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The investigators carried out animal trials with the engineered AsCas12f system, partnering it with other genes and administering it to live mice. The encouraging results indicated that engineered AsCas12f has the potential to be used for human gene therapies, such as treating hemophilia.
The team discovered numerous potentially effective combinations for engineering an improved AsCas12f gene-editing system, and acknowledged the possibility that the selected mutations may not have been the most optimal of all the available mixes. As a next step, computational modeling or machine learning could be used to sift through the combinations and predict which might offer even better improvements.
And as the authors noted, by applying the same approach to other Cas enzymes, it may be possible to generate efficient genome-editing enzymes capable of targeting a wide range of genes. “The compact size of AsCas12f offers an attractive feature for AAV-deliverable gRNA and partner genes, such as base editors and epigenome modifiers. Therefore, our newly engineered AsCas12f systems could be a promising genome-editing platform … Moreover, with suitable adaptations to the evaluation system, this approach can be applied to enzymes beyond the scope of genome editing.”
Venture Investing To Catalyze The Next Generation Of Founder-Led, Longevity Biotech Companies — Dr. Alex Colville, Ph.D., Co-Founder and General Partner — age1.
Dr. Alex Colville, Ph.D. is Co-Founder and General Partner of age1 (https://age1.com/), a venture capital firm focused on catalyzing the next generation of founder-led, longevity biotech companies, with a strategy of building a community of visionaries advancing new therapeutics, tools, and technologies targeting aging and age-related diseases.
With a recent initial closing of US$35 million, age1 will be focusing on founders and companies at the earliest stages of first-money in, pre-seed and seed funding, and is resourced to continue to support companies through later rounds.
Dr. Colville previously established the biotech arm of Starbloom Capital and served as founding Chief of Staff of Amaranth Foundation, where he led: the foundation’s support of skilled researchers and ambitious moonshot projects in the longevity field, and helped to advance their lobbying efforts; the TIME Initiative (a group with mission to activate undergraduate students’ interest in aging biology); the Marine Biology Laboratory Biology of Aging Summer Course, among other programs.
Dr. Colville completed his Ph.D. in Genetics at Stanford University studying the biology of aging in Dr. Thomas Rando’s lab while consulting for several family offices, the R&D team of Rubedo Life Sciences, and the business development team of Maze Therapeutics. Prior to his Ph.D., while at Northeastern University completing his Bachelor of Science (B.S.) in Chemical Engineering with a Minor in Biochemical Engineering, he advised pharma companies as a management consultant at Putnam Associates, a boutique life sciences consulting firm.
Professor René Ketting’s team at the Institute of Molecular Biology (IMB) in Mainz, Germany, along with Dr. Sebastian Falk’s group at the Max Perutz Labs in Vienna, Austria, have discovered a new enzyme, PUCH, which plays a key role in preventing the spread of parasitic DNA
DNA, or deoxyribonucleic acid, is a molecule composed of two long strands of nucleotides that coil around each other to form a double helix. It is the hereditary material in humans and almost all other organisms that carries genetic instructions for development, functioning, growth, and reproduction. Nearly every cell in a person’s body has the same DNA. Most DNA is located in the cell nucleus (where it is called nuclear DNA), but a small amount of DNA can also be found in the mitochondria (where it is called mitochondrial DNA or mtDNA).
George Church at his most optimistic. June 1, 2022.
Dr George Church talks about combination therapies for age reversal, recently published papers from his lab and expresses his wish on developing inexpensive gene therapies like vaccine that can be equitably distributed to human.
Dr George Church is the Robert Winthrop Professor of Genetics at Harvard Medical School, a Professor of Health Sciences and Technology at Harvard and the Massachusetts Institute of Technology (MIT), and a core faculty member of the Wyss Institute.
Same as Dr David Sinclair, Dr George Church currently runs the Church Lab at Harvard Medical School. Both labs collaborate many projects together especially on age reversal topics. Dr Church also directs the Personal Genome Project, a long-term cohort study that allows scientists to connect human genetic information (human DNA sequence, gene expression, associated microbial sequence data, and more) with human trait information (medical information, biospecimens, and physical traits) and environmental exposures.
DISCLAIMER: Please note that none of the information in this video constitutes health advice or should be substituted in lieu of professional guidance. The video content is purely for informational purposes.
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A new compound called d16 that reduces tumor growth and overcomes treatment resistance in mutant p53-bearing cancers has been developed by researchers at the Baylor College of Medicine. Their findings testing the compound, published in the journal Cancer Research Communications, suggests the new compound could be used in combination therapies to provide more effective treatment against these kinds of cancer.
“One of the most common alterations in many human cancers are mutations in p53, a gene that normally provides one of the most powerful shields against tumor growth,” says Helena Folly-Kossi, PhD, a postdoctoral associate in Weei-Chin Lin’s lab at Baylor and the study’s first author. “Mutations that alter the normal function of p53 can promote tumor growth, cancer progression and resistance to therapy, which are associated with poor prognosis. It is important to understand how p53 mutations help cancer grow to develop therapies to counteract their effects.”
According to Lin, finding ways to target p53 mutations directly as a form of therapy for cancer has been difficult. His lab has been working for many years to not interfere directly with p53, but rather to identify vulnerabilities in the cells carrying p53 mutations that they could target to prevent cancer growth. “One of the challenges has been to develop drugs that act on mutant p53 directly. Some of these drugs are under development, but they appear to be toxic,” he said.