NESH (Abi‐3) is present in the Abi/WAVE complex but does not promote c‐Abl‐mediated phosphorylation
Open accessAbstract
Abl interactor (Abi) was identified as an Abl tyrosine kinase‐binding protein and subsequently shown to be a component of the macromolecular Abi/WAVE complex, which is a key regulator of Rac‐dependent actin polymerization. Previous studies showed that Abi‐1 promotes c‐Abl‐mediated phosphorylation of Mammalian Enabled (Mena) and WAVE2. In addition to Abi‐1, mammals possess Abi‐2 and NESH (Abi‐3). In this study, we compared the three Abi proteins in terms of the promotion of c‐Abl‐mediated phosphorylation and the formation of Abi/WAVE complex. Although Abi‐2, like Abi‐1, promoted the c‐Abl‐mediated phosphorylation of Mena and WAVE2, NESH (Abi‐3) had no such effect. This difference was likely due to their binding abilities as to c‐Abl. 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.
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WRC containing ABI3 is functionally distinct from that containing ABI1.
“WRC containing ABI3 is functionally distinct from that containing ABI1 (17,18).”
From Microglia express ABI3 in the brains of Alzheimer's disease and Nasu-Hakola disease (2017) · cites this paper as [17]
The Introduction reports that ABI1 promotes c-Abl-mediated phosphorylation of Mena and WAVE2 whereas ABI3 does not, and that both participate in the Abi/WAVE complex. The Discussion says it is *possible* that complexes containing them differ in regulation by c-Abl; it does not establish the broader, unqualified claim that the complexes are functionally distinct. (LLM, conf=0.85)
Experimental — accuracy not yet measuredBoth ABI1 and ABI2 but not ABI3 promote the c-ABL-mediated phosphorylation of WAVE2, since ABI3 does not directly interact with c-ABL.
“Both ABI1 and ABI2 but not ABI3 promote the c-ABL-mediated phosphorylation of WAVE2, since ABI3 does not directly interact with c-ABL (17,18).”
From Microglia express ABI3 in the brains of Alzheimer's disease and Nasu-Hakola disease (2017) · cites this paper as [17]
Section 3.1 reports that Abi-1 and Abi-2 promoted c-Abl-mediated WAVE2 phosphorylation, whereas NESH (Abi-3) did not. Sections 3.2 and 4 say NESH was not detected interacting with c-Abl in the assay and that reduced or absent binding is the most likely explanation; they do not establish that it cannot interact directly or that this explanation is certain. (LLM, conf=0.87)
Experimental — accuracy not yet measuredABI3 is a regulator of actin cytoskeleton organization.
“A recent study demonstrated that a rare coding variant p.Ser209Phe in the ABI family member 3 (ABI3) gene, a regulator of actin cytoskeleton organization, confers risk of developing of LOAD, although the pattern of ABI3 expression in AD and NHD brains with relevance to microglial pathology remains to be characterized.”
From Microglia express ABI3 in the brains of Alzheimer's disease and Nasu-Hakola disease (2017) · cites this paper as [17]
The Introduction identifies ABI3 as NESH and says its involvement in regulating the cellular cytoskeleton is suggested, while its mechanism remains unclear. The paper also shows that NESH belongs to the actin-regulating Abi/WAVE complex, but it does not establish ABI3 itself as a regulator of actin cytoskeleton organization as definitively as the citing sentence states. (LLM, conf=0.83)
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Cites
Kunda, P., Craig, G., Dominguez, V., & Baum, B. (2003) · Current Biology · doi:10.1016/j.cub.2003.10.005 · Cited by 341 · see citing works
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Research works printed but not linked: 2
- Leng, Y., Zhang, J., Badour, K., Arpaia, E., Freeman, S., Cheung, P., Siu, M. and Siminovitch, K. (2005) Abelson- interactor-1 promotes WAVE2 membrane translocation and Abelson-mediated tyrosine phosphorylation required for WAVE2 activation. Proc. Natl. Acad. Sci. USA 102, 1098-1103.
- Gautreau, A., Ho, H.Y., Li, J., Steen, H., Gygi, S.P. and Kirschner, M.W. (2004) Purification and architecture of the ubiquitous Wave complex. Proc. Natl. Acad. Sci. USA 101, 4379- 4383.
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The NESH/Abi-3-based WAVE2 complex is functionally distinct from the Abi-1-based WAVE2 complex
Sekino, S., Kashiwagi, Y., Kanazawa, H., Takada, K., Baba, T., Sato, S., Inoue, H., Kojima, M., & Tani, K. (2015) · Cell Communication and Signaling · doi:10.1186/s12964-015-0119-5 · Cited by 43 · see citing works
Self-citationMicroglia express ABI3 in the brains of Alzheimer's disease and Nasu-Hakola disease
Satoh, J.-I., Kino, Y., Yanaizu, M., Tosaki, Y., Sakai, K., Ishida, T., & Saito, Y. (2017) · Intractable & Rare Diseases Research · doi:10.5582/irdr.2017.01073 · Cited by 55 · see citing works
- Authors
- Hirao, N., Sato, S., Gotoh, T., Maruoka, M., Suzuki, J., Matsuda, S., Shishido, T., & Tani, K.
- Affiliations
- Tokyo University of Pharmacy and Life Sciences (JP)
- Nara Institute of Science and Technology (JP)
- Nara Women's University (JP)
- Corresponding author
- Tani, Katsuko
- Venue
- FEBS Letters
- Publisher
- Wiley
- Published
- 2006-11-07
- Volume
- 580
- Issue
- 27
- Pages
- 6464-6470
- ISSN
- 0014-5793 (ISSN-L)
- 1873-3468
- OpenAlex
- W2057704178
- Cited by
- 25
- References
- 1
- Citations by year
- 2026: 1 · 2024: 2 · 2023: 1 · 2021: 2 · 2019: 1 · 2017: 3 · 2016: 1 · 2015: 3 · 2014: 3 · 2012: 3
- FWCI
- 0.38
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- FEBS Letters (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Japan Society for the Promotion of Science (16022259)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular Mechanics and Interactions
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Axon Guidance and Neuronal Signaling
- Keywords
- c-Abl, Abi-1, Middle East and North Africa, WAVE2, Abl tyrosine kinase, protein-protein interaction
- MeSH terms
- Animals, Chlorocebus aethiops, Cytoskeletal Proteins, Gene Expression Regulation, Humans, Microfilament Proteins, Phosphorylation, Protein Processing, Post-Translational, Proto-Oncogene Proteins c-abl, COS Cells, Multiprotein Complexes, Adaptor Proteins, Signal Transducing, Wiskott-Aldrich Syndrome Protein Family, Mice
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