Human FGFR2 Antibody Pair - BSA and Azide free (RMAB-0252221)
Cat. No.: RMAB-0252221
Category: Antibody Pair
INQUIRY
10 x 96 tests
Human FGFR2 Antibody Pair - BSA and Azide free is a matched pair of unconjugated recombinant rabbit monoclonal capture and detection antibodies used to (quantify human FGFR2) in sandwich ELISAs and many other pair-based applications. _x000D_
Product Features
| Conjugate | Unconjugated capture and detector antibodies |
|---|---|
| Species Reactivity | Human |
| Range | 7.81 pg/mL - 1000 pg/mL |
| Applications | Sandwich ELISA |
| Key Features | Unconjugated capture and detector antibodies; Adaptable to any antibody pair-based assay format; Antibody concentration ~ 1 mg/mL; BSA and azide free buffer - ready for conjugation; Reacts with: Human |
Target Information
| Target Symbol | FGFR2 |
|---|---|
| Target Name | Fibroblast growth factor receptor 2 |
| UniProt ID | P21802 |
| Cellular Localization | Secreted and Cell membrane. |
| Function | Receptor for acidic and basic fibroblast growth factors. |
| Involvement in Disease | Defects in FGFR2 are the cause of Crouzon syndrome (CS); 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). JWS is an autosomal dominant craniosynostosis syndrome characterized by craniofacialities andity of the feet: broad great toes with medial deviation and tarsal-metatarsal coalescence.Defects in FGFR2 are a cause of Apert syndrome (APRS); 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); 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). 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 anogenitalities and early death.Defects in FGFR2 are the cause of familial scaphocephaly syndrome (FSPC); 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); also known as Levy-Hollister syndrome. LADDS is a form of ectodermal dysplasia, a heterogeneous group of disorders due to 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 genitalia have been reported. Craniosynostosis and severe syndactyly are not observed.Defects in FGFR2 are the cause of Antley-Bixler syndrome. multiple congenital anomaly syndrome characterized by craniosynostosis, radiohumeral synostosis, midface hypoplasia, malformed ears, arachnodactyly and multiple joint contractures. heterogeneous disorder and occurs with and without genitalia in both sexes. |
| 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. |
Storage & Shipping
| Storage & Shipping | Store at 4°C. Please refer to protocols. |
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For research use only. Not for clinical use.
