Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Automatic assignment of GO terms using logical inference, based on inter-ontology links
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
WIP, a protein associated with wiskott-aldrich syndrome protein, induces actin polymerization and redistribution in lymphoid cells.
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WIP identified as WASP-interacting protein
"WIP binds to WASP at a site distinct from the Cdc42 binding site"
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WIP has actin and profilin binding motifs
"WIP binds to WASP at a site distinct from the Cdc42 binding site and has actin as well as profilin binding motifs"
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WIP expression increases polymerized actin content
"Expression of WIP in human B cells, but not of a WIP truncation mutant that lacks the actin binding motif, increased polymerized actin content and induced the appearance of actin-containing cerebriform projections on the cell surface"
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WIP colocalizes with actin stress fibers
"WIP binds to WASP at a site distinct from the Cdc42 binding site and has actin as well as profilin binding motifs"
Mutations that cause the Wiskott-Aldrich syndrome impair the interaction of Wiskott-Aldrich syndrome protein (WASP) with WASP interacting protein.
A complex of N-WASP and WIP integrates signalling cascades that lead to actin polymerization.
WIP regulates N-WASP-mediated actin polymerization and filopodium formation.
Identification of novel SH3 domain ligands for the Src family kinase Hck. Wiskott-Aldrich syndrome protein (WASP), WASP-interacting protein (WIP), and ELMO1.
Structure of the N-WASP EVH1 domain-WIP complex: insight into the molecular basis of Wiskott-Aldrich Syndrome.
X-linked thrombocytopenia caused by a mutation in the Wiskott-Aldrich syndrome (WAS) gene that disrupts interaction with the WAS protein (WASP)-interacting protein (WIP).
Cortactin interacts with WIP in regulating Arp2/3 activation and membrane protrusion.
WASP suppresses the growth defect of Saccharomyces cerevisiae las17Delta strain in the presence of WIP.
Wiskott-Aldrich syndrome protein is involved in alphaIIb beta3-mediated cell adhesion.
WIP regulates the stability and localization of WASP to podosomes in migrating dendritic cells.
WIP is a chaperone for Wiskott-Aldrich syndrome protein (WASP).
Src phosphorylation of cortactin enhances actin assembly.
Requirements for F-BAR proteins TOCA-1 and TOCA-2 in actin dynamics and membrane trafficking during Caenorhabditis elegans oocyte growth and embryonic epidermal morphogenesis.
Phosphorylation of WASp is a key regulator of activity and stability in vivo.
Characterization of Wiskott-Aldrich syndrome (WAS) mutants using Saccharomyces cerevisiae.
A human MAP kinase interactome.
Hematopoietic lineage cell-specific protein 1 functions in concert with the Wiskott-Aldrich syndrome protein to promote podosome array organization and chemotaxis in dendritic cells.
Next-generation sequencing to generate interactome datasets.
Selected reaction monitoring mass spectrometry reveals the dynamics of signaling through the GRB2 adaptor.
Toward an understanding of the protein interaction network of the human liver.
A human skeletal muscle interactome centered on proteins involved in muscular dystrophies: LGMD interactome.
NMR determines transient structure and dynamics in the disordered C-terminal domain of WASp interacting protein.
A proteome-scale map of the human interactome network.
Architecture of the human interactome defines protein communities and disease networks.
An interactome perturbation framework prioritizes damaging missense mutations for developmental disorders.
Dual proteome-scale networks reveal cell-specific remodeling of the human interactome.
OpenCell: Endogenous tagging for the cartography of human cellular organization.
CLDN6 inhibits breast cancer metastasis through WIP-dependent actin cytoskeleton-mediated autophagy.
Multimodal cell maps as a foundation for structural and functional genomics.
WASPs WAVE G-actin ARP2/3 binds F-actin
WIP binds WASP N-WASP activating them
Src phosphorylate WASP N-WASP
Deep research summary for WIPF1
Cyberian deep research on WIPF1 function