Nature Medicine
11, 175 - 182 (2005)
Published online: 30 January 2005; | doi:10.1038/nm1187
Deletion of Cdkn1b ameliorates hyperglycemia by maintaining compensatory hyperinsulinemia in diabetic miceTohru Uchida, Takehiro Nakamura, Naoko Hashimoto, Tomokazu Matsuda, Ko Kotani, Hiroshi Sakaue, Yoshiaki Kido, Yoshitake Hayashi, Keiichi I Nakayama, Morris F White
& Masato KasugaSupplementary Fig. 1 (pdf 163K)
Expression of p21Cip1 in islets of Irs2-/- and Lepr-/- mice. Supplementary Fig. 2 (pdf 80K)
Detection of phosphorylated p27. Supplementary Fig. 3 (pdf 581K)
Decreased Pcna-positive  cells in RIP-p27 mice. Supplementary Fig. 4 (pdf 736K)
The effect of p27 deletion on apoptosis in the islets of Lepr-/- mice. Supplementary Fig. 5 (pdf 204K)
The effect of p27 on apoptosis in Min6 insulinoma cells. Supplementary Fig. 6 (pdf 674K)
Deletion of p27 increases Pcna-positive cells in Irs2-/- mice. Supplementary Fig. 7 (pdf 124K)
Igf-1 and leptin each induce Akt activation in Min6 cells. Supplementary Fig. 8 (pdf 34K)
p27 mRNA is not increased in the islets of diabetic mice. Supplementary Fig. 9 (pdf 123K)
Deletion of p27 does not affect insulin resistance in Irs2-/- mice Supplementary Fig. 10 (pdf 320K)
Abundance of p27 in various tissues of Lepr-/- or Lepr+/- mice.
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