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#GSK-3

3 public questions tagged with this topic.

Sea urchin -lll

Blocking GSK-3 in sea urchin embryos leads to:

GSK-three normally phosphorylates beta-catenin within destruction complex containing Axin and APC, marking it for degradation by beta-TrCP ubiquitin ligase and proteasome. Vegetal Dishevelled inhibits GSK-three locally, allowing beta-catenin accumulation in micromeres and macromeres vegetally. Chemical inhibition of GSK-three with lithium chloride or genetic dominant negative constructs eliminates degradation globally in all blastomeres. Consequently beta-catenin accumulates in all nuclei including animal pole cells that normally remain ectodermal. Animal blastomeres then ectopically activate endoderm genes like Endo16 and mesenchyme genes Msp130. Result is severe vegetalization with expanded gut and excess skeleton production.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 10: GSK-3 block causes beta-catenin accumulation all nuclei vegetalization.

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amphibian -ll

GSK-3 normally functions by:

In resting cells GSK-3 beta resides in destruction complex with scaffold Axin and tumor suppressor APC, phosphorylating N-terminal residues Ser33, Ser37, Thr41 of beta-catenin. Phosphorylated beta-catenin recognized by beta-TrCP E3 ubiquitin ligase leading to ubiquitination and proteasomal degradation, keeping cytoplasmic levels low. Wnt signaling displaces complex via Dishevelled and GBP inhibiting GSK-3, preventing phosphorylation. Thus GSK-3 normally functions by degrading beta-catenin ventrally. Dorsal Wnt11 signaling inhibits GSK-3 allowing beta-catenin accumulation, nuclear translocation and organizer gene activation, fundamental regulatory mechanism of dorsal axis specification.

Ref: NCBI Bookshelf, Molecular Biology of the Cell, Chapter 19: GSK-3 function - beta-catenin degradation in Wnt pathway.

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Cell Signaling ELR Pathways - I

GSK-3 negatively regulates:

Glycogen synthase, is consistent with established principles of cell signaling, receptor pharmacology and cellular regulation. Experimental measurements of binding parameters, genetic loss-of-function studies and pharmacological interventions all converge on the same interpretation. Related options address neighboring concepts but do not satisfy the precise criterion stated in the question.

Ref: NCERT Biology Class 11–12 Alberts et al Molecular Biology of the Cell Lodish et al, Molecular Cell Biology Cooper & Hausman, The Cell Abbas et al., Cellular and Molecular Immunology (for immunology sections)

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