Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Automatic assignment of GO terms using logical inference, based on inter-ontology links
The cell migration molecule UNC-53/NAV2 is linked to the ARP2/3 complex by ABI-1.
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C. elegans ABI-1 binds the N-terminal calponin-homology domain of UNC-53/NAV2 to link UNC-53 to the Arp2/3 complex during excretory cell and neuronal migration.
"We have identified ABI-1 as a novel molecular partner of UNC-53/NAV2 and have found that a restricted calponin homology (CH) domain of UNC-53 is sufficient to bind ABI-1."
Abl kinase inhibits the engulfment of apoptotic [corrected] cells in Caenorhabditis elegans.
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ABI-1 physically interacts with ABL-1 in vitro and is required for apoptotic cell engulfment and distal tip cell migration, with ABL-1 inhibiting ABI-1.
"ABL-1 and ABI-1 interact physically in vitro. We propose that ABL-1 opposes the engulfment of apoptotic cells by inhibiting ABI-1 via a pathway that is distinct from the two known engulfment pathways."
Shifted Transversal Design smart-pooling for high coverage interactome mapping.
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.
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In vitro translated C. elegans ABI-1 binds directly to the SH3 domain of CeTOCA-2, conserving the mammalian TOCA-1 SH3 interaction with ABI-1.
"In keeping with this notion, we found that in vitro translated C. elegans ABI-1 readily interacted with the SH3 domain of CeTOCA-2 (Figure 7C), indicating that this interaction is conserved in the nematode."
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CeTOCA-1/2 associate indirectly with WVE-1 via ABI-1 to support clathrin-mediated endocytosis and embryonic epidermal morphogenesis.
"Furthermore, mammalian TOCA-1 and C. elegans CeTOCAs physically associated with N-WASP and WSP-1 directly, or WAVE2 indirectly via ABI-1."
Abelson interactor-1 (ABI-1) interacts with MRL adaptor protein MIG-10 and is required in guided cell migrations and process outgrowth in C. elegans.
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The C-terminal SH3 domain of ABI-1 binds MIG-10/Lamellipodin to drive ALM neuron migration and excretory canal outgrowth.
"Further analysis using a co-immunoprecipitation system confirmed the interaction of MIG-10 and ABI-1 and showed that it requires the SH3 domain of ABI-1. Single mutants for mig-10 and abi-1 displayed similar phenotypes of incomplete migration of the ALM neurons and truncated outgrowth of the excretory cell canals, suggesting that the ABI-1/MIG-10 interaction is relevant in vivo."
Synaptic vesicle clustering requires a distinct MIG-10/Lamellipodin isoform and ABI-1 downstream from Netrin.
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MIG-10B binds ABI-1 in the WAVE complex downstream of Netrin to organize presynaptic F-actin and cluster synaptic vesicles.
"MIG-10B interacts with Abl-interacting protein-1 (ABI-1)/Abi1, a component of the WAVE complex, to organize the actin cytoskeleton at presynaptic sites and instruct vesicle clustering through SNN-1/Synapsin."
MIG-10 functions with ABI-1 to mediate the UNC-6 and SLT-1 axon guidance signaling pathways.
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ABI-1 binds MIG-10 via its SH3 domain and acts with WVE-1 in UNC-6/netrin and SLT-1/slit axon guidance pathways.
"The SH3 domain of ABI-1 binds to MIG-10, and loss of function of either of these proteins causes similar axon guidance defects. Like MIG-10, ABI-1 functions in both the attractive UNC-6 (netrin) pathway and the repulsive SLT-1 (slit) pathway."
SH3 interactome conserves general function over specific form.
WormBase gene description for abi-1 (worm)