Wntcatenin

Wntcatenin refers informally to the canonical Wnt signaling pathway centered on the stabilization and transcriptional activity of β-catenin. The preferred term is Wnt/β-catenin signaling, which transduces extracellular Wnt cues into gene expression changes inside the nucleus.

Under resting conditions, β-catenin is phosphorylated by a destruction complex composed of APC, Axin, GSK-3β, and CK1, leading to ubiquitin-dependent degradation and repression of target genes. When Wnt ligands bind to Frizzled receptors and LRP5/6 co-receptors, Dishevelled is activated and inhibits the destruction complex. As a result, β-catenin accumulates in the cytoplasm and translocates to the nucleus, where it associates with TCF/LEF transcription factors to activate genes such as c-Myc, cyclin D1, and Axin2.

The pathway regulates cell fate, proliferation, and differentiation during development and in adult tissues. It plays key roles in the intestine, skin, and bone, and in maintaining stem cell populations and tissue renewal. Aberrant activation can alter cell behavior and tissue homeostasis.

Dysregulation of Wnt/β-catenin signaling is linked to disease, most notably cancer. Mutations in APC or β-catenin, or overproduction of Wnt ligands, can drive oncogenesis. Therapeutic approaches include targeting ligand secretion with porcupine inhibitors or promoting β-catenin destruction by stabilizing Axin through tankyrase inhibitors; however, broad inhibition risks affecting normal tissue function.

Terminology: The term Wntcatenin is not standard; it may appear in informal contexts. In scientific writing, canonical Wnt signaling or Wnt/β-catenin signaling is preferred to distinguish it from non-canonical Wnt pathways, which do not rely on β-catenin stabilization and mediate calcium or planar cell polarity signals.

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