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- Bb7599ffb72de333bd957e62628eefa15 NCIT_P378 "KEGG" @default.
- Bb7599ffb72de333bd957e62628eefa15 type Axiom @default.
- Bb7599ffb72de333bd957e62628eefa15 annotatedProperty NCIT_P325 @default.
- Bb7599ffb72de333bd957e62628eefa15 annotatedSource NCIT_C91513 @default.
- Bb7599ffb72de333bd957e62628eefa15 annotatedTarget "The development of basal cell carcinoma is associated with constitutive activation of sonic hedgehog signaling. Normally, ligand-dependent signaling by Hedgehog (Hh) homologs proceeds through binding to the Patched receptor. This binding relieves the Patched-mediated inhibition of signaling through the Smoothened (SMOH) gene product. This signaling ultimately results in the dissociation of the Gli1 transcription factor from an inhibitory complex in the cytoplasm, its subsequent translocation to the nucleus, and activation of target gene expression. The mutations in SMOH, PTCH1, and SHH in BCCs result in continuous activation of target genes. At a cellular level, sonic hedgehog signaling promotes cell proliferation. Mutations in TP53 are also found with high frequency (>50%) in sporadic BCC." @default.