A study led by Dr. Hyun Kyoung Lee, associate professor at Baylor College of Medicine and investigator at the Jan and Dan Duncan Neurological Research Institute at Texas Children's Hospital, has discovered a new biological mechanism to regenerate and repair myelin, a protective sheath that insulates neuronal fibers and plays a vital role in ensuring rapid and accurate neurotransmission.
Colorectal cancer is the fourth most common and second deadliest cancer. How colorectal cancer develops is not well understood, but a team led by researchers at Baylor College of Medicine reports in the Journal of Experimental & Clinical Cancer Research that silencing the gene p16, even though the DNA itself does not change, can drive colorectal cancer progression in animal models.
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SETD2 is a protein well known as a chromatin remodeler, one that helps turn genes on or off by modifying histone proteins in the nucleus of the cell. When researchers discovered that SETD2 is mutated or lost in several cancer types, most commonly a type of kidney cancer called clear-cell renal cell carcinoma, all eyes turned toward SETD2 function in the nucleus of the cell to explain these cancers.
In 2016, the lab of Dr. Cheryl Walker, director of the Center for Precision Environmental Health at Baylor College of Medicine, made the unexpected discovery that SETD2 not only remodels chromosomes in the nucleus, but also microtubules of the cytoskeleton outside the nucleus. The cytoskeleton is a dynamic network of interlinking protein thread-like structures, including filaments and microtubules that extend throughout the cell. It gives a cell its shape and internal organization and provides mechanical support that enables cells to carry out essential functions like division