Allison L. Brill on Muck Rack

Allison L. Brill

Cambridge
As seen in: Nature, Science Magazine, Cell Reports, Diabetes Magazine
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Articles

BOK controls apoptosis by Ca2+ transfer through ER-mitochondrial contact sites

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By Robert Means, Allison L. Brill, Marcos A. Carpio, Alva Sainz
| Cell Reports Verified
Highlights • BOK interacts with the IP3Rs in mitochondria-associated membranes (MAMs) • BOK potentiates ER-mitochondrial contact sites and protein expression in MAMs • BOK regulates Ca2+ transfer from the ER to the mitochondria • The transfer of Ca2+ at MAMs by BOK is an apoptotic control point Summary Calcium transfer from the endoplasmic reticulum (ER) to mitochondria is a critical contributor to apoptosis.
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Glucagon stimulates gluconeogenesis by INSP3R1-mediated hepatic lipolysis

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By Mateus T Guerra, Allison L. Brill, Barbara E. Ehrlich, Gerald I. Shulman
| Nature Verified
Abstract Although it is well-established that reductions in the ratio of insulin to glucagon in the portal vein have a major role in the dysregulation of hepatic glucose metabolism in type-2 diabetes1,2,3, the mechanisms by which glucagon affects hepatic glucose production and mitochondrial oxidation are poorly understood.
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Polycystin 2 regulates mitochondrial Ca2+ signaling, bioenergetics, and dynamics through mitofusin 2

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By Ivana Y. Kuo, Allison L. Brill, Jason Jiang, Fernanda O. Lemos
| Science Magazine Verified
Patients with loss-of-function mutations in polycystin (PC) 1 or 2 develop fluid-filled cysts due to excessive proliferation of kidney epithelial cells. Kuo et al. found that loss of the ER cation channel PC2 led to increased abundance of the mitochondrial fusion factor MFN2 and enhanced tethering of mitochondria to the ER.
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