Anti-N-WASP

Anti-N-WASP

AB1963

The antibody recognizes human N-WASP.

~64 kDa

Full-length human recombinant N-WASP protein.

Members of the Wiskott-Aldrich syndrome protein (WASP) family regulate the formation of actin-based cell structures in many cell types. These proteins contain C-terminal actin binding domains that can stimulate actin polymerization. In addition, these proteins bind the ARP2/3 complex, which can nucleate actin polymerization at sites that lead to branched actin structures. WASP is expressed primarily in hematopoietic cells, while its homolog N-WASP is widely expressed. These proteins have 48% identity in human with the highest homology in the functional regions of these proteins. Serine and tyrosine phosphorylation regulates the activity of both proteins. WASP is observed as a ~63 kDa protein in hematopoietic cells, while N-WASP is observed as a ~65 kDa in many tissues, especially brain.

• Human
• Mouse
• Rat

Human, mouse, rat. Reactivity with other species has not been tested.

HEK293 cell lysates

Evaluated on a representative lot by Western blot on HEK293 cell lysate using 1:1000 dilution of Anti-N-WASP.

Rabbit serum containing 0.05% NaN3.

Maintain at -20°C for up to 1 year from date of receipt.

P42768

NP_003932

• N-WASP
• NWASP
• MGC48327

• Wiskott-Aldrich syndrome gene-like
• Wiskott-Aldrich syndrome gene-like protein
• Wiskott-Aldrich syndrome-like
• neural Wiskott-Aldrich syndrome protein

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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. The WASL gene product is a homolog of WAS protein, however, unlike the latter, it is ubiquitously expressed and shows highest expression in neural tissues. It has been shown to bind Cdc42 directly, and induce formation of long actin microspikes. [provided by RefSeq]

Western Blotting

FUNCTION: Effector protein for Rho-type GTPases, providing a link with the Arp2/3 complex that regulates the structure and dynamics of the actin cytoskeleton. Important for efficient actin polymerization. Possible regulator of lymphocyte and platelet function.
SUBUNIT STRUCTURE: Binds to CDC42, RAC, NCK, FYN, SRC kinase FGR, BTK, ABL, PSTPIP1, WIP, and to the p85 subunit of PLC-gamma. Binds the Arp2/3 complex.
SUBCELLULAR LOCATION: Cytoplasm › cytoskeleton.
TISSUE SPECIFICTY: Expressed predominantly in the thymus. Also found, to a much lesser extent, in the spleen. Ref.1
DOMIAN: The WH1 (Wasp homology 1) domain may bind a Pro-rich ligand.
The CRIB (Cdc42/Rac-interactive-binding) region binds to the C-terminal WH2 domain in the autoinhibited state of the protein. Binding of Rho-type GTPases to the CRIB induces a conformation change and leads to activation.
INVOLVEMENT IN DISEASE: Defects in WAS are the cause of Wiskott-Aldrich syndrome (WAS) [MIM:301000]; also known as eczema-thrombocytopenia-immunodeficiency syndrome. WAS is an X-linked recessive immunodeficiency characterized by eczema, thrombocytopenia, recurrent infections, and bloody diarrhea. Death usually occurs before age 10.
Defects in WAS are the cause of thrombocytopenia type 1 (THC1) [MIM:313900]. Thrombocytopenia is defined by a decrease in the number of platelets in circulating blood, resulting in the potential for increased bleeding and decreased ability for clotting.
Defects in WAS are a cause of X-linked severe congenital neutropenia (XLN) [MIM:300299]. XLN is an X-linked immunodeficiency syndrome characterized by recurrent major bacterial infections, severe congenital neutropenia, and monocytopenia.
SEQUENCE SIMILARITIES: Contains 1 CRIB domain.
Contains 1 WH1 domain.
Contains 1 WH2 domain.

100 µL

Serum

Rabbit

Anti-N-WASP

Polyclonal Antibody