Product nameAnti-FGFR2 antibody [EPR5180]
See all FGFR2 primary antibodies
DescriptionRabbit monoclonal [EPR5180] to FGFR2
Tested applicationsSuitable for: WB, IPmore details
Unsuitable for: Flow Cyt,ICC or IHC-P
Species reactivityReacts with: Mouse, Rat, Human
- MCF7, Jurkat, HeLa, K562, and T47-D cell lysates
Our RabMAb® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMab® patents.
We are constantly working hard to ensure we provide our customers with best in class antibodies. As a result of this work we are pleased to now offer this antibody in purified format. We are in the process of updating our datasheets. The purified format is designated 'PUR' on our product labels. If you have any questions regarding this update, please contact our Scientific Support team.
This product is a recombinant rabbit monoclonal antibody.
Storage instructionsShipped at 4°C. Store at -20°C. Stable for 12 months at -20°C.
Storage bufferpH: 7.40
Preservative: 0.01% Sodium azide
Constituents: 59% PBS, 40% Glycerol, 0.5% BSA
Concentration information loading...
PurityProtein A purified
Our Abpromise guarantee covers the use of ab109372 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||1/1000 - 1/10000. Detects a band of approximately 145 kDa (predicted molecular weight: 92 kDa).|
|IP||1/10 - 1/100.|
FunctionReceptor for acidic and basic fibroblast growth factors.
Involvement in diseaseDefects in FGFR2 are the cause of Crouzon syndrome (CS) [MIM:123500]; also called craniofacial dysostosis type I (CFD1). CS is an autosomal dominant syndrome characterized by craniosynostosis (premature fusion of the skull sutures), hypertelorism, exophthalmos and external strabismus, parrot-beaked nose, short upper lip, hypoplastic maxilla, and a relative mandibular prognathism.
Defects in FGFR2 are a cause of Jackson-Weiss syndrome (JWS) [MIM:123150]. JWS is an autosomal dominant craniosynostosis syndrome characterized by craniofacial abnormalities and abnormality of the feet: broad great toes with medial deviation and tarsal-metatarsal coalescence.
Defects in FGFR2 are a cause of Apert syndrome (APRS) [MIM:101200]; also known as acrocephalosyndactyly type 1 (ACS1). APRS is a syndrome characterized by facio-cranio-synostosis, osseous and membranous syndactyly of the four extremities, and midface hypoplasia. The craniosynostosis is bicoronal and results in acrocephaly of brachysphenocephalic type. Syndactyly of the fingers and toes may be total (mitten hands and sock feet) or partial affecting the second, third, and fourth digits. Intellectual deficit is frequent and often severe, usually being associated with cerebral malformations.
Defects in FGFR2 are a cause of Pfeiffer syndrome (PS) [MIM:101600]; also known as acrocephalosyndactyly type V (ACS5). PS is characterized by craniosynostosis (premature fusion of the skull sutures) with deviation and enlargement of the thumbs and great toes, brachymesophalangy, with phalangeal ankylosis and a varying degree of soft tissue syndactyly. Three subtypes of Pfeiffer syndrome have been described: mild autosomal dominant form (type 1); cloverleaf skull, elbow ankylosis, early death, sporadic (type 2); craniosynostosis, early demise, sporadic (type 3).
Defects in FGFR2 are the cause of Beare-Stevenson cutis gyrata syndrome (BSCGS) [MIM:123790]. BSCGS is an autosomal dominant condition is characterized by the furrowed skin disorder of cutis gyrata, acanthosis nigricans, craniosynostosis, craniofacial dysmorphism, digital anomalies, umbilical and anogenital abnormalities and early death.
Defects in FGFR2 are the cause of familial scaphocephaly syndrome (FSPC) [MIM:609579]; also known as scaphocephaly with maxillary retrusion and mental retardation. FSPC is an autosomal dominant craniosynostosis syndrome characterized by scaphocephaly, macrocephaly, hypertelorism, maxillary retrusion, and mild intellectual disability. Scaphocephaly is the most common of the craniosynostosis conditions and is characterized by a long, narrow head. It is due to premature fusion of the sagittal suture or from external deformation.
Defects in FGFR2 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 FGFR2 are the cause of Antley-Bixler syndrome (ABS) [MIM:207410]. ABS is a multiple congenital anomaly syndrome characterized by craniosynostosis, radiohumeral synostosis, midface hypoplasia, malformed ears, arachnodactyly and multiple joint contractures. ABS is a heterogeneous disorder and occurs with and without abnormal genitalia in both sexes.
Sequence similaritiesBelongs 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 localizationSecreted and Cell membrane.
- Information by UniProt
- bacteria-expressed kinase antibody
- BBDS antibody
- BEK antibody
Lane 1: Wild-type HAP1 cell lysate (20 µg)
Lane 2: FGFR2 knockout HAP1 cell lysate (20 µg)
Lane 3: HeLa cell lysate (20 µg)
Lane 4: Jurkat cell lysate (20 µg)
Lanes 1 - 4: Merged signal (red and green). Green - ab109372 observed at 160 kDa. Red - loading control, ab8245, observed at 37 kDa.
ab109372 was shown to specifically react with FGFR2 when FGFR2 knockout samples were used. Wild-type and FGFR2 knockout samples were subjected to SDS-PAGE. Ab109372 and ab8245 (loading control to GAPDH) were diluted at 1/1000 and 1/10,000 dilution respectively and incubated overnight at 4C. Blots were developed with Goat anti-Rabbit IgG H&L (IRDye® 800CW) preadsorbed (ab216773) and Goat anti-Mouse IgG H&L (IRDye® 680RD) preadsorbed (ab216776) secondary antibodies at 1/10,000 dilution for 1 hour at room temperature before imaging.
All lanes : Anti-FGFR2 antibody [EPR5180] (ab109372) at 1/1000 dilution
Lane 1 : MCF7 cell lysate
Lane 2 : Jurkat cell lysate
Lane 3 : HeLa cell lysate
Lane 4 : K562 cell lysate
Lane 5 : T47-D cell lysate
Lysates/proteins at 10 µg per lane.
Predicted band size: 92 kDa
Observed band size: 145 kDa why is the actual band size different from the predicted?
This product has been referenced in:
- Lee KW et al. FGF11 influences 3T3-L1 preadipocyte differentiation by modulating the expression of PPAR? regulators. FEBS Open Bio 9:769-780 (2019). Read more (PubMed: 30984550) »
- Xu L et al. Gambogenic acid inhibits fibroblast growth factor receptor signaling pathway in erlotinib-resistant non-small-cell lung cancer and suppresses patient-derived xenograft growth. Cell Death Dis 9:262 (2018). Read more (PubMed: 29449529) »