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Table 1 Summary of mutations targeting cyclin D1 phosphorylation or ligase function

From: Speeding through cell cycle roadblocks: Nuclear cyclin D1-dependent kinase and neoplastic transformation

Target Mutation Consequence Tumor Type Reference
Cyclin D1 T286R Constitutively Nuclear Esophageal [18]
Cyclin D1 Δ266–295 Constitutively Nuclear Esophageal [18]
Cyclin D1 P287A Constitutively Nuclear Tumor-derived esophageal carcinoma cell lines TE3, TE7, and TE12 [18]
Cyclin D1 P287S/T Constitutively Nuclear Endometrial [17]
Cyclin D1 Δ289–292 Constitutively Nuclear Endometrial [17]
αB crystallin Chromosome 11 deletion Impaired ligase activity Tumor-derived breast cancer cell lines (MCF-7, MDA-MB 231) [14]
Fbx4 S8R Impaired ligase activity Esophageal [26]
Fbx4 S12L Disrupts phosphorylation Esophageal [26]
Fbx4 P13S Disrupts phosphorylation Esophageal [26]
Fbx4 L23Q Dimerization-deficient Esophageal [26]
Fbx4 P76T Impaired Skp1 binding Esophageal [26]
  1. Mutations disrupting GSK3β-dependent cyclin D1 phosphorylation and nuclear export include mutation of Thr-286, Pro-287, and deletion of residues corresponding to the CRM1 binding site. Mutations targeting the SCFFbx4-αB crystallin E3 ubiquitin ligase result in impaired ligase activity and subsequent cyclin D1/CDK4 accumulation in the nucleus.