Category Archives: Protein Folding

Googles DeepMind AI team solved a long-running biological problem

Scientists are not about to lose their jobs to more sophisticated artificial intelligence instead it will help them work even better, an expert in the field has said following a Google breakthrough.

Last week, the tech giants DeepMind AI specialists based in the UK made a leap forward in solving one of biologys biggest challenges, the five-decade-old protein folding problem.

Determining the structure of a protein opens up a world of possibilities, from understanding neurological diseases like Parkinsons, to discovering new drugs.

The problem is there are so many and it takes time to understand them all we have only managed to unfold a fraction of the millions of known proteins in living things.

But what does this mean for scientists going forward?

Like many jobs touched by technology, it does not mean their skills will no longer be needed, according to Dr Aldo Faisal, professor of AI and neuroscience at Imperial College London.

Instead it will cut down on mundane tasks, allow research to be carried out faster, and enable scientists to concentrate on more in-depth experiments.

I think what were going to see is that AI is going to empower scientists, its not about replacing scientists, its about empowering them to be able to do more and effectively taking away the boring parts of the work so to speak that are routine and mundane and allowing them to move quicker, discover things faster and I think thats one of the biggest appeals of AI, Dr Faisal told the PA news agency.

The protein folding and AlphaFold is beautiful because it shows that one can test hypotheses much, much quicker than with current conventional technologies about how protein folds and of course how protein folds tell us something about how they can function, interact and so this will basically save time and allow people to very quickly explore protein structures without having to do costly and slow great experiments.

Although AI has been used to revolutionise science for several years, Dr Faisal said we are seeing loads of other applications arrive and he expects more to come.

For example, earlier this year a group of scientists from Massachusetts Institute of Technology (MIT) used AI to help them uncover new types of powerful antibiotics, capable of killing some of the worlds most problematic disease-causing bacteria.

That was a very fortuitous discovery they made using AI and were seeing loads of other applications in understanding, basically, bringing together data about health care and environment and the context in which people live in relating that to the genes and the function of proteins inside their body, Dr Faisal continued.

Establishing these links, basically connecting healthcare data, connecting daily life data,

See the article here:
Will AI empower scientists or replace them? - Techerati

The Tech.eu Podcast is a show in which we discuss some of the most interesting stories from the European technology scene and interview leading entrepreneurs and investors from across the region.

This week, we talk about whats going on in European tech, including some of the biggest funding rounds of the week, new VC funds, science and research news, and much more. Weve also spoken to Sebastian Peck, managing director of InMotion Ventures.

You can find the latest episode embedded below. Subscribe today and dont miss new episodes:

And here are the notes and links for this weeks episode:

Voi, the European micromobility rental company, raises $160 million additional equity and debt funding

UK-based HungryPanda raises $70 million to expand its online Asian food delivery business worldwide

Monzo, the UK challenger bank, picks up additional 60 million in funding

UK edtech startup MEL Science snags $14 million Series B

SoftBank buys 10.1 percent stake in Sinch after its meteoric surge

This is where Target Global wants to invest its new 300+ million fund

Firstminute Capital launches second $111 million fund, featuring a whos-who of founders as LPs

The European Investment Bank Group debuts new 150 million financing instrument to support European AI tech firms

London AI lab claims breakthrough that could accelerate drug discovery

Interview with Sebastian Peck, managing director of InMotion Ventures, a firm backed by Jaguar Land Rover

We hope you enjoy(ed) the podcast! Please feel free to email us with any questions, suggestions, and opinions topodcast@tech.eu or tweet at us @tech_eu.

Image credit: National Cancer Institute on Unsplash

Link:
Tech.eu Podcast #198: Even more money for e-scooters, new VC funds, protein folding, and we talk to Sebastian Peck of InMotion Ventures - Tech.eu

Did you ever wonder where all that tech money came from all of a sudden? Turns out, a lot of it comes from online programmatic ads, an industry that gets little attention even from the companies, such as Google, that it made wealthy. That lack of attention is pretty ironic, because lack of attention is whats going to kill the industry, according to Tim Hwang, former Google policy maven and current research fellow at the Center for Security and Emerging Technology (CSET).

In our interview, Tim Hwang explains the remarkably complex industry and the dynamics that are gradually leaching the value out of its value proposition. Tim thinks were in an attention bubble, and the popping will be messy. Im persuaded the bubble is here but not that its end will be disastrous outside of Silicon Valley.

Sultan Meghji and I celebrate what seems like excellent news about a practical artificial intelligence (AI) achievement in predicting protein folding. Its a big deal, and an ideal problem for AI, with one exception. The parts of the problem that AI hasnt solved would be a lot easier for humans to work on if AI could tell us how it solved the parts it did figure out. Explainability, it turns out, is the key to collaborative AI-human work.

We welcome first time participant and long-time listener Jordan Schneider to the panel. Jordan is the host of the unmissable ChinaTalk podcast. Given his expertise, we naturally ask him about Australia. Actually, its natural, because Australia is now the testing ground for many of Chinas efforts to exercise power over independent countries using cyber power along with trade. Among the highlights: Chinese tweets highlighting a report about Australian war crimes followed by ham-handed tweet-boosting bot campaigns. And in a move that ought to be featured in future justifications of the Trump administrations ban on WeChat, the platform refused to carry the Australian prime ministers criticism of the war-crimes tweet.

Sen. Ted Cruz, call your office! And this will have to be Sen. Cruzs fight, because it looks more and more as though the Trump administration has thrown in the towel. Its claim that it is negotiating a TikTok sale after ordering divestment is getting thinner; now the divestment deadline has completely disappeared, as the government simply says that negotiations continue. Nick Weaver is on track to win his bet with me that CFIUS wont make good on its order before the mess is shoveled onto President-elect Joe Bidens plate.

Whoever was in charge of beating up WeChat and TikTok may have left the government early, but the team thats sticking pins in other Chinese companies is still hard at work. Jordan and Brian Egan talk about the addition of SMIC to the amorphous defense blacklist. And Congress has passed a law (awaiting the presidents signature) that will make life hard for Chinese firms listed on U.S. exchanges.

China, meanwhile, isnt taking this lying down, Jordan reports. It is mirror-imaging all the Western laws that it sees as targeting China, including bans on exports of Chinese products and technology. It is racing (on what Jordan thinks is a twenty-year pace) to create its own chip design capabilities. And with some success. Sultan takes some of the hype out of Chinas claims to quantum supremacy. Though even dehyped, Chinas achievement should be making those who rely on RSA-style crypto just a bit nervous (thats all of us, by the way).

Michael Weiner previews the still veiled state antitrust lawsuit against Facebook and promises to come back with details as soon as its filed.

In quick hits, I explain why we havent covered the Iranian claim that their scientist was rubbed out by an Israeli killer robot machine gun: I dont actually believe them. Brian explains that another law aimed at China and its use of Xinjian forced labor is attracting lobbyists but likely to pass. Apple, Nike, and Coca-Cola have all taken hits for lobbying on the bill; none of them say they oppose the bill, but it turns out theres a reason for that. Lobbyists have largely picked the bones clean.

President Trump is leaving office in typical fashiongesturing in the right direction but uninteresting in actually getting there. In a Too Much Too Late negotiating move, the President has threatened to veto the defense authorization act if it doesnt include a repeal of Section 230 of the Communications Decency Act. If hes yearning to wield the veto, the Democrats and GOP alike seem willing to give him the chance. They may even override, or wait until Jan. 20 to pass it again.

Finally, I commend to interested listeners the oral argument in the Supreme Courts Van Buren case, about the Computer Fraud and Abuse Act. The solicitor generals footwork in making up quasi textual limitations on the more sweeping readings of the act is admirable, and it may well be enough to keep van Buren in jail, where he probably belongs for some crime, if not this one.

And more.

Download the 341st Episode (mp3)

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The Cyberlaw Podcast: It's Time to Pay Attention When Attention Stops Paying - Lawfare

Aging is a significant risk factor for developing many chronic diseases, and gaining a better understanding of the genetic, molecular, and cellular processes responsible for the aging process is vital to improving quality of life. To this end, two studies, funded in part by NIA and published in Nature, used mouse models to catalog and identify multiple cell-specific and cellular composition changes in different cell types and organs related to the aging process.

The first study describes the creation of a single-cell transcriptomic mouse cell atlas that captures cell-type-specific hallmarks across the lifespan of the mouse. The Tabula Muris Senis or Mouse Aging Cell Atlas provides molecular information on age-related changes in specific cell types across 23 tissues and organs. In the second study, using data from the atlas, researchers found that not only do cell-specific changes occur across multiple cell types and organs, but age-related changes also occur in the cellular composition of different organs.

To create the mouse atlas, researchers performed single-cell RNA sequencing on more than 350,000 cells from male and female mice ranging from one to 30 months old, which models the human aging process from infancy to approximately 100 years old. Data were collected for mice in six age groups at 1, 3, 18, 21, 24 and 30 months. By analyzing multiple organs from the same mouse over that time span, researchers were able to obtain data controlled for age, environment, and epigenetic effects.

Researchers observed that changes in the relative composition of a given cell type with age are more meaningful than comparing proportions of different cell types at a single age. In one analysis of their data, they used the Genome Analysis ToolKit to identify specific gene mutations across all samples simultaneously. They focused on genes that were expressed in at least 75% of cells for each age group within a particular tissue and observed an age-related increase in mutations across all the organs they analyzed. This supports other studies indicating that genomic instability is a hallmark of aging and suggests it occurs in many organs of the body.

In the second study, researchers performed bulk RNA sequencing of proteins and data from the mouse atlas to demonstrate a progression of aging both within and among different organs.

They measured plasma proteins and sequenced RNA from 17 isolated organ types from male and female mice from one month old to maturity (3-6 months old) and aging through adulthood (median 27 months old). Researchers then analyzed whether differentially expressed genes (DEGs) arise and whether they persist with advancing age. Differential gene expression is the activation of different genes within a cell that define its function.

Few DEGs were observed between organs at similar ages but they increased markedly with advancing mouse age, especially when compared with one-month-old mice that were undergoing development. Among their findings on DEGs, they discovered gene expression trajectories that were similar to aging-related processes, including mitochondria dysfunction, impaired protein folding, and inflammation. They also noted that changes in DEGs for common biological pathways in tissues did not seem to be driven by changes in transcription regulatory factors, which turn gene expression on and off. This suggests that additional gene regulatory sites may come into play in the dynamics of DEGs with aging. Further, researchers found that DEGs that began in middle age were highly correlated to similar patterns in later life, indicating that some harmful changes begin earlier in life. The researchers noted that better understanding of these processes may lead to improved interventions to enhance healthspan benefits.

These studies highlight the utility of the Mouse Aging Cell Atlas, as well as the work that can stem from enhanced understanding of aging processes at the cellular, tissue, and organ system level. Future research using these characterizations of aging may help with the development and application of interventions to increase the healthspan and delay aging-related diseases. The mouse atlas data set is available at https://tabula-muris-senis.ds.czbiohub.org/.

This research was supported in part by NIA grants R01-AG045034 and DP1-AG053015.

References: Tabula Muris Consortium. A single-cell transcriptomic atlas characterizes ageing tissues in the mouse. Nature. 2020;583(7817):590-595. doi: 10.1038/s41586-020-2496-1.

Schaum N, et al. Ageing hallmarks exhibit organ-specific temporal signatures. Nature. 2020;583(7817):596-602. doi: 10.1038/s41586-020-2499-y.

Original post:
Mouse Aging Cell Atlas enables discovery of cellular-specific aging changes in different cell types and organs - National Institute on Aging

As human lifespans have gotten longer, certain proteins in our bodies are increasingly prone to take on alternative shapes. These misfolded proteins can ultimately trigger neurodegenerative diseases such as Alzheimers, Parkinsons and Lou Gehrigs disease, formally known as amyotrophic lateral sclerosis (ALS).

Meredith Jackrel, assistant professor of chemistry in Arts & Sciences at Washington University in St. Louis, and her lab group study protein misfolding disorders. They are especially interested in how protein misfolding occurs, how it leads to disease and how scientists might be able to prevent or even reverse protein misfolding. Their work promises applications in flu vaccines as well as in the current coronavirus pandemic.

In this Q&A, Jackrel describes how her labs expertise in protein misfolding and neurodegenerative diseases has made them uniquely qualified to work on developing new amyloid-inspired vaccine technologies aimed at elderly populations.

How does your research relate to the current pandemic?

We are working on the development of new vaccine technologies specifically tailored to elderly populations. We originally initiated this project to evaluate new flu vaccine technologies, but this approach could also be relevant to COVID-19 since seniors are particularly susceptible to its severe complications.

A general problem with vaccination of elderly individuals is immuosenescence, or age-related dysfunction of the immune system. Immunosenescence is typically overcome by the addition of adjuvants to improve immune response and efficacy. However, adjuvants create local inflammation, which obstructs the immune system and makes vaccines less effective.

A colleague at WashU in biomedical engineering, Jai Rudra, studies self-assembling peptides as materials for developing novel vaccines that do not require the use of adjuvants. These self-adjuvanting peptide nanofibers are hypothesized to trigger the autophagy pathway, a kind of cellular recycling that can also promote good immunological functions, which has emerged as a potential vaccine target. Administration of these peptide nanofibers leads to robust, high-affinity, and neutralizing antibody responses without local reactions, making them attractive for vaccine delivery in the elderly.

To further pursue application of these nanofibers, we must now investigate the toxicity and clearance mechanism of these materials.

How are you using your expertise in protein folding/misfolding in your work on vaccine technology?

Peptide nanofiber materials rapidly assemble into configurations that closely resemble the underlying causes of neurodegenerative disorders. These amyloids are recognized as clumps of proteins that accumulate in patients with Alzheimers, Huntingtons and Parkinsons disease.

While there are key differences that we anticipate will not make use of these materials problematic, it is nonetheless essential that the safety and clearance mechanism of the peptide nanofiber vaccines be thoroughly tested. My labs expertise in the development of model systems to study the toxicity and mechanism of disease-associated amyloid proteins is therefore highly relevant to this project.

Furthermore, due to the complexities of studying the peptide nanofibers in mammalian cells, my labs expertise in the use of Bakers yeast as a model system is proving highly relevant for studying the mechanism of clearance of these new materials.

What are your specific goals in this project?

The primary goals for my lab are to determine the toxicity and mechanism of clearance of the peptide nanofiber vaccines in a yeast model system. We aim to compare the toxicity of the nanofibers to the toxicity of disease-associated proteins. We will also employ autophagy-deficient yeast models to establish the mechanism of clearance of the nanofibers. The Rudra lab then aims to assess the efficacy of the nanofiber-based vaccines in aged mice.

Where does the project stand now? What are the next steps?

We have established a yeast model system of these peptide nanofibers and completed much of the preliminary work. Excitingly, we have confirmed that these peptide nanofibers are not toxic in yeast and have made some new insights into their mechanism of clearance. We aim to complete the early stage of this project shortly, and the Rudra lab has begun work in animal systems. Once we complete work with the nanofibers alone, we will begin to test conjugates to various vaccine targets, notably those that underpin COVID-19.

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Building better vaccines for the elderly | The Source - Washington University in St. Louis Newsroom

A breakthrough on protein folding could unlock new possibilities into disease understanding and drug discovery, among other fields.(Photo: DeepMind)

Anew discovery about "protein folding" could unlock a world of possibilities into the understanding ofeverything from diseases to drugs, researchers say.

The breakthrough that is sending ripples of excitement throughthe science and medical communities this week deals with theshapestiny proteins in our bodies essential to all life fold into.

The so-called "protein-folding problem" has puzzled scientists for five decades, and the discovery this week from the London-based artificial intelligence lab DeepMind has been heralded as a major milestone.

"This computational work represents a stunning advance on the protein-folding problem, a 50-year old grand challenge in biology," said Venki Ramakrishnan, president of the U.K.'s Royal Society. "It has occurred decades before many people in the field would have predicted. It will be exciting to see the many ways in which it will fundamentally change biological research.

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Proteins are essential to life, supporting practically all of its functions, according to DeepMind, which is owned by Google. They are large, complex molecules, made up of chains of amino acids, and what a protein does largely depends on its unique 3D structure.

The ability to predict protein structures accurately enables a better understanding of what they do and how they work.

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When proteins are translated from their DNA codes, they quickly transform from a non-functional, unfolded state into their folded, functional state. Problems in folding can lead to diseases such asAlzheimer's and Parkinson's.

The companys breakthrough essentially means that it figured out how to use artificial intelligence to deliver relatively quick answers to questions about protein structure and function that would take many months or years to solve using currently available methods, according to STAT News.

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DeepMinds program, called AlphaFold, outperformed about 100 other teams in a biennial protein-structure prediction challenge called CASP, short for Critical Assessment of Structure Prediction, according to the journal Nature.

We have been stuck on this one problem how do proteins fold up for nearly 50 years," said University of Maryland professor John Moult, co-founder and chair of CASP. "To see DeepMind produce a solution for this, having worked personally on this problem for so long and after so many stops and starts wondering if wed ever get there, is a very special moment.

Researchers from DeepMind plan to publish their results in a peer-reviewed journal in the near future.

Read or Share this story: https://www.usatoday.com/story/news/nation/2020/12/03/protein-folding-discovery-major-breakthrough-deepmind/3809693001/

Read more here:
'Stunning advance' on 'protein folding': A 50-year-old science problem solved and that could mean big things - USA TODAY