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Baylor College of Medicine


Research improves understanding of mechanism of atrial fibrillation

Researchers at Baylor College of Medicine have discovered a functional link between noncoding DNA regions called Pitx2 enhancers and the expression of the Pitx2 gene in relation to atrial fibrillation. This interaction prevents predisposition to the condition by looping and folding distant Pitx2 enhancers to make contact with the gene.

SourceBaylor College of Medicine·JournalProceedings of the National Academy of Sciences·DateOct 21, 2019

New insights into the healing capacity of the heart

Researchers at Baylor College of Medicine discovered that inactivating the Hippo pathway in cardiac fibroblasts promotes cardiac fibrosis and adversely affects cardiac function. This finding highlights the need for specific targeting of the Hippo pathway in cardiac muscle cells for safe and effective heart failure therapy.

SourceBaylor College of Medicine·JournalGenes & Development·DateSep 25, 2019

What's at the 'heart' of a heartbeat?

Atrial fibrillation is a major concern due to its association with serious complications like heart failure and stroke. Researchers have identified a new piece of the puzzle that has changed the field's understanding of the molecular mechanisms leading to atrial fibrillation, involving a phosphatase regulatory subunit known as PPP1R3A.

SourceBaylor College of Medicine·JournalCirculation·DateAug 20, 2019

New insights into how the brain works

Researchers at Baylor College of Medicine discovered that removing inhibitory interneurons' ability to regulate excitatory neurons dramatically changed odor responses. The study highlights the need for better understanding cell type relationships in brain function.

SourceBaylor College of Medicine·JournalNature Communications·DateJul 29, 2019

SHANK3: the good, the bad and the hopeful

A deficiency in the SHANK3 protein, which regulates synaptic communication between brain cells, is associated with various neurological conditions. Researchers have identified kinases that can regulate SHANK3 stability, offering hope for developing treatments by increasing its abundance.

SourceBaylor College of Medicine·JournalMolecular Psychiatry·DateMar 7, 2019