ArticleProceedings of the National Academy of Sciences of the United States of America2015
Ubl4A is required for insulin-induced Akt plasma membrane translocation through promotion of Arp2/3-dependent actin branching.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed, 43 citations in OpenAlex.
- Impact of Prematurity on Nutrient Signaling and Protein Synthesis in Skeletal Muscle.Annual review of nutrition · 2026Review
- Structural and mechanistic basis of mTORC2 activation of protein kinase AKT/PKB.The Biochemical journal · 2026Review
- mAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Preterm birth alters the feeding-induced activation of Akt signaling in the muscle of neonatal piglets.Pediatric research · 2023Article
- Molecular mechanisms underlying the promotion of wound repair by coenzyme Q10: PI3K/Akt signal activation via alterations to cell membrane domains.Journal of clinical biochemistry and nutrition · 2022Article
- The Molecular Biodiversity of Protein Targeting and Protein Transport Related to the Endoplasmic Reticulum.International journal of molecular sciences · 2021Review
- HIV-1 Tat and Heparan Sulfate Proteoglycans Orchestrate the Setup ofMolecules (Basel, Switzerland) · 2021Article
- Pharmacological Manipulation of Translation as a Therapeutic Target for Chronic Pain.Pharmacological reviews · 2021Review
- Ubl4A is critical for mitochondrial fusion process under nutrient deprivation stress.PloS one · 2020Article
- UBL4A inhibits autophagy-mediated proliferation and metastasis of pancreatic ductal adenocarcinoma via targeting LAMP1.Journal of experimental & clinical cancer research : CR · 2019Article
- The Ways of Tails: the GET Pathway and more.The protein journal · 2019Review
- Crosstalk in transition: the translocation of Akt.Journal of mathematical biology · 2019Article
- Akt-ing Up Just About Everywhere: Compartment-Specific Akt Activation and Function in Receptor Tyrosine Kinase Signaling.Frontiers in cell and developmental biology · 2019Review
- Absence of GdX/UBL4A Protects against Inflammatory Diseases by Regulating NF-кB Signaling in Macrophages and Dendritic Cells.Theranostics · 2019Article
- The roles of cytosolic quality control proteins, SGTA and the BAG6 complex, in disease.Advances in protein chemistry and structural biology · 2019Review
- The C-terminus of Ubl4A is critical for pro-death activity and association with the Arp2/3 complex.Biochemical and biophysical research communications · 2018Article
- GRAMD1B regulates cell migration in breast cancer cells through JAK/STAT and Akt signaling.Scientific reports · 2018Article
- Inositol Pyrophosphate Synthesis by Diphosphoinositol Pentakisphosphate Kinase-1 is Regulated by Phosphatidylinositol(4,5)bisphosphate.Bioscience reports · 2018Article
- Targeted AKT Inhibition in Prostate Cancer Cells and Spheroids Reduces Aerobic Glycolysis and Generation of Hyperpolarized [1-Molecular cancer research : MCR · 2018Article
- Prolactin Signaling Stimulates Invasion via Na(+)/H(+) Exchanger NHE1 in T47D Human Breast Cancer Cells.Molecular endocrinology (Baltimore, Md.) · 2016Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
The serine-threonine kinase Akt is a key regulator of cell proliferation and survival, glucose metabolism, cell mobility, and tumorigenesis. Activation of Akt by extracellular stimuli such as insulin centers on the interaction of Akt with PIP3 on the plasma membrane, where it is subsequently phosphorylated and activated by upstream protein kinases. However, it is not known how Akt is recruited to the plasma membrane upon stimulation. Here we report that ubiquitin-like protein 4A (Ubl4A) plays a crucial role in insulin-induced Akt plasma membrane translocation. Ubl4A knockout newborn mice have defective Akt-dependent glycogen synthesis and increased neonatal mortality. Loss of Ubl4A results in the impairment of insulin-induced Akt translocation to the plasma membrane and activation. Akt binds actin-filaments and colocalizes with actin-related protein 2 and 3 (Arp2/3) complex in the membrane ruffles and lamellipodia. Ubl4A directly interacts with Arp2/3 to accelerate actin branching and networking, allowing Akt to be in close proximity to the plasma membrane for activation upon insulin stimulation. Our finding reveals a new mechanism by which Akt is recruited to the plasma membrane for activation, thereby providing a missing link in Akt signaling.
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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.