S. Tam

Germline deletion of AMP‐activated protein kinase β subunits reduces bone mass without altering osteoclast differentiation or function

B. Kemp, I. J. Poulton, N. Sims, 2010, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

The Outcome of Renal Ischemia-Reperfusion Injury Is Unchanged in AMPK-β1 Deficient Mice

D. Power, G. Fingerle-Rowson, R. Bucala, 2012, PloS one.

Inhibition of Adenosine Monophosphate–Activated Protein Kinase–3‐Hydroxy‐3‐Methylglutaryl Coenzyme A Reductase Signaling Leads to Hypercholesterolemia and Promotes Hepatic Steatosis and Insulin Resistance

P. Meikle, B. Kemp, G. Steinberg, 2018, Hepatology communications.

Use of Click Chemistry to Define the Substrate Specificity of Leishmania β‐1,2‐Mannosyltransferases

Spencer J. Williams, M. McConville, Phillip L van der Peet, 2006, Chembiochem : a European journal of chemical biology.

AMPK Is a Direct Adenylate Charge-Regulated Protein Kinase

B. Kemp, Zhi-ping Chen, Naomi X. Y. Ling, 2011, Science.

Mice lacking AMP-activated kinase (AMPK) subunits β1 or β2 have low bone mass, while AICAR acts AMPK-independently to increase osteoclast formation

B. Kemp, N. Sims, M. Gillespie, 2009 .

AMPK Is a Direct Adenylate Charge-Regulated Protein Kinase

B. Kemp, Zhi-ping Chen, Naomi X. Y. Ling, 2011, Science.