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Society of
General physiologists

Cranefield Postdoc and Student Awards

In 2005, SGP instituted two new Paul F. Cranefield awards, one each to be given annually to a deserving postdoctoral fellow and a graduate student who are the first authors of manuscripts published in Journal of General Physiology. In truly exceptional cases, undergraduate students will be considered for a third award. Awardees will receive $1000 in addition to being featured on the Society's website.

To be considered for such an award, the candidate must have had a major role in the planning, execution, and analysis of the results - and contributed significantly to the writing. Candidates shall write a one-page summary of the work, emphasizing its overall significance and describing specifically his or her contributions to the research and writing, and email it to

2024 Cranefield Postdoc Awardee: Shuya Ishii, Ph.D.

Shuya Ishii
for “Myosin and tropomyosin–troponin complementarily regulate thermal activation of muscles”

J Gen Physiol (2023) 155 (12): e202313414

Through studies of muscle contractile regulation in the physiological temperature range, Ishii and colleagues show that the lower thermal activation of thin filaments is compensated by the higher thermal activity of myosin, and that the inverse relationship holds for thin filaments and myosin in cardiac muscle. The higher temperature dependence of skeletal vs cardiac muscle may enable fast skeletal muscle contraction as the body temperature increases with exercise while maintaining efficient cardiac contraction.

2024 Cranefield Student Awardee
: Teresa Crespo, Ph.D.

Teresa Crespo for A Cantú syndrome mutation produces dual effects on KATP channels by disrupting ankyrin B regulation”;

J Gen Physiol (2023) 155 (1): e202112995

Inhibition of the KATP channel complex by physiological ATP links cellular electrical activity and metabolism. Mutations relieving this block cause Cantù syndrome, with larger reliefs correlating with more severe disease phenotypes. Crespo and colleagues reveal that mutations can also impair surface protein expression and interactions with ankyrin B, thus identifying a novel partner of the KATP complex. These results explain why a mutation with a predicted severe phenotype causes a mild form of the disease.

(click here for past award winners)

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