The DOI matches its Crossref record; 30 of the 31 references it cites were found in a registry or an index.
SHIP is a negative regulator of growth factor receptor-mediated PKB/Akt activation and myeloid cell survival
Open accessAbstract
SHIP is an inositol 5' phosphatase that hydrolyzes the PI3'K product PI(3,4,5)P3. We show that SHIP-deficient mice exhibit dramatic chronic hyperplasia of myeloid cells resulting in splenomegaly, lymphadenopathy, and myeloid infiltration of vital organs. Neutrophils and bone marrow-derived mast cells from SHIP-/- mice are less susceptible to programmed cell death induced by various apoptotic stimuli or by growth factor withdrawal. Engagement of IL3-R and GM-CSF-R in these cells leads to increased and prolonged PI3'K-dependent PI(3,4,5)P3 accumulation and PKB activation. These data indicate that SHIP is a negative regulator of growth factor-mediated PKB activation and myeloid cell survival.
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“This strategy also avoids the developmental effects that can occur in constitutive knockouts.16,17”
From Microglial INPP5D limits plaque formation and glial reactivity in the PSAPP mouse model of Alzheimer's disease (2023) · cites this paper as [16]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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“which are both processes that can be mediated by Inpp5d. 6 , 20”
From Loss of Inpp5d has disease‐relevant and sex‐specific effects on glial transcriptomes (2024) · cites this paper as [6]
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“Upon binding to PI(3,4,5)P3, the 5’ phosphatase catalytic domain phosphorylates PI(3,4,5)P3 to generate PI(3,4)P2, which can bind to the C2 domain near the C-terminus [92, 107, 108].”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [92]
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“SHIP1 is a phosphatase involved in phosphoinositide signaling.”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [92]
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“PI(3,4,5)P3 can be converted back to PI(4,5)P2 by the protein phosphatase and tensin homology (PTEN) or converted into PI(3,4)P2 by SHIP1, which negatively regulates PI3K/Akt signaling (Fig. 2) [89–92].”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [92]
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Cites
Maehama, T., & Dixon, J. E. (1998) · Journal of Biological Chemistry · doi:10.1074/jbc.273.22.13375 · Cited by 3,104
Alessi, D. R., James, S. R., Downes, C. P., Holmes, A. B., Gaffney, P. R. J., Reese, C. B., & Cohen, P. (1997) · Current Biology · doi:10.1016/s0960-9822(06)00122-9 · Cited by 2,874
Negative regulation of PKB/Akt-dependent cell survival by the tumor suppressor PTEN
Stambolic, V., Suzuki, A., de la Pompa, J. L., Brothers, G. M., Mirtsos, C., Sasaki, T., Ruland, J., Penninger, J. M., Siderovski, D. P., & Mak, T. W. (1998) · Cell · doi:10.1016/s0092-8674(00)81780-8 · Cited by 2,551
Self-citationPI3K: Downstream AKTion Blocks Apoptosis
Franke, T. F., Kaplan, D. R., & Cantley, L. C. (1997) · Cell · doi:10.1016/s0092-8674(00)81883-8 · Cited by 1,665
Mechanisms and consequences of activation of protein kinase B/Akt
Downward, J. (1998) · Current Opinion in Cell Biology · doi:10.1016/s0955-0674(98)80149-x · Cited by 1,304
The lipid phosphatase activity of PTEN is critical for its tumor supressor function
Myers, M. P., Pass, I., Batty, I. H., KAAY, J. V. D., Stolarov, J. P., Hemmings, B. A., Wigler, M. H., Downes, C. P., & Tonks, N. K. (1998) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.95.23.13513 · Cited by 1,161
Delcommenne, M., Tan, C., Gray, V., Rue, L., Woodgett, J. R., & Dedhar, S. (1998) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.95.19.11211 · Cited by 1,102
Rozakis-Adcock, M., McGlade, J. C., Mbamalu, G., Pelicci, G., Daly, R. J., Li, W., Batzer, A., Thomas, S. Μ., Brugge, J. S., Pelicci, P. G., et al. (1992) · Nature · doi:10.1038/360689a0 · Cited by 973
Ono, M., Bolland, S. M., Tempst, P., & Ravetch, J. V. (1996) · Nature · doi:10.1038/383263a0 · Cited by 773
RAFF, M. C. (1998) · Nature · doi:10.1038/24055 · Cited by 690
Cited by
Sorted by citations
The phosphatidylinositol 3-Kinase–AKT pathway in human cancer
Vivanco, I., & Sawyers, C. L. (2002) · Nature reviews. Cancer · doi:10.1038/nrc839 · Cited by 6,155
Cellular survival: a play in three Akts
Datta, S. R., Brunet, A., & Greenberg, M. E. (1999) · Genes & Development · doi:10.1101/gad.13.22.2905 · Cited by 4,216
Ravetch, J. V., & Bolland, S. M. (2001) · Annual Review of Immunology · doi:10.1146/annurev.immunol.19.1.275 · Cited by 1,687
Phosphoinositides: Tiny Lipids With Giant Impact on Cell Regulation
Balla, T. (2013) · Physiological Reviews · doi:10.1152/physrev.00028.2012 · Cited by 1,638
The protein kinase B/Akt signalling pathway in human malignancy
Nicholson, K. M., & Anderson, N. G. (2002) · Cellular Signalling · doi:10.1016/s0898-6568(01)00271-6 · Cited by 1,665
Metadata
- Authors
- Liu, Q., Sasaki, T., Kozieradzki, I., Wakeham, A., Itie, A., Dumont, D. J., & Penninger, J. M.
- Affiliations
- University of Toronto (CA)
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 1999-04-01
- Volume
- 13
- Issue
- 7
- Pages
- 786-791
- ISSN
- 0890-9369 (ISSN-L)
- PMC
- PMC316591
- OpenAlex
- W2151313755
- Cited by
- 341
- References
- 31
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 7 · 2023: 12 · 2022: 5 · 2021: 4 · 2020: 5 · 2019: 3 · 2018: 10 · 2017: 8 · 2016: 9 · 2015: 7 · 2014: 10 · 2013: 14 · 2012: 17
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Genes & Development (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Tyrosine Phosphatases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Keywords
- ships, inositol polyphosphate 5-phosphatase, phosphatidylinositol 3-kinase, phosphatidylinositol 3,4,5-trisphosphate, Akt signaling, apoptosis, GM-CSF receptor, growth factor withdrawal, myeloid hyperplasia, splenomegaly, mast cells, neutrophils
- MeSH terms
- Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases, Animals, Anisomycin, Bone Marrow, Cell Line, Cell Survival, Cycloheximide, Enzyme Activation, Interleukin-3, Mice, Inbred C57BL, Neutrophils, Phosphoric Monoester Hydrolases, Precipitin Tests, Proto-Oncogene Proteins, Sorbitol, Spleen, Time Factors, Blotting, Southern, Blotting, Western, Down-Regulation, Apoptosis, Protein Serine-Threonine Kinases, Mice, Knockout, Proto-Oncogene Proteins c-akt, Mice
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