使用敲除细胞株进行验证RabMAb

Anti-FGFR2抗体[EPR5180] (ab109372)

概述

  • 产品名称Anti-FGFR2抗体[EPR5180]
    参阅全部 FGFR2 一抗
  • 描述
    兔单克隆抗体[EPR5180] to FGFR2
  • 经测试应用适用于: WB, IPmore details
    不适用于: Flow Cyt,ICC or IHC-P
  • 种属反应性
    与反应: Mouse, Rat, Human
  • 免疫原

    Synthetic peptide corresponding to residues in the extracellular domain of Human FGFR2.

  • 阳性对照
    • MCF7, Jurkat, HeLa, K562, and T47-D cell lysates
  • 常规说明

    This product is a recombinant rabbit monoclonal antibody.

    Produced using Abcam’s RabMAb® technology. RabMAb® technology is covered by the following U.S. Patents, No. 5,675,063 and/or 7,429,487.

性能

应用

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.

应用 Ab评论 说明
WB 1/1000 - 1/10000. Detects a band of approximately 145 kDa (predicted molecular weight: 92 kDa).
IP 1/10 - 1/100.
  • 应用说明Is unsuitable for Flow Cyt,ICC or IHC-P.
  • 靶标

    • 功能Receptor for acidic and basic fibroblast growth factors.
    • 疾病相关Defects 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.
    • 序列相似性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.
    • 细胞定位Secreted and Cell membrane.
    • Information by UniProt
    • 数据库链接
    • 别名
      • bacteria-expressed kinase antibody
      • BBDS antibody
      • BEK antibody
      • BEK fibroblast growth factor receptor antibody
      • BFR1 antibody
      • CD332 antibody
      • CD332 antigen antibody
      • CEK3 antibody
      • CFD1 antibody
      • Craniofacial dysostosis 1 antibody
      • ECT1 antibody
      • FGF receptor antibody
      • FGFR 2 antibody
      • FGFR-2 antibody
      • Fgfr2 antibody
      • FGFR2_HUMAN antibody
      • Fibroblast growth factor receptor 2 antibody
      • Hydroxyaryl protein kinase antibody
      • Jackson Weiss syndrome antibody
      • JWS antibody
      • K SAM antibody
      • K-sam antibody
      • Keratinocyte growth factor receptor 2 antibody
      • Keratinocyte growth factor receptor antibody
      • KGFR antibody
      • KSAM antibody
      • protein tyrosine kinase, receptor like 14 antibody
      • soluble FGFR4 variant 4 antibody
      • TK14 antibody
      • TK25 antibody
      see all

    Anti-FGFR2 antibody [EPR5180] 图像



    • Predicted band size : 92 kDa

      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) ab216773 and Goat anti-Mouse IgG H&L (IRDye® 680RD) 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?)

    Anti-FGFR2 antibody [EPR5180] (ab109372)参考文献

    ab109372 has not yet been referenced specifically in any publications.

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