Anti-Filamin A (phospho S2152) antibody (ab51229)
Key features and details
- Rabbit polyclonal to Filamin A (phospho S2152)
- Suitable for: WB
- Reacts with: Human
- Isotype: IgG
Overview
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Product name
Anti-Filamin A (phospho S2152) antibody
See all Filamin A primary antibodies -
Description
Rabbit polyclonal to Filamin A (phospho S2152) -
Host species
Rabbit -
Tested applications
Suitable for: WBmore details -
Species reactivity
Reacts with: Human
Predicted to work with: Mouse, Rat -
Immunogen
Synthetic peptide corresponding to Human Filamin A aa 2100-2200 (phospho S2152).
Database link: P21333 -
Positive control
- Extracts from 293 cells treated with EGF (200ng/ml, 5min)
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General notes
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Properties
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Form
Liquid -
Storage instructions
Shipped at 4°C. Store at -20°C. Stable for 12 months at -20°C. -
Storage buffer
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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Purity
Immunogen affinity purified -
Purification notes
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. -
Clonality
Polyclonal -
Isotype
IgG -
Research areas
Associated products
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Compatible Secondaries
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Corresponding non-phospho antibody
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Isotype control
Applications
The Abpromise guarantee
Our Abpromise guarantee covers the use of ab51229 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Application | Abreviews | Notes |
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WB |
1/300 - 1/1000. Predicted molecular weight: 281 kDa.
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Notes |
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WB
1/300 - 1/1000. Predicted molecular weight: 281 kDa. |
Target
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Function
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. -
Tissue specificity
Ubiquitous. -
Involvement in disease
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. -
Sequence similarities
Belongs to the filamin family.
Contains 1 actin-binding domain.
Contains 2 CH (calponin-homology) domains.
Contains 24 filamin repeats. -
Domain
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. -
Post-translational
modificationsPhosphorylated upon DNA damage, probably by ATM or ATR (By similarity). Phosphorylation extent changes in response to cell activation.
The N-terminus is blocked. -
Cellular localization
Cytoplasm > cell cortex. Cytoplasm > cytoskeleton. - Information by UniProt
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Database links
- 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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Alternative names
- ABP 280 antibody
- ABP-280 antibody
- Actin-binding protein 280 antibody
see all
Images
Datasheets and documents
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SDS download
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Datasheet download
References (2)
ab51229 has been referenced in 2 publications.
- 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