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WAS Antibody(Center)

Affinity Purified Rabbit Polyclonal Antibody (Pab)

     
  • 1 - WAS Antibody(Center) AP19544c
    WAS Antibody (Center) (Cat. #AP19544c) western blot analysis in K562 cell line lysates (35ug/lane).This demonstrates the WAS antibody detected the WAS protein (arrow).
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Product Information
Application
  • Applications Legend:
  • E=ELISA
  • WB=Western Blotting
  • IHC=Immunohistochemistry
  • IHC-P=Immunohistochemistry (Paraffin)
  • IP=Immunoprecipitation
  • IF=Immunofluorescence
  • IC=Immunochemistry
  • ICC=Immunocytochemistry
  • FC=Flow Cytometry
  • DB=Dot Blot
WB, E
Primary Accession P42768
Other Accession NP_000368.1
Reactivity Human
Host Rabbit
Clonality Polyclonal
Isotype Rabbit IgG
Calculated MW 52913 Da
Antigen Region 205-234 aa
Additional Information
Gene ID 7454
Other Names Wiskott-Aldrich syndrome protein, WASp, WAS, IMD2
Target/Specificity This WAS antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 205-234 amino acids from the Central region of human WAS.
Dilution WB~~1:1000
E~~Use at an assay dependent concentration.
Format Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification.
StorageMaintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.
PrecautionsWAS Antibody(Center) is for research use only and not for use in diagnostic or therapeutic procedures.
Protein Information
Name WAS
Synonyms IMD2
Function Effector protein for Rho-type GTPases that regulates actin filament reorganization via its interaction with the Arp2/3 complex (PubMed:12235133, PubMed:12769847, PubMed:16275905). Important for efficient actin polymerization (PubMed:12235133, PubMed:16275905, PubMed:8625410). Possible regulator of lymphocyte and platelet function (PubMed:9405671). Mediates actin filament reorganization and the formation of actin pedestals upon infection by pathogenic bacteria (PubMed:18650809). In addition to its role in the cytoplasmic cytoskeleton, also promotes actin polymerization in the nucleus, thereby regulating gene transcription and repair of damaged DNA (PubMed:20574068). Promotes homologous recombination (HR) repair in response to DNA damage by promoting nuclear actin polymerization, leading to drive motility of double-strand breaks (DSBs) (PubMed:29925947).
Cellular Location Cytoplasm, cytoskeleton. Nucleus
Tissue Location Expressed predominantly in the thymus. Also found, to a much lesser extent, in the spleen.
Research Areas

For Research Use Only. Not For Use In Diagnostic Procedures.

BACKGROUND

The Wiskott-Aldrich syndrome (WAS) family of proteins share similar domain structure, and are involved in transduction of signals from receptors on the cell surface to the actin cytoskeleton. The presence of a number of different motifs suggests that they are regulated by a number of different stimuli, and interact with multiple proteins. Recent studies have demonstrated that these proteins, directly or indirectly, associate with the small GTPase, Cdc42, known to regulate formation of actin filaments, and the cytoskeletal organizing complex, Arp2/3. Wiskott-Aldrich syndrome is a rare, inherited, X-linked, recessive disease characterized by immune dysregulation and microthrombocytopenia, and is caused by mutations in the WAS gene. The WAS gene product is a cytoplasmic protein, expressed exclusively in hematopoietic cells, which show signalling and cytoskeletal abnormalities in WAS patients. A transcript variant arising as a result of alternative promoter usage, and containing a different 5' UTR sequence, has been described, however, its full-length nature is not known.

REFERENCES

Burns, S.O., et al. Blood 115(26):5355-5365(2010)
Taylor, M.D., et al. Sci Transl Med 2 (37), 37RA44 (2010) :
Rajmohan, R., et al. FEMS Yeast Res. 9(8):1226-1235(2009)
Dovas, A., et al. J. Cell. Sci. 122 (PT 21), 3873-3882 (2009) :
Ameratunga, R., et al. N. Z. Med. J. 122(1304):46-53(2009)

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