product is provided under an intellectual property license from Life Technologies Corporation. As this product contains the Alexa Fluor® dye, the purchase of this product conveys to the buyer the non-transferable right to use the purchased product and components of the product only in research conducted by the buyer (whether the buyer is an academic or for-profit entity). As this product contains the Alexa Fluor® dye the sale of this product is expressly conditioned on the buyer not using the product or its components, or any materials made using the product or its components, in any activity to generate revenue, which may include, but is not limited to use of the product or its components: in manufacturing; (ii) to provide a service, information, or data in return for payment (iii) for therapeutic, diagnostic or prophylactic purposes; or (iv) for resale, regardless of whether they are sold for use in research. For information on purchasing a license to this product for purposes other than research, contact Life Technologies Corporation, 5781 Van Allen Way, Carlsbad, CA 92008 USA or outlicensing@thermofisher.com.

    This product is a recombinant rabbit monoclonal antibody.

Properties

Applications

Our Abpromise guarantee covers the use of ab237164 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

Application Abreviews Notes
Flow Cyt 1/500.
ICC/IF 1/100.

This product gave a positive signal in MCF7 cells treated with Pervanadate (1mM, 30min) fixed with 4% formaldehyde (10 min)

Target

  • Function

    Receptor for acidic and basic fibroblast growth factors. Preferentially binds FGF1.
  • Tissue specificity

    Expressed in brain, kidney and testis. Very low or no expression in spleen, heart, and muscle. In 20- to 22-week old fetuses it is expressed at high level in kidney, lung, small intestine and brain, and to a lower degree in spleen, liver, and muscle. Isoform 2 is detected in epithelial cells. Isoform 1 is not detected in epithelial cells. Isoform 1 and isoform 2 are detected in fibroblastic cells.
  • Involvement in disease

    Defects in FGFR3 are the cause of achondroplasia (ACH) [MIM:100800]. ACH is an autosomal dominant disease and is the most frequent form of short-limb dwarfism. It is characterized by a long, narrow trunk, short extremities, particularly in the proximal (rhizomelic) segments, a large head with frontal bossing, hypoplasia of the midface and a trident configuration of the hands.
    Defects in FGFR3 are the cause of Crouzon syndrome with acanthosis nigricans (CAN) [MIM:612247]. Classic Crouzon disease which is caused by mutations in the FGFR2 gene is characterized by craniosynostosis (premature fusion of the skull sutures), and facial hypoplasia. Crouzon syndrome with acanthosis nigricans (a skin disorder characterized by pigmentation anomalies), CAN, is considered to be an independent disorder from classic Crouzon syndrome. CAN is characterized by additional more severe physical manifestation, such as Chiari malformation, hydrocephalus, and atresia or stenosis of the choanas, and is caused by a specific mutation (Ala-391 to Glu) in the transmembrane domain of FGFR3. It is proposed to have an autosomal dominant mode of inheritance.
    Defects in FGFR3 are a cause of thanatophoric dysplasia type (TD) [MIM:187600, 187601]; also known as thanatophoric dwarfism or platyspondylic lethal skeletal dysplasia Sand Diego type (PLSD-SD). TD is the most common neonatal lethal skeletal dysplasia. Affected individuals display features similar to those seen in homozygous achondroplasia. It causes severe shortening of the limbs with macrocephaly, narrow thorax and short ribs. In the most common subtype, TD1, femur are curved, while in TD2, straight femurs are associated with cloverleaf skull. Mutations affecting different functional domains of FGFR3 cause different forms of this lethal disorder.
    Defects in FGFR3 are a cause of hypochondroplasia (HCH) [MIM:146000]. HCH is an autosomal dominant disease and is characterized by disproportionate short stature. It resembles achondroplasia, but with a less severe phenotype.
    Defects in FGFR3 are a cause of susceptibility to bladder cancer (BLC) [MIM:109800]. A malignancy originating in tissues of the urinary bladder. It often presents with multiple tumors appearing at different times and at different sites in the bladder. Most bladder cancers are transitional cell carcinomas. They begin in cells that normally make up the inner lining of the bladder. Other types of bladder cancer include squamous cell carcinoma (cancer that begins in thin, flat cells) and adenocarcinoma (cancer that begins in cells that make and release mucus and other fluids). Bladder cancer is a complex disorder with both genetic and environmental influences. Note=Somatic mutations can constitutively activate FGFR3.
    Defects in FGFR3 are a cause of cervical cancer (CERCA) [MIM:603956]. A malignant neoplasm of the cervix, typically originating from a dysplastic or premalignant lesion previously present at the active squamocolumnar junction. The transformation from mild dysplastic to invasive carcinoma generally occurs slowly within several years, although the rate of this process varies widely. Carcinoma in situ is particularly known to precede invasive cervical cancer in most cases. Cervical cancer is strongly associated with infection by oncogenic types of human papillomavirus.
    Defects in FGFR3 are the cause of camptodactyly tall stature and hearing loss syndrome (CATSHL syndrome) [MIM:610474]. CATSHL syndrome is an autosomal dominant syndrome characterized by permanent and irreducible flexion of one or more fingers of the hand and/or feet, tall stature, scoliosis and/or a pectus excavatum, and hearing loss. Affected individuals have developmental delay and/or mental retardation, and several of these have microcephaly. Radiographic findings included tall vertebral bodies with irregular borders and broad femoral metaphyses with long tubular shafts. On audiological exam, each tested member have bilateral sensorineural hearing loss and absent otoacoustic emissions. The hearing loss was congenital or developed in early infancy, progressed variably in early childhood, and range from mild to severe. Computed tomography and magnetic resonance imaging reveal that the brain, middle ear, and inner ear are structurally normal.
    Defects in FGFR3 are a cause of multiple myeloma (MM) [MIM:254500]. MM is a malignant tumor of plasma cells usually arising in the bone marrow and characterized by diffuse involvement of the skeletal system, hyperglobulinemia, Bence-Jones proteinuria and anemia. Complications of multiple myeloma are bone pain, hypercalcemia, renal failure and spinal cord compression. The aberrant antibodies that are produced lead to impaired humoral immunity and patients have a high prevalence of infection. Amyloidosis may develop in some patients. Multiple myeloma is part of a spectrum of diseases ranging from monoclonal gammopathy of unknown significance (MGUS) to plasma cell leukemia. Note=A chromosomal aberration involving FGFR3 is found in multiple myeloma. Translocation t(4;14)(p16.3;q32.3) with the IgH locus.
    Defects in FGFR3 are a cause of lacrimo-auriculo-dento-digital syndrome (LADDS) [MIM:149730]; also known as Levy-Hollister syndrome. LADDS is a form of ectodermal dysplasia, a heterogeneous group of disorders due to abnormal development of two or more ectodermal structures. LADDS is an autosomal dominant syndrome characterized by aplastic/hypoplastic lacrimal and salivary glands and ducts, cup-shaped ears, hearing loss, hypodontia and enamel hypoplasia, and distal limb segments anomalies. In addition to these cardinal features, facial dysmorphism, malformations of the kidney and respiratory system and abnormal genitalia have been reported. Craniosynostosis and severe syndactyly are not observed.
    Defects in FGFR3 are a cause of keratinocytic non-epidermolytic nevus (KNEN) [MIM:162900]; also known as pigmented moles. Epidermal nevi of the common, non-organoid and non-epidermolytic type are benign skin lesions and may vary in their extent from a single (usually linear) lesion to widespread and systematized involvement. They may be present at birth or develop early during childhood.
    Defects in FGFR3 are a cause of Muenke syndrome (MNKS) [MIM:602849]; also known as Muenke non-syndromic coronal craniosynostosis. MNKS is a condition characterized by premature closure of coronal suture of skull during development (coronal craniosynostosis), which affects the shape of the head and face. It may be uni- or bilateral. When bilateral, it is characterized by a skull with a small antero-posterior diameter (brachycephaly), often with a decrease in the depth of the orbits and hypoplasia of the maxillae. Unilateral closure of the coronal sutures leads to flattening of the orbit on the involved side (plagiocephaly). The intellect is normal. In addition to coronal craniosynostosis some affected individuals show skeletal abnormalities of hands and feet, sensorineural hearing loss, mental retardation and respiratory insufficiency.
    Defects in FGFR3 are a cause of keratosis seborrheic (KERSEB) [MIM:182000]. A common benign skin tumor. Seborrheic keratoses usually begin with the appearance of one or more sharply defined, light brown, flat macules. The lesions may be sparse or numerous. As they initially grow, they develop a velvety to finely verrucous surface, followed by an uneven warty surface with multiple plugged follicles and a dull or lackluster appearance.
  • Sequence similarities

    Belongs to the protein kinase superfamily. Tyr protein kinase family. Fibroblast growth factor receptor subfamily.
    Contains 3 Ig-like C2-type (immunoglobulin-like) domains.
    Contains 1 protein kinase domain.
  • Cellular localization

    Membrane.
  • Information by UniProt
  • Database links

  • Alternative names

    • ACH antibody
    • CD 333 antibody
    • CD333 antibody
    • CD333 antigen antibody
    • CEK 2 antibody
    • CEK2 antibody
    • FGFR 3 antibody
    • FGFR-3 antibody
    • FGFR3 antibody
    • FGFR3_HUMAN antibody
    • Fibroblast growth factor receptor 3 (achondroplasia thanatophoric dwarfism) antibody
    • Fibroblast growth factor receptor 3 antibody
    • Heparin binding growth factor receptor antibody
    • HSFGFR3EX antibody
    • Hydroxyaryl protein kinase antibody
    • JTK 4 antibody
    • JTK4 antibody
    • MFR 3 antibody
    • SAM 3 antibody
    • Tyrosine kinase JTK 4 antibody
    • Tyrosine kinase JTK4 antibody
    • Z FGFR 3 antibody
    see all

Images

  • Overlay histogram showing MCF7 cells untreated (green line) and MCF7 cells treated with Pervanadate, 1mM, 30 minutes, (red line) stained with ab237164. The cells were fixed with 4% formaldehyde (10 min) and then permeabilized with 90% methanol. The cells were then incubated in 1x PBS / 10% normal goat serum to block non-specific protein-protein interactions followed by the antibody (ab237164, 1/500 dilution) for 30 min at 22°C.

    Isotype control antibody (black line) was Rabbit IgG (monoclonal) Alexa Fluor® 488 (ab199091) used at the same concentration and conditions as the primary antibody. Unlabelled sample (blue line) was also used as a control.

    Acquisition of >5,000 events were collected using a 20mW solid-state laser (488nm) and 530/30 bandpass filter.

  • ab237164 staining FGFR3 (phospho Y724) in MCF7 cells +/- Pervanadate (1mM, 30min). The cells were fixed with 4% formaldehyde (10 min), permeabilized with 0.1% Triton X-100 for 5 minutes and then blocked with 1% BSA/10% normal goat serum/0.3M glycine in 0.1% PBS-Tween for 1h.

    The cells were then incubated overnight at +4°C with ab237164 at 1/100 dilution (shown in green) and ab195889, Mouse monoclonal to alpha Tubulin (Alexa Fluor® 594), at 1/250 dilution (shown in red). Nuclear DNA was labelled with DAPI (shown in blue).

    Image was taken with a confocal microscope (Leica-Microsystems, TCS SP8).

References

ab237164 has not yet been referenced specifically in any publications.

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