Posts Tagged ‘suggest’

When Government is Not Enough for Research Funding

Two research executives from the University of Minnesota see there isn’t enough government funding to pay for all the innovative research that needs to be taking place. Might business take up the slack?

The post When Government is Not Enough for Research Funding appeared first on Social Science Space.

Fixing Peer Review, a Biologist’s View

Peer review clearly isn’t perfect, but rather than simply bypassing it and releasing even more information into an overloaded system, we should focus on making it better, says this life sciences editor. The first step is to reset and clearly state our standards for quality in both publishing and peer reviewing.

The post Fixing Peer Review, a Biologist’s View appeared first on Social Science Space.

Kids are ‘natural scientists’ with live fish in class

Raising live fish in class helps children and teens learn fundamentals of biology—and improves their attitudes about […]

The post Kids are ‘natural scientists’ with live fish in class appeared first on Futurity.

Control of mitochondrial function and cell growth by the atypical cadherin Fat1

Mitochondrial products such as ATP, reactive oxygen species, and aspartate are key regulators of cellular metabolism and growth. Abnormal mitochondrial function compromises integrated growth-related processes such as development and tissue repair, as well as homeostatic mechanisms that counteract ageing and neurodegeneration, cardiovascular disease, and cancer. Physiologic mechanisms that control mitochondrial activity in such settings remain incompletely understood. Here we show that the atypical Fat1 cadherin acts as a molecular ‘brake’ on mitochondrial respiration that regulates vascular smooth muscle cell (SMC) proliferation after arterial injury. Fragments of Fat1 accumulate in SMC mitochondria, and the Fat1 intracellular domain interacts with multiple mitochondrial proteins, including critical factors associated with the inner mitochondrial membrane. SMCs lacking Fat1 (Fat1KO) grow faster, consume more oxygen for ATP production, and contain more aspartate. Notably, expression in Fat1KO cells of a modified Fat1 intracellular domain that localizes exclusively to mitochondria largely normalizes oxygen consumption, and the growth advantage of these cells can be suppressed by inhibition of mitochondrial respiration, which suggest that a Fat1-mediated growth control mechanism is intrinsic to mitochondria. Consistent with this idea, Fat1 species associate with multiple respiratory complexes, and Fat1 deletion both increases the activity of complexes I and II and promotes the formation of complex-I-containing supercomplexes. In vivo, Fat1 is expressed in injured human and mouse arteries, and inactivation of SMC Fat1 in mice potentiates the response to vascular damage, with markedly increased medial hyperplasia and neointimal growth, and evidence of higher SMC mitochondrial respiration. These studies suggest that Fat1 controls mitochondrial activity to restrain cell growth during the reparative, proliferative state induced by vascular injury. Given recent reports linking Fat1 to cancer, abnormal kidney and muscle development, and neuropsychiatric disease, this Fat1 function may have importance in other settings of altered cell growth and metabolism.

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