InnateDB: Systems Biology of the Innate Immune Response

Bos taurus Gene: WAS

Summary

InnateDB Gene

IDBG-636860.3

Last Modified

2014-10-13 [Report errors or provide feedback]

Gene Symbol

WAS

Gene Name

Uncharacterized protein

Synonyms

Species

Bos taurus

Ensembl Gene

ENSBTAG00000046555

Encoded Proteins

IDBP-688840

Wiskott-Aldrich syndrome (eczema-thrombocytopenia)

Protein Structure

Useful resources

Stemformatics EHFPI ImmGen

InnateDB Annotation from Orthologs

Summary

PMID 22253930

[Homo sapiens] WAS interacts with BTK to induce the LPS signalling cascade in macrophages. (Demonstrated in mice)

PMID 22253930

[Mus musculus] Was interacts with Btk to induce the LPS signalling cascade in macrophages.

Entrez Gene

Summary

This gene does not have any Entrez summary - the following is the summary from its human ortholog ENSG00000015285:
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. [provided by RefSeq, Jul 2008]
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. [provided by RefSeq, Jul 2008]

Gene Information

Type

Protein coding

Genomic Location

Chromosome X:91842944-91855473

Strand

Forward strand

Band

Transcripts

ENSBTAT00000062988

ENSBTAP00000056444

Interactions

Number of Interactions

This gene and/or its encoded proteins are associated with 0 experimentally validated interaction(s) in this database.
They are also associated with 72 interaction(s) predicted by orthology.

Predicted by orthology
Total	72 [view]

Gene Ontology

Molecular Function

Accession	GO Term
GO:0003779	actin binding
GO:0005515	protein binding
GO:0042802	identical protein binding

Biological Process

GO:0006955	immune response
GO:0007015	actin filament organization
GO:0008154	actin polymerization or depolymerization
GO:0016197	endosomal transport
GO:0030041	actin filament polymerization
GO:0030048	actin filament-based movement
GO:0042110	T cell activation
GO:2000601	positive regulation of Arp2/3 complex-mediated actin nucleation