10108294001

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Cell-free expression and in meso crystallisation of an integral membrane kinase for structure determination.

Coilín Boland et al.

Cellular and molecular life sciences : CMLS, 71(24), 4895-4910 (2014-07-12)

Membrane proteins are key elements in cell physiology and drug targeting, but getting a high-resolution structure by crystallographic means is still enormously challenging. Novel strategies are in big demand to facilitate the structure determination process that will ultimately hasten the

Uremic metabolites impair skeletal muscle mitochondrial energetics through disruption of the electron transport system and matrix dehydrogenase activity.

Trace Thome et al.

American journal of physiology. Cell physiology, 317(4), C701-C713 (2019-07-11)

Chronic kidney disease (CKD) leads to increased skeletal muscle fatigue, weakness, and atrophy. Previous work has implicated mitochondria within the skeletal muscle as a mediator of muscle dysfunction in CKD; however, the mechanisms underlying mitochondrial dysfunction in CKD are not

Synthesis of phosphoenol pyruvate (PEP) analogues and evaluation as inhibitors of PEP-utilizing enzymes.

Garcia A, et al.

FEBS Journal, 269(13), 3226-3236 (2002)

Improving cell-free glycoprotein synthesis by characterizing and enriching native membrane vesicles.

Jasmine M Hershewe et al.

Nature communications, 12(1), 2363-2363 (2021-04-24)

Cell-free gene expression (CFE) systems from crude cellular extracts have attracted much attention for biomanufacturing and synthetic biology. However, activating membrane-dependent functionality of cell-derived vesicles in bacterial CFE systems has been limited. Here, we address this limitation by characterizing native

Gαo is a major determinant of cAMP signaling in the pathophysiology of movement disorders.

Brian S Muntean et al.

Cell reports, 34(5), 108718-108718 (2021-02-04)

The G protein alpha subunit o (Gαo) is one of the most abundant proteins in the nervous system, and pathogenic mutations in its gene (GNAO1) cause movement disorder. However, the function of Gαo is ill defined mechanistically. Here, we show

Misrouting of v-ATPase subunit V0a1 dysregulates lysosomal acidification in a neurodegenerative lysosomal storage disease model.

Maria B Bagh et al.

Nature communications, 8, 14612-14612 (2017-03-08)

Defective lysosomal acidification contributes to virtually all lysosomal storage disorders (LSDs) and to common neurodegenerative diseases like Alzheimer's and Parkinson's. Despite its fundamental importance, the mechanism(s) underlying this defect remains unclear. The v-ATPase, a multisubunit protein complex composed of cytosolic

Glutathione participates in the modulation of starvation-induced autophagy in carcinoma cells.

Desideri E

Autophagy, 8(12), 1769-1781 (2012)

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