Novel splice isoforms of STRADα differentially affect LKB1 activity, complex assembly and subcellular localization.
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Summary
The discovery of several novel splice isoforms of STRADα that differentially affect the kinase activity, complex assembly, subcellular localization of L KB1 and the activation of the LKB1-dependent AMPK pathway are reported.
- Type
- article
- Published
- 2007-10-01
- Cited by
- 20
- References
- 29
- Access
- Open access
- OpenAlex
- https://openalex.org/W1964497584
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:20065914
Keywords
Scaffold protein, Heterotrimeric G protein, HEK 293 cells, Cell biology, Biology
References
- A serine/threonine kinase gene defective in Peutz–Jeghers syndrome
- Epithelial polarity, villin expression, and enterocytic differentiation of cultured human colon carcinoma cells: a survey of twenty cell lines.
- STK11 mutations in Peutz-Jeghers syndrome and sporadic colon cancer.
- Evidence that translation reinitiation leads to a partially functional Menkes protein containing two copper-binding sites.
- MO25alpha/beta interact with STRADalpha/beta enhancing their ability to bind, activate and localize LKB1 in the cytoplasm.
- Vav2 is required for cell spreading
- Emerging roles of pseudokinases.
- LKB1, a protein kinase regulating cell proliferation and polarity
- LKB1 Associates with Brg1 and Is Necessary for Brg1-induced Growth Arrest*
- Vascular Abnormalities and Deregulation of VEGF in Lkb1-Deficient Mice
- Peutz-Jeghers syndrome is caused by mutations in a novel serine threonine kinase.
- A novel cell type-specific role of p38α in the control of autophagy and cell death in colorectal cancer cells
- The position of premature termination codons in the hepatocyte nuclear factor −1 beta gene determines susceptibility to nonsense-mediated decay
- Butyrate-Induced Differentiation of Colon Cancer Cells Is PKC and JNK Dependent
- Mutation analysis of three genes encoding novel LKB1-interacting proteins, BRG1, STRADα, and MO25α, in Peutz–Jeghers syndrome
- Analysis of the LKB1-STRAD-MO25 complex
- Complete polarization of single intestinal epithelial cells upon activation of LKB1 by STRAD.
- LKB1 catalytically deficient mutants enhance cyclin D1 expression.
- Growth suppression by Lkb1 is mediated by a G(1) cell cycle arrest.
- The AMP-activated protein kinase pathway – new players upstream and downstream
Cited by
- Characterization of the LKB1-MO25-STRAD AMPKK Complex in Adult Mouse Skeletal Muscle
- LKB1: cancer, polarity, metabolism, and now fertility
- Characterization of an Alternative Splice Variant of LKB1*
- The role of pseudokinases in cancer.
- Characterization of the liver kinase B1-mouse protein-25 -Ste-20-related adaptor protein complex in adult mouse skeletal muscle.
- Omega-3 polyunsaturated fatty acid promotes the inhibition of glycolytic enzymes and mTOR signaling by regulating the tumor suppressor LKB1
- The LKB1-AMPK pathway: metabolism and growth control in tumor suppression
- LKB1 catalytic activity contributes to estrogen receptor alpha signaling.
- The LKB1 complex-AMPK pathway: the tree that hides the forest
- STRAD pseudokinases regulate axogenesis and LKB1 stability
- Identification of TGFβ signaling, p53, and actin stress fibers as targets of LKB1 tumor suppressor activity
- A 21-year-old female patient with Peutz-Jeghers syndrome.
- Hydrogen sulfide and autophagy: A double edged sword
- Targeting mTOR and Glycolysis in HER2-Positive Breast Cancer
- No Tumor Suppressor Role for LKB1 in Prostate Cancer
- The Tumor Suppressor Kinase LKB1: Metabolic Nexus
- Insights into targeting LKB1 in tumorigenesis
- 6-phosphogluconate dehydrogenase links oxidative PPP, lipogenesis and tumor growth by inhibiting LKB1-AMPK signaling
- Pseudokinases Regulate Axogenesis and LKB 1 Stability
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