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The CRISPR gene-editing system is a powerful tool that could revolutionize medicine and other sciences, but unfortunately it has a tendency to make edits to the wrong sections of DNA. Now, researchers at the University of Texas at Austin have identified a previously unknown structure of the protein that drives these mistakes, and tweaked it to reduce the likelihood of off-target mutations by 4,000 times.

CRISPR tools use certain proteins, most often Cas9, to make precise edits to specific DNA sequences in living cells. This can involve cutting out problematic genes, such as those that cause disease, and/or slotting in beneficial ones. The problem is that sometimes the tool can make changes to the wrong parts, potentially triggering a range of other health issues.

And in the new study, the UT researchers discovered how some of these errors can happen. Usually, the Cas9 protein is hunting for a specific sequence of 20 letters in the DNA code, but if it finds one where 18 out of 20 match its target, it might make its edit anyway. To find out why this occurs, the team used cryo-electron microscopy to observe what Cas9 is doing when it interacts with a mismatched sequence.

Circa 2012 o.o

For decades, the idea of a future where meals were condensed into tablets was so popular that it became cliché. So why are we not eating them now?

A research team led by scientists at Roswell Park Comprehensive Cancer Center has discovered a molecule that inhibits the growth and metastasis of pancreatic cancer cells through the iron metabolism pathway. Their findings, recently published in Molecular Cancer Therapeutics, pave the way toward the development of a new drug candidate for the treatment of pancreatic cancer.

The molecule, MMRi62, targets iron metabolism to kill cancer cells and the harmful proteins that encourage their growth and spread, suggesting that further development and refinement of this compound could lead to a new type of pancreatic cancer therapy.

“MMRi62 causes degradation of an iron-storage protein called FTH1, as well as a protein that is mutated in PDAC, resulting [in] inhibition of metastasis and ferroptosis, a form of cell death triggered by free cellular iron,” says Xinjiang Wang, Ph.D., Associate Professor in the Department of Pharmacology and Therapeutics at Roswell Park.

Tesla has gained approval to begin commercial production at its new factory near Berlin, local German officials announced Friday.

The conditional license for the vehicle and battery plants in Brandenburg was expected following months of delays. Tesla had intended to start production of vehicles by early summer of 2021 in Brandenburg, but the Covid pandemic, supply chain complications and clashes with environmentalists all slowed their pace.

The project, which was approved with the 536-page decision, includes the plant for the production of up to 500,000 vehicles per year, according to a translated release.

Have not heard from Dr West in awhile. Two things stood out in this technical hour: Telomerase in gene therapy has never been properly developed, and their iTR technology has not had animal trials as they wait for funding.

In this #webinar, Dr Michael West, a bioentrepreneur and CEO of AgeX Therapeutics, discussed the work of AgeX Therapeutics, their mission and plan to extend human health and longevity, and exciting new #technologies that could combat #ageing and unlock cellular immortality.

Continue reading “AgeX Therapeutics: Targeting Biological Ageing | Dr Michael D. West” »

Scientists from Roswell Park Comprehensive Cancer Center have shed light on a different way of overcoming mechanisms of resistance to specific therapeutic agents used to treat cancer. In a new article published March 1 in the journal Cell Reports, the researchers propose a new approach to cancer treatment based on the way different cancer cells divide.

A collaborative team led by Agnieszka Witkiewicz, MD, Professor of Oncology, and Erik Knudsen, Ph.D., Professor of Oncology and Chair of Molecular and Cellular Biology, from Roswell Park investigated over 500 cell lines from a multitude of cancer types, as well as preclinical tumor models. The researchers then analyzed cancer cells based on their dependency for CDK and CCN, two genes that drive the cell cycle and determine how often a cancer cell divides.

“We found that the way cancer cells divide is highly varied, and that diversity represents a tremendous challenge for some widely used cancer therapies because it often contributes to treatment resistance,” says Dr. Witkiewicz, the study’s senior author. “However, with a better understanding of these heterogenous features of cancer cell division, different therapies could be deployed in a more precise and effective fashion.”