ArticleGenesis (New York, N.Y. : 2000)2010
Appl1 is dispensable for Akt signaling in vivo and mouse T-cell development.
Article in Genesis (New York, N.Y. : 2000), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- APPL1 Is a Prognostic Biomarker and Correlated with Treg Cell Infiltration via Oxygen-Consuming Metabolism in Renal Clear Cell Carcinoma.Oxidative medicine and cellular longevity · 2023Article
- Endosomes as Signaling Platforms for IL-6 Family Cytokine Receptors.Frontiers in cell and developmental biology · 2021Review
- Appl1 and Appl2 are Expendable for Mouse Development But Are Essential for HGF-Induced Akt Activation and Migration in Mouse Embryonic Fibroblasts.Journal of cellular physiology · 2016Article
- The Osteogenesis Effect and Underlying Mechanisms of Local Delivery of gAPN in Extraction Sockets of Beagle Dogs.International journal of molecular sciences · 2015Article
- Rab31 and APPL2 enhance FcγR-mediated phagocytosis through PI3K/Akt signaling in macrophages.Molecular biology of the cell · 2015Article
- APPL1 potentiates insulin sensitivity by facilitating the binding of IRS1/2 to the insulin receptor.Cell reports · 2014Article
- Reconstruction of an integrated genome-scale co-expression network reveals key modules involved in lung adenocarcinoma.PloS one · 2013Article
- Adaptor protein APPL1 couples synaptic NMDA receptor with neuronal prosurvival phosphatidylinositol 3-kinase/Akt pathway.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- APPL1 potentiates insulin secretion in pancreatic β cells by enhancing protein kinase Akt-dependent expression of SNARE proteins in mice.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Recruitment of OCRL and Inpp5B to phagosomes by Rab5 and APPL1 depletes phosphoinositides and attenuates Akt signaling.Molecular biology of the cell · 2012Article
- Hormonal regulation of hepatic glucose production in health and disease.Cell metabolism · 2011Review
- The adapter protein APPL1 links FSH receptor to inositol 1,4,5-trisphosphate production and is implicated in intracellular Ca(2+) mobilization.Endocrinology · 2011Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Appl1 (Adaptor protein containing pleckstrin homology [PH], phosphotyrosine binding [PTB], and Leucine zipper motifs) is an adaptor that participates in cell signaling by interacting with various signaling molecules including Akt, PI3-kinase (PI3K), Rab5, adiponectin receptor, and TrkA. By using RNA knockdown technology, Appl1 has been implicated in zebrafish development and murine glucose metabolism. To investigate the unambiguous role of Appl1 in vivo, we generated a knockout mouse in which exon1 of the Appl1 gene was disrupted using gene trap methodology. Homozygous Appl1 knockout mice with ubiquitous loss of Appl1 protein expression were viable, grossly normal, and born at expected Mendelian ratios. Moreover, activation of Akt and the downstream effecter Gsk3β was unaffected in vivo. We next performed glucose and insulin tolerance tests and found that glucose metabolism is normal in Appl1-null mice. We also tested the effect of Appl1 loss on Akt signaling in T cells, because we discovered that Appl1 strongly interacts with the p110β subunit of PI3K in T lymphocytes. However, such interaction was found to be dispensable for Akt signaling in thymic T cells and T-cell development. Moreover, Appl1 loss did not affect DNA synthesis in cultured thymocytes, although loss of Appl1 was associated with a slight increase in ConA-stimulated splenic T-cell viability/proliferation. Collectively, our findings indicate that Appl1 is dispensable for Akt signaling in vivo and T-cell differentiation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.