Anti-Filamin A (phospho S2152) 抗体 (ab51229)
Key features and details
- Rabbit polyclonal to Filamin A (phospho S2152)
- Suitable for: WB
- Reacts with: Human
- Isotype: IgG
製品の概要
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製品名
Anti-Filamin A (phospho S2152) antibody
Filamin A 一次抗体 製品一覧 -
製品の詳細
Rabbit polyclonal to Filamin A (phospho S2152) -
由来種
Rabbit -
アプリケーション
適用あり: WBmore details -
種交差性
交差種: Human
交差が予測される動物種: Mouse, Rat -
免疫原
Synthetic peptide corresponding to Human Filamin A aa 2100-2200 (phospho S2152).
Database link: P21333 -
ポジティブ・コントロール
- Extracts from 293 cells treated with EGF (200ng/ml, 5min)
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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.
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製品の特性
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製品の状態
Liquid -
保存方法
Shipped at 4°C. Store at -20°C. Stable for 12 months at -20°C. -
バッファー
pH: 7.40
Preservative: 0.02% Sodium azide
Constituents: 50% Glycerol (glycerin, glycerine), 0.87% Sodium chloride, PBS
Without Mg+2 and Ca+2 -
Concentration information loading...
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精製度
Immunogen affinity purified -
特記事項(精製)
ab51229 was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific phosphopeptide. The antibody against non-phosphopeptide was removed by chromatography using non-phosphopeptide corresponding to the phosphorylation site. -
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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Corresponding non-phospho antibody
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Isotype control
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ab51229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 |
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WB |
1/300 - 1/1000. Predicted molecular weight: 281 kDa.
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特記事項 |
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WB
1/300 - 1/1000. Predicted molecular weight: 281 kDa. |
ターゲット情報
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機能
Promotes orthogonal branching of actin filaments and links actin filaments to membrane glycoproteins. Anchors various transmembrane proteins to the actin cytoskeleton and serves as a scaffold for a wide range of cytoplasmic signaling proteins. Interaction with FLNA may allow neuroblast migration from the ventricular zone into the cortical plate. Tethers cell surface-localized furin, modulates its rate of internalization and directs its intracellular trafficking. -
組織特異性
Ubiquitous. -
関連疾患
Defects in FLNA are the cause of periventricular nodular heterotopia type 1 (PVNH1) [MIM:300049]; also called nodular heterotopia, bilateral periventricular (NHBP or BPNH). PVNH is a developmental disorder characterized by the presence of periventricular nodules of cerebral gray matter, resulting from a failure of neurons to migrate normally from the lateral ventricular proliferative zone, where they are formed, to the cerebral cortex. PVNH1 is an X-linked dominant form. Heterozygous females have normal intelligence but suffer from seizures and various manifestations outside the central nervous system, especially related to the vascular system. Hemizygous affected males die in the prenatal or perinatal period.
Defects in FLNA are the cause of periventricular nodular heterotopia type 4 (PVNH4) [MIM:300537]; also known as periventricular heterotopia Ehlers-Danlos variant. PVNH4 is characterized by nodular brain heterotopia, joint hypermobility and development of aortic dilation in early adulthood.
Defects in FLNA are the cause of otopalatodigital syndrome type 1 (OPD1) [MIM:311300]. OPD1 is an X-linked dominant multiple congenital anomalies disease mainly characterized by a generalized skeletal dysplasia, mild mental retardation, hearing loss, cleft palate, and typical facial anomalies. OPD1 belongs to a group of X-linked skeletal dysplasias known as oto-palato-digital syndrome spectrum disorders that also include OPD2, Melnick-Needles syndrome (MNS), and frontometaphyseal dysplasia (FMD). Remodeling of the cytoskeleton is central to the modulation of cell shape and migration. FLNA is a widely expressed protein that regulates re-organization of the actin cytoskeleton by interacting with integrins, transmembrane receptor complexes and second messengers. Males with OPD1 have cleft palate, malformations of the ossicles causing deafness and milder bone and limb defects than those associated with OPD2. Obligate female carriers of mutations causing both OPD1 and OPD2 have variable (often milder) expression of a similar phenotypic spectrum.
Defects in FLNA are the cause of otopalatodigital syndrome type 2 (OPD2) [MIM:304120]; also known as cranioorodigital syndrome. OPD2 is a congenital bone disorder that is characterized by abnormally modeled, bowed bones, small or absent first digits and, more variably, cleft palate, posterior fossa brain anomalies, omphalocele and cardiac defects.
Defects in FLNA are the cause of frontometaphyseal dysplasia (FMD) [MIM:305620]. FMD is a congenital bone disease characterized by supraorbital hyperostosis, deafness and digital anomalies.
Defects in FLNA are the cause of Melnick-Needles syndrome (MNS) [MIM:309350]. MNS is a severe congenital bone disorder characterized by typical facies (exophthalmos, full cheeks, micrognathia and malalignment of teeth), flaring of the metaphyses of long bones, s-like curvature of bones of legs, irregular constrictions in the ribs, and sclerosis of base of skull.
Defects in FLNA are the cause of X-linked congenital idiopathic intestinal pseudoobstruction (CIIPX) [MIM:300048]. CIIPX is characterized by a severe abnormality of gastrointestinal motility due to primary qualitative defects of enteric ganglia and nerve fibers. Affected individuals manifest recurrent signs of intestinal obstruction in the absence of any mechanical lesion.
Defects in FLNA are the cause of FG syndrome type 2 (FGS2) [MIM:300321]. FG syndrome (FGS) is an X-linked disorder characterized by mental retardation, relative macrocephaly, hypotonia and constipation.
Defects in FLNA are the cause of terminal osseous dysplasia (TOD) [MIM:300244]. A rare X-linked dominant male-lethal disease characterized by skeletal dysplasia of the limbs, pigmentary defects of the skin and recurrent digital fibroma during infancy. A significant phenotypic variability is observed in affected females.
Defects in FLNA are the cause of cardiac valvular dysplasia X-linked (CVDX) [MIM:314400]. A rare X-linked heart disease characterized by mitral and/or aortic valve regurgitation. The histologic features include fragmentation of collagenous bundles within the valve fibrosa and accumulation of proteoglycans, which produces excessive valve tissue leading to billowing of the valve leaflets. -
配列類似性
Belongs to the filamin family.
Contains 1 actin-binding domain.
Contains 2 CH (calponin-homology) domains.
Contains 24 filamin repeats. -
ドメイン
Comprised of a NH2-terminal actin-binding domain, 24 internally homologous repeats and two hinge regions. Repeat 24 and the second hinge domain are important for dimer formation. -
翻訳後修飾
Phosphorylated upon DNA damage, probably by ATM or ATR (By similarity). Phosphorylation extent changes in response to cell activation.
The N-terminus is blocked. -
細胞内局在
Cytoplasm > cell cortex. Cytoplasm > cytoskeleton. - Information by UniProt
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参照データベース
- Entrez Gene: 2316 Human
- Entrez Gene: 192176 Mouse
- Entrez Gene: 293860 Rat
- Omim: 300017 Human
- SwissProt: P21333 Human
- SwissProt: Q8BTM8 Mouse
- Unigene: 195464 Human
- Unigene: 295533 Mouse
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別名
- ABP 280 antibody
- ABP-280 antibody
- Actin-binding protein 280 antibody
see all
画像
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)
ab51229 は 2 報の論文で使用されています。
- Urra H et al. IRE1a governs cytoskeleton remodelling and cell migration through a direct interaction with filamin A. Nat Cell Biol 20:942-953 (2018). PubMed: 30013108
- Sayner SL et al. Filamin A is a phosphorylation target of membrane but not cytosolic adenylyl cyclase activity. Am J Physiol Lung Cell Mol Physiol 301:L117-24 (2011). WB ; Rat . PubMed: 21478251