PTEN controls β-cell regeneration in aged mice by regulating cell cycle inhibitor p16ink4a
Article first published online: 6 AUG 2013
© 2013 the Anatomical Society and John Wiley & Sons Ltd
Volume 12, Issue 6, pages 1000–1011, December 2013
How to Cite
Zeng, N., Yang, K.-T., Bayan, J.-A., He, L., Aggarwal, R., Stiles, J. W., Hou, X., Medina, V., Abad, D., Palian, B. M., Al-Abdullah, I., Kandeel, F., Johnson, D. L. and Stiles, B. L. (2013), PTEN controls β-cell regeneration in aged mice by regulating cell cycle inhibitor p16ink4a. Aging Cell, 12: 1000–1011. doi: 10.1111/acel.12132
- Issue published online: 21 NOV 2013
- Article first published online: 6 AUG 2013
- Accepted manuscript online: 4 JUL 2013 05:50AM EST
- Manuscript Accepted: 17 JUN 2013
- Zumberg Individual Award. Grant Numbers: NIDDK R21 DK075928-02, R01 DK084241-01A1
- USC CBM training fellowship
Fig. S1 PTEN loss leads to increased β-cell size.
Fig. S2 PTEN controls increases islet mass and β-cell mitotic activity in adult.
Fig. S3 High dose STZ treatment induces beta cell apoptosis in Pten null islets.
Fig. S4 PTEN loss leads to upregulation of cyclin D1 and downregulation of p16 expression.
Fig. S5 Increased p16 but not p53 signaling in aged β-cells.
Fig. S6 Loss of p16ink4a leads to increased proliferation in b-cells from old mice.
Fig. S7 PTEN loss allows cells to escape cell cycle arrest after cell division.
Fig. S8 Inducing Pten deletion in vivo leads to downregulation of p16 and increased proliferation in β-cells.
Fig. S9 Protein levels of Ezh2, Bmi-1 and p16 in mEFs where Ezh2 and Bmi-1 are downregulated.
Table S1 Primers used for qPCR analysis for mouse genes.
Table S2 Primers used for qPCR analysis of human genes.
Table S3 Primers used for Chip assay.
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