Skip to main content
. 2017 Jan 30;114(7):E1224–E1233. doi: 10.1073/pnas.1614893114

Fig. 7.

Fig. 7.

(A) Western blotting analysis and quantitative analysis of DYRK1A, Cyclin D1, and p21 levels in the hypothalamus of WT and Hap1-KO mouse hypothalami. (B) The relative levels of DYRK1A, Cyclin D1, and p21 on the Western blots. Actin was used as loading control. n = 3 per group. *P < 0.05. (C) A schematic of imbalanced Hap1–Dcaf7 and DYRK1A–Dcaf7 interactions in Hap1-KO mouse and DS hypothalamic neurons. (Left) In WT hypothalamic neurons, Dcaf7 binds both Hap1 and DYRK1A in the cytoplasm. The Hap1–Dcaf7 interaction may be critical for postnatal growth. (Center) In a Hap1-KO hypothalamic neuron, more Dcaf7 binds to DYRK1A, increasing the DYRK1A protein level. Absence of the Hap1–Dcaf7 complex may impair postnatal growth. (Right) In a DS hypothalamic neuron, an elevated level of DYRK1A leads to more Dcaf7 being bound to DYRK1A and less to Hap1, possibly resulting in delayed postnatal growth.