Yishu He

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Activation induced cytidine deaminase (AID) is required for somatic hypermutation and immunoglobulin class switching in activated B cells. Because AID possesses no known target site specificity, there have been efforts to identify non-immunoglobulin AID targets. We show that AID acts promiscuously, generating widespread DNA double strand breaks (DSB),(More)
Signaling through RAS/MAP kinase pathway is central to biology. ERK has long been perceived as the only substrate for MEK. Here, we report that HSF1, the master regulator of the proteotoxic stress response, is a new MEK substrate. Beyond mediating cell-environment interactions, the MEK-HSF1 regulation impacts malignancy. In tumor cells, MEK blockade(More)
To cope with proteotoxic stress, cells attenuate protein synthesis. However, the precise mechanisms underlying this fundamental adaptation remain poorly defined. Here we report that mTORC1 acts as an immediate cellular sensor of proteotoxic stress. Surprisingly, the multifaceted stress-responsive kinase JNK constitutively associates with mTORC1 under normal(More)
his constant encouragement and the opportunity to work on this research project. His innovative ideas and encouragement have made this work interesting and challenging. I would also like to thank Dr, Randy Chow and Dr. Jih-Kwon Peir for agreeing to serve on my committee. I thank my parents for their inspiration and support throughout my academic career. I(More)
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