Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity
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
Gene Ontology annotation based on curation of intracellular localizations of expressed fusion proteins in living cells
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Combined Automated Annotation using Multiple IEA Methods
Forced expression of NESH suppresses motility and metastatic dissemination of malignant cells.
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NESH/ABI3 forced expression suppresses cell motility and metastatic dissemination. NESH interacts with PAK via its SH3 domain and decreases PAK phosphorylation at Thr402.
"every clone of NESH transfectants caused a marked reduction in motility, although the clones exhibited no significant differences in intrinsic cell growth compared with the control cells in vitro. The NESH transfectants also exhibited significant reduction in tumor metastatic potential in vivo."
Towards a proteome-scale map of the human protein-protein interaction network.
NESH (Abi-3) is present in the Abi/WAVE complex but does not promote c-Abl-mediated phosphorylation.
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ABI3/NESH is present in the Abi/WAVE complex by immunoprecipitation but does not bind c-Abl and does not promote c-Abl-mediated phosphorylation of Mena or WAVE2, distinguishing it from ABI1 and ABI2.
"Immunoprecipitation revealed that NESH (Abi-3) is present in the Abi/WAVE complex. Our results suggest that NESH (Abi-3), like Abi-1 and Abi-2, is a component of the Abi/WAVE complex, but likely plays a different role in the regulation of c-Abl."
Insulin receptor substrate protein 53 (IRSp53) as a binding partner of antimetastasis molecule NESH, a member of Abelson interactor protein family.
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IRSp53 identified as a binding partner of NESH/ABI3. IRSp53 is involved in PDGF-stimulated membrane ruffling.
"Insulin receptor substrate protein 53 (IRSp53) as a binding partner of antimetastasis molecule NESH, a member of Abelson interactor protein family."
An empirical framework for binary interactome mapping.
Defining the membrane proteome of NK cells.
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ABI3 detected in the membrane proteome of NK cells by high-throughput proteomics.
"The present study was initiated to define the composition of the membrane proteome of the Natural Killer (NK) like cell line YTS"
ABI3 ectopic expression reduces in vitro and in vivo cell growth properties while inducing senescence.
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ABI3 re-expression in thyroid and colon carcinoma cells reduces transforming activity, inhibits anchorage-independent growth, suppresses in vivo tumor formation, and induces cellular senescence via p21WAF1 upregulation and ERK phosphorylation reduction.
Next-generation sequencing to generate interactome datasets.
A proteome-scale map of the human interactome network.
The NESH/Abi-3-based WAVE2 complex is functionally distinct from the Abi-1-based WAVE2 complex.
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ABI3 expression in NIH3T3 cells causes degradation of endogenous ABI1 and formation of a distinct ABI3-based WAVE2 complex that reduces WAVE2 translocation to the plasma membrane and impairs lamellipodial protrusions. In v-src transformed cells, ABI3 promotes invadopodia formation under certain conditions.
An inter-species protein-protein interaction network across vast evolutionary distance.
An interactome perturbation framework prioritizes damaging missense mutations for developmental disorders.
A reference map of the human binary protein interactome.
Multimodal cell maps as a foundation for structural and functional genomics.
Falcon deep research report for ABI3