Anti-FGFR2 抗体 (ab10647)
Key features and details
- Rabbit polyclonal to FGFR2
- Suitable for: IHC-P, IP, WB
- Reacts with: Human
- Isotype: IgG
リコンビナント抗体で、ロット間での高い再現性を実現
- 異なるロット間での安定した再現性
- 容易なスケールアップ
- 評価試験による特異性の確認済み
- 倫理基準に準拠 - アニマル・フリーの生産
製品の概要
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製品名
Anti-FGFR2 antibody
FGFR2 一次抗体 製品一覧 -
製品の詳細
Rabbit polyclonal to FGFR2 -
由来種
Rabbit -
アプリケーション
適用あり: IHC-P, IP, WBmore details -
種交差性
交差種: Human
交差が予測される動物種: Mouse, Rat
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免疫原
Synthetic peptide:
KLPQYPHINGSVKT
conjugated to KLH by a Glutaraldehyde linker, corresponding to amino acids 809-821 of the cytoplasmic region of Human FGFR2. -
ポジティブ･コントロール
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特記事項
The Life Science industry has been in the grips of a reproducibility crisis for a number of years. Abcam is leading the way in addressing this with our range of recombinant monoclonal antibodies and knockout edited cell lines for gold-standard validation. Please check that this product meets your needs before purchasing.
If you have any questions, special requirements or concerns, please send us an inquiry and/or contact our Support team ahead of purchase. Recommended alternatives for this product can be found below, along with publications, customer reviews and Q&As
製品の特性
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製品の状態
Liquid -
保存方法
Shipped at 4°C. Upon delivery aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles. -
バッファー
pH: 7.40
Preservative: 0.097% Sodium azide
Constituents: 0.0268% PBS, 1% BSA -
Concentration information loading... -
精製度
Immunogen affinity purified -
特記事項（精製）
The antibody is affinity-purified using the immunizing peptide immobilized on agarose. -
ポリ/モノ
ポリクローナル -
アイソタイプ
IgG -
研究分野
関連製品
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Compatible Secondaries
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Isotype control
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Recombinant Protein
アプリケーション
The Abpromise guarantee
Abpromise保証は、 次のテスト済みアプリケーションにおけるab10647の使用に適用されます
アプリケーションノートには、推奨の開始希釈率がありますが、適切な希釈率につきましてはご検討ください。
| アプリケーション | Abreviews | 特記事項 |
|---|---|---|
| IHC-P | ||
| IP | ||
| WB |
| 特記事項 |
|---|
追加情報
IHC-P: Use at an assay dependent dilution, this concentration is determined by indirect immunoperoxidase staining of trypsin or protease-digested human and animal tissue sections.
IP: 1/2000. This concentration is determined by immunoprecipitation using a whole lysate of transfected cells expressing recombinant human FGFR2.
WB: 1/2000. This concentration is determined by immunoblotting using a whole extract of transfected cells expressing recombinant human FGFR2. Predicted molecular weight: 110 kDa.
Not tested in other applications.
Optimal dilutions/concentrations should be determined by the end user.
IP: 1/2000. This concentration is determined by immunoprecipitation using a whole lysate of transfected cells expressing recombinant human FGFR2.
WB: 1/2000. This concentration is determined by immunoblotting using a whole extract of transfected cells expressing recombinant human FGFR2. Predicted molecular weight: 110 kDa.
Not tested in other applications.
Optimal dilutions/concentrations should be determined by the end user.
ターゲット情報
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機能
Receptor for acidic and basic fibroblast growth factors. -
関連疾患
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. -
配列類似性
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. -
細胞内局在
Secreted and Cell membrane. - Information by UniProt
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参照データベース
- Entrez Gene: 2263 Human
- Entrez Gene: 14183 Mouse
- Entrez Gene: 25022 Rat
- Omim: 176943 Human
- SwissProt: P21802 Human
- SwissProt: P21803 Mouse
- Unigene: 533683 Human
- Unigene: 16340 Mouse
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別名
- bacteria-expressed kinase antibody
- BBDS antibody
- BEK antibody
see all
プロトコール
データシートおよび資料
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SDS download
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Datasheet download
参考文献 (2)
ab10647 は 2 報の論文で使用されています。
- Vesterlund L et al. Co-localization of neural cell adhesion molecule and fibroblast growth factor receptor 2 in early embryo development. Int J Dev Biol 55:313-9 (2011). PubMed: 21710437
- Spence JR et al. Retina regeneration in the chick embryo is not induced by spontaneous Mitf downregulation but requires FGF/FGFR/MEK/Erk dependent upregulation of Pax6. Mol Vis 13:57-65 (2007). PubMed: 17277739