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. 2014 Apr 11;42(9):5765–5775. doi: 10.1093/nar/gku225

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© The Author(s) 2014. Published by Oxford University Press on behalf of Nucleic Acids Research.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 3. — UBE3A interacts with BMAL1 both in the presence and absence of E6/E7. (A) Co-IP of HA-UBE3A and V5-BMAL1 in HEK 293T cells. IP was performed using an anti-HA antibody and precipitated V5-BMAL1 or HA-UBE3A was detected by IB using an anti-V5 or anti-HA antibody (top and middle panels). (B) V5 Co-IP showing that V5-BMAL1 could pull down Myc-UBE3A. MG132 (5 μM) was applied in all cases. (C) Co-IP of V5-BMAL1 and myc-UBE3A in HEK 293T cells in the presence or absence of MG132. IP was performed using an anti-V5 antibody and precipitated myc-UBE3A or V5-BMAL1 was detected by IB (top two panels). (D) Endogenous Co-IP between UBE3A and BMAL1 in SW1353 human chondrocytes in the presence of MG132. IP was performed using an anti-UBE3A antibody and the precipitated BMAL1 was detected by IB (top two panels).