Category Archives: Cell Biology

Cell Biology

Glycan shield of the ebolavirus envelope glycoprotein GP | Communications Biology – Nature.com

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Glycan shield of the ebolavirus envelope glycoprotein GP | Communications Biology - Nature.com

Cell Biology

Associate Professor / Professor of Cancer Biology job with UNIVERSITY OF SOUTHAMPTON | 303905 – Times Higher Education

Cancer Sciences

Location: Southampton General HospitalSalary: 53,353 to 99,330Full Time PermanentClosing Date: Thursday 01 September 2022Interview Date: To be confirmedReference: 1928122CM

Associate Professor Salary: 53,353 67,060 per annum recruitment package will be commensurate with qualifications and experience (Level 6)

Professor Salary: Competitive from 70,119 per annum recruitment package will be commensurate with qualifications and experience (Level 7)

The University of Southampton seeks to recruit a new Associate Professor or Professor of Cancer Biology to expand our existing programmes and track record in this area, ideally in the field of lymphoid malignancy.

Over the last 30 years, our collaborative research teams, based on a single hospital site, have made important contributions to the study of normal and malignant lymphoid biology. Our research has helped transform the understanding and treatment of the most common adult leukaemia, Chronic Lymphocytic Leukaemia (CLL). Our discovery of two distinct CLL subsets has given clinicians and patients a much clearer indication of the likely disease course and has inspired the development of novel therapeutics. In parallel, our observations have driven major advances in lymphoma care, leading to the development and standardisation of effective new antibody treatments and optimal drug regimens (e.g. antibodies that target the CD20 protein). Through our leadership of international clinical trials, we have transformed the standard of care for different lymphoid malignancies (e.g. Hodgkin and Burkitt lymphoma) in the UK and internationally, affecting all stages of patient experience from diagnosis to treatment.

We now wish to further strengthen this area of our research with additional expertise in the fundamental biology of lymphoid malignancy. For the Professorial appointment, we seek an experienced and internationally recognised candidate with outstanding credentials in the field, someone with proven experience who will be attracted to a role in Southampton by our record in B cell biology and cancer immunology/immunotherapy, and our proven capabilities in clinical translation, taking results from the laboratory directly to patients. At the Associate Professor level, we would like to attract a rising star, with the potential, evidenced by early indicators, to become an international scientific leader of the future.

Successful candidates at both Associate Professor and Professor level will have a developing, or strong international profile in the molecular and cellular biology of cancer, respectively, and add synergy and/or a new dimension to our research activities. The successful individual will join a passionate team of basic and translational scientists working in close collaboration with clinical colleagues in our Biomedical Campus at Southampton General Hospital, in purpose-built laboratories in the Somers Building and the Centre for Cancer Immunology. Our work is under-pinned by multiple programme and accelerator awards from Cancer Research UK (CRUK), and houses a CRUK Centre, a CRUK/NIHR Experimental Cancer Medicine Centre, and a CRUK Clinical Trials Unit. Successful candidates at the Professorial level will also have senior research leadership experience and a more established track record of attracting substantive external research funding from research councils, charities and the commercial sector.

More than 250 researchers, clinicians and associated staff focus on all aspects of cancer research, with particular focus on cancer immunology/immunotherapy, cell biology and engineering antibodies to generate therapeutics. Through close interactions of our researchers with the clinical trials unit,we bring ideas and discoveries made in the laboratory into clinical practice as rapidly as possible and ensure that the mechanisms underlying cancer treatments are understood.

We welcome applications from all candidates with an interest in the role, and those who are committed to helping us create an inclusive work environment. We especially encourage applications from candidates from Black, Asian and Minority Ethnic communities, people who identify as LGBTQ+ and people with disabilities.

For further details about the post you are invited to contact the Head of School, Professor Jonathan Strefford jcs@soton.ac.uk

You should submit your completed online application form at https://jobs.soton.ac.uk. The application deadline will be midnight on the closing date stated above. Please submit details for 3 referees and include your CV and publication list with your application. If you need any assistance, please call Lauren Ward (Recruitment Team) on +44 (0) 23 8059 2750, or email recruitment@soton.ac.uk. Please quote reference 1928122CM on all correspondence.

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Associate Professor / Professor of Cancer Biology job with UNIVERSITY OF SOUTHAMPTON | 303905 - Times Higher Education

Cell Biology

NeuroVoices: Ralph Nixon, MD, PhD, on Autolysosome Acidification in Alzheimer Disease and Changing Perceptions of Amyloid – Neurology Live

Despite the billions of dollars poured into developing therapies for Alzheimer disease (AD), little regulatory success has been achieved, with a list of failed or discontinued agents that has continued to grow. A popular approach has been to target amyloid- plaques; however, some in the field argue that this does not result in the intended sustained disease-modifying effects. Most notably, the 2021 FDA approval of aducanumab (Aduhelm; Biogen), an antiamyloid medication, sparked discussion as to whether these drugs are worth the investment.

Led by researchers at NYU Grossman School of Medicine and the Nathan Kline Institute, a newly published paper in Nature continues to challenge the traditional approaches to AD drug development. The latest study findings argue instead that neuronal damage characteristic of AD takes root inside cells and well before these thread-like amyloid plaques fully form and clump together in the brain. Using AD mouse models in vivo, investigators identified small sacs inside cells that were filled with acidic enzymes involved in the routine breakdown, removal, and recycling of metabolic waste from everyday cell reactions, as well as from disease.

In an interview with NeurologyLive, senior investigator Ralph Nixon, MD, PhD, provided in-depth detail on the findings observed and the specific underlying processes taking place. Nixon, a professor of psychiatry and cell biology at NYU Langone, sat down as part of a new iteration of NeuroVoices, and discussed the reasons why the community should seriously consider changing their perceptions on amyloid-, AD drug development, and the root causes of the disease.

Ralph Nixon, MD, PhD: As the audience knows well, Alzheimer disease is a disorder where toxic proteins accumulate in the brain and ultimately kill neurons and cause cognitive decline. Weve been interested in the mechanisms in neurons for clearing these types of proteins since it lives for the life of the individual. This process must be efficient for the cell to survive for that long. One of the principal ways that clearance takes place is the process of autophagy. It basically is 2 steps. One, to sequester unneeded or obsolete or damaged proteins, especially as they accumulate in aging and stress, and to deliver them to a lysosome, which is the digestive compartment of the cell, filled with dozens of digestive enzymes of various sorts. The fusion of that with the sequestered material in that vesicle is followed by acidifying the compartment, because the lysosome is highly acidic. In order for these proteases and hydrolases to work, that acidification takes place upon fusion, and then the process of digestion occurs, hopefully, if it's successful, to completely digest the contents. This is an area that we've been investigating for a long time, and mostly, initially in human brain. Over the years, we've documented what appears to be a unique degree of pathology of this system, the autophagy system, and the lysosomal dysfunction. The degree seemed to us to be unique among all the different age-related disorders.

Another feature was that amyloid- and metabolites of APP [amyloid precursor protein] were accumulating in these autophagy vacuoles, which are the packets of waste that accumulate. We thought that there was a close connection between autophagy failure and the accumulation of amyloid and other things. The goal at that point was to track this process in mouse models, where we could look at the very earliest stages, we knew in a genetically identical model that had a mutation of Alzheimer disease so that we could know that these mice are going to develop pathology. We could follow that evolution from the beginning to the end stages of the process. This was difficult to do because there were no tools available that were really reliable.

We decided to construct a mouse model in which we transgenically introduced a protein that is a marker of the autophagic vacuoles, and in particular, auto phagosomes. That construct was tagged with two fluorescent probes, a red and a green probe. The concept behind it is that once it attaches to the first stage of autophagy, sequestration, we can follow the whole efficiency and progress of that pathway all the way from sequestration to clearance. In addition, the dual fluorescence allowed us to track the pH (potential hydrogen) of the compartments because this turns out to be the key change that allows us to identify the vesicles. As digestion occurs, the color of the fluorescence turns from yellow to red, which indicates successful fusion of the lysosome and digestion of the materials. To introduce this particular construct into a mouse that was also engineered to have mutations that mimic certain aspects of Alzheimer's disease pathology, we could then follow the progress of autophagy and its disruption during the evolution of the disease, and as before the onset of anything that was previously associated with Alzheimer's, and then to all of the consequences of any disruption that occurred. This worked out beyond our dreams as to how successful we could reveal pathology that had not been seen before.

There were a bunch of surprises, but one of the things we were most interested in and were able to confirm is that the very first thing that happens in a in these mice is an abnormality of the lysosome. The lysosomes start to lose the ability to acidify. We know why that happens now, but the important thing is that this was happening very, very early before any manifestations of the Alzheimer process that most people track, ie, amyloid outside the cell, plaques, and cytoskeleton changes. This is the first thing that we can detect during this Alzheimer evolution in these mice.

The other interesting thing is that amyloid- and other metabolites that we consider toxic in Alzheimer's disease, one of them ill call C99, are the first cleavage of APP to generate this c-terminal fragment. We sometimes call it CTF, or call it C99. That then gets cleaved to amyloid-. It's been one of these molecules that has a lot of interesting toxicities and has been generally ignored in the amyloid cascade hypothesis because the focus has been exclusively on amyloid-. These molecules are accumulating along with other waste in the affected neurons in this mouse model. There was a close connection there between the earliest changes, and even earlier changes in lysosomes than in the amyloid, that is considered to be the earliest stage of disease.

The biggest surprises were some other things that the probe was able to reveal. One of which is that this failure of autophagy resulted in massive accumulation of waste vesicles in the cells, so much so that they are pushing the circumference of the cell body, of the neuron, and causing these balloon-like blebs that are deeply fluorescent because they're basically packed with autophagy waste. They're all around the surface of the cell, which made it look like a flower. That was the source of the description of these phenomena as PANTHOS. P for poison and anthos, the Greek word for flower.

This process, to our knowledge, has never been described. The probe allowed us to see it. In addition to that process, the accumulation of these waste artifact vacuoles was encroaching on the center of the cell and transformed, coalesced into this network of membrane tubules that actually had fibrils of amyloid. Again, this was something that to my knowledge had never been visualized: an intact cell that's still alive accumulates the amyloid that's normally just associated it with the outside of the cell. If you had just stayed within amyloid, you would think this is a plaque. But in fact, it's an intact cell that has all the features of an amyloid plaque within it but is still alive.

The other important piece of information is that all the plaques that develop in these mouse models originated from the death of these PANTHO cells, or PANTHOS neurons. Once the cell dies, the ghost becomes the plaque outside the cell. The bottom line here, and one of the main messages, is the importance of lysosome dysfunction at the earliest possible stage of Alzheimer. This connects with the genetics that we now know. That C99 that I mentioned earlier, the APP fragment, we now know, inhibits the acidification process. When it accumulates, it actually sets a vicious cycle to further de-acidify the lysosome. The lysosome is genetically and pathologically at the earliest outset of evolution at the least in amyloid- models.

The other thing that was important in terms of the clinical relevance, is that, as many people know, to this point, the vaccines for amyloid have not been very successful. When you think of what the sequence is that we've defined, it's an inside-out process rather than the cascade hypothesis that the lesion and the amyloid outside is killing the cell as a secondary process. In the case of if we are correct, which I think the pathology speaks for itself, there's very little logic in removing the amyloid on the outside because the cell has already, you know, been so compromised, that it's going to die. There's no reason to remove the amyloid on the outside because it originated from basically a dying cell. One has to now attack the process inside the cell, and to target these individual processes, lysosomes or whatever other autophagy dysfunction that you can reverse, and to cure the cell from inside route rather than by removing amyloid. This is a paradigm shift. Of course, so far, we haven't heard a response from many in the amyloid vaccine field, I'm sure there'll be still some people that will say, well, we need more work, which of course, we do.

Transcript edited for clarity. Click here for more NeuroVoices

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NeuroVoices: Ralph Nixon, MD, PhD, on Autolysosome Acidification in Alzheimer Disease and Changing Perceptions of Amyloid - Neurology Live

Cell Biology

Research Assistant Cellimage Project, College of Medicine, (NUIG RES 199-22) job with NATIONAL UNIVERSITY OF IRELAND, GALWAY | 303808 – Times Higher…

Research Assistant Cellimage Project

Regenerative Medicine Institute, College of Medicine

NUIG RES 199-22

Information on project/centre

The Regenerative Medicine Institute (REMEDI) is a world-class biomedical research centre which focuses on research in cell and gene therapies to address a number of major disease targets. Our research spans a broad spectrum of translational strategies including basic stem cell biology, advanced manufacturing, contemporary analytics and clinical trials.

The CELLIMAGE Project, funded under the Disruptive Technologies innovation fund is designed to develop novel artificial intelligence tools to support next generation cell therapy manufacturing. The project is a partnership between REMEDI, Valitacell Ltd., and Intel.

Job Description:

Duties:

Employment permit restrictions apply for this category of post

Salary: 27.874 30,742 per annum

Continuing Professional Development/Training:

Researchers at NUI Galway are encouraged to avail of a range of training and development opportunities designed to support their personal career development plans.

Further information on research and working at NUI Galway is available on Research at NUI Galway

For information on moving to Ireland please see http://www.euraxess.ie

Further information about NUI Galway School of Medicine is available at this link.

Informal enquiries concerning the post may be made to Professor Frank Barry at frank.barry@nuigalway.ie

To Apply:

Applications to include a covering letter, CV, and the contact details of three referees should be sent, via e-mail (in word or PDF only) to Ms. Amy Hogan amy.hogan@nuigalway.ie

Please put reference number NUIG RES 199-22 in subject line of e-mail application.

Closing date for receipt of applications is 5.00 pm 16/08/2022

We reserve the right to re-advertise or extend the closing date for this post.

National University of Ireland, Galway is an equal opportunities employer.

All positions are recruited in line with Open, Transparent, Merit (OTM) and Competency based recruitment

'NUI Galway provides continuing professional development supports for all researchers seeking to build their own career pathways either within or beyond academia. Researchers are encouraged to engage with our Researcher Development Centre (RDC) upon commencing employment - see http://www.nuigalway.ie/rdc for further information.'

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Research Assistant Cellimage Project, College of Medicine, (NUIG RES 199-22) job with NATIONAL UNIVERSITY OF IRELAND, GALWAY | 303808 - Times Higher...

Cell Biology

These sterile mice have been modified to make rat sperm – Popular Science

Biologists have successfully engineered animals that produce the sperm of a different species, which brings labs one step closer to animal reproduction that uses nothing but the animals DNA. And while theres potential to rebuild endangered species populations, or even bring extinct species back to life, dont worryJurassic Park will probably stay fiction.

The new research published today in Stem Cell Reports has demonstrated that it is possible to produce rat sperm in sterile hybrid mice. While the technique still needs to be fine-tuned, the study authors say that their approach of adding engineered stem cells from one species to embryos of another species, called blastocyst complementation, has the potential to boost endangered species. If at-risk species arent able to maintain healthy numbers, generating their eggs and sperm in a lab could be used as a new tool to build populations up.

The teams process used stem cells, specifically pluripotent stem cells. Stem cells are the raw materials that make all kinds of cells, but the pluripotent stem cells can produce the greatest number of different cell types. These stem cells naturally develop only in embryos, but its also possible for other types of cells, such as those from a regular tissue sample, to be transformed into pluripotent stem cells. So this gives scientists a more readily available source to brew these stem cells in the lab. Adding them to the sterile embryos of a different living animal ultimately converts these stem cells into germ cells, such as sperm or eggs.

Previous research had already shown that rat sperm could be made in mice using pluripotent stem cells, says Ori Bar-Nur, a biologist at the Swiss university ETH Zurich and a coauthor of the study. The process involves creating a chimera, which is an artificial genetic hybrid of multiple animalsin this case, mice and rats. But past experiments with rat-mice chimera produced mouse sperm in addition to rat, resulting in a mix that was difficult to distinguish, isolate, and use. Unlike these past experiments, Bar-Nur and his team used mice that were genetically sterile. By adding the pluripotent stem cells of a rat to a sterile mouse embryo at a particular stage in its development (in this case the blastocyst stage) only the rats sperm formed in the resulting rat-mouse chimera.

Its removed a hurdle, especially if the process can work with other species, says Kevin Gonzales, a postdoctoral stem cell biology researcher at the Rockefeller University who was not involved with the study.

This new system wasnt a perfect success, though. The sperm produced by the chimeras could fertilize rat eggs, but at a relatively low rate, and the resulting embryos didnt develop into live offspring. Bar-Nur and his team arent sure why this is, but they suggest that it could be because the cells had been frozen and thawed, which is known to reduce viability. Its something we still need to pursue and are working on, Bar-Nur says.

Still, Gonzales says that the teams ability to engineer a chimera that exclusively produced the sperm of a different species shows promising progress for the future of stem cell propagation in conservation efforts. Continuing down this line of research has the potential to repopulate endangered (or even extinct) species with dwindling numbers. Small populations lead to a dangerous lack of genetic diversity, which increases the risk of extinction. If you think about critically endangered species, you probably wont have access to spermatozoa, explains Bar-Nur. But you might have tissue samples, and if we could transform that into pluripotent stem cells and find an evolutionarily close species, we could potentially, eventually, repopulate the species.

[Related: Airborne animal DNA could help biologists track endangered species]

There are a number of steps left before this technology can be put to practical use. First, biologists have yet to actually develop a living creature with sperm made from this particular type of stem cell propagation, blastocyst complementation. Additionally, no one has been able to produce female eggs with this method. However, both Bar-Nur and Gonzales say theres every reason to think its possible.

Gonzales points out that future use of the application will depend on having or making pluripotent stem cells. Samples of endangered species tissue are being collected and preserved, so labs could gain access, he says. However, the specific set of genetic keys needed to transform cells into pluripotent stem cells varies from species to species. The DNA sequences of lab mice, for instance, are relatively well known, but those of a rare tiger might not be.

The reproductive systems of mammal species present another barrier: they will need hosts to carry any viable embryos, says Gonzales. Even if sperm and eggs are successfully created and combined, its unknown whether the embryo could healthily develop in the uterus of a different species, even one that is closely related.

So as Jurassic Park-esque as it sounds to use cell samples to bring an extinct species back to lifeor even a nearly-extinct species back from the brinkresearchers still have a few hurdles to overcome before the technology can be put into practice.

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These sterile mice have been modified to make rat sperm - Popular Science

Cell Biology

Postdoc Position in Metabolomics and Proteomics Biomarkers Discovery job with MASARYK UNIVERSITY | 303929 – Times Higher Education

Department:Biomarkers of Disease and HealthFaculty of ScienceDeadline:31 Aug 2022Start date:upon agreementJob type:full-timeJob field:Science and research

Bursar of the Faculty of Science, Masaryk Universityannounces an open competition for the positionPostdoc Position in Metabolomics and Proteomics BiomarkersDiscovery

Workplace:RECETOX, Faculty of Science, Masaryk University in Brno, Czech RepublicType of Contract:temporary position with 1-year contract (with possible extension), non-academicWorking Hours: 1,0 FTE(full-time employment of40 hours per week)Expected Start Date: as soon as possible, or negotiable concerning immigration timelines for non-EU candidatesNumber of Open Positions:1Pay:negotiable Application Deadline:31.8.2022 EU Researcher Profile:R2

About the Workplace

Masaryk Universityis modern, dynamic and the most attractive university in the Czech Republic with ten faculties, more than 6000 staff and 30000 students, awide range of research areas and astrong international position. We are the largest academic employer in the South Moravian Region.

Faculty of ScienceMU,holder of theHR Excellence in Research Awardby the European Commission, is aresearch-oriented faculty, offering university education (Bachelors, Masters, and Doctoral degree programs) closely linked to both primary and applied research and high school teaching of the following sciences: Mathematics, Physics, Chemistry, Biology, and Earth sciences. We are the most productive scientific unit of the Masaryk University generating around 40 % of MU research results.

RECETOXfocuses on interdisciplinary research and education in the area of Environment & Health, studying toxic compounds and their behavior, transport & bioaccumulation to evaluate environmental effects, assess the exposure and health risks to humans, and develop technologies and biotechnologies to break them down.http://www.recetox.muni.cz/en/career/career-at-recetox

Job description

Clinically relevant biochemical, immunological and cellular biomarkers of Alzheimer'sdisease and aging

Dr. Zdenek Spacilis searching for atalented and highly motivated scientistexperienced in mass spectrometry and cell culture. The primary responsibilities will include cerebral organoids' cell culture as amodel system for Alzheimer'sdisease and the application of mass spectrometry-based metabolomics and proteomics to study the underlying mechanisms and early disease biomarkers. The candidate will be involved in amultidisciplinary project combining advanced analytical technology with state-of-the-art cell biology to advance life sciences and medicine.

Biomarkers of health and diseaseresearch group led by Zdenek Spilzdenek.spacil@recetox.muni.czis engaged in metabolomics and targeted proteomics, pioneering non-genetic factors affecting human health.https://www.recetox.muni.cz/en/research/principal-investigators/dr-zdenek-spacil

Skills and Qualifications

The applicant must have:

The applicant should have:

Informalinquiries about the positioncan be sent to Ji Dobe,jiri.dobes@recetox.muni.cz,+420549493268.

We Offer

Application Process

The application shall besubmitted online by 31.8.2022 via an e-application,please find the reference to the e-application in the beginning and end of the advertisement.

The candidate shall provide following:

After submitting your application successfully, you will receive an automatic confirmation email from jobs.muni.cz. In case of problems with filling in the e-application form, please contact us by e-mail:rcx-hr@recetox.muni.cz.

Selection Process

Received applications will be considered carefully in line withprinciples of the EU Charter and Code for Researchers. Selection criteria: (i) meeting qualification requirements described above, (ii) all required documents provided.

If we do not contact you within 10 working days after the application deadline at the latest, it means that we have shortlisted other candidates meeting the position requirements.

Shortlisted candidates will be invited for apersonal or online interview.The Faculty Recruitment Policy (OTM-R) can be seenhere.

Faculty of Science, Masaryk University is an equal opportunity employer. We support diversity and are committed to creating an inclusive environment for all employees.

Visit ourCareer pageand alsoCareer page of Faculty of science.

We are looking forward to hearing from you!

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Postdoc Position in Metabolomics and Proteomics Biomarkers Discovery job with MASARYK UNIVERSITY | 303929 - Times Higher Education

Cell Biology

Mitochondrial DNA mutations are associated with an increased risk of atherosclerosis – News-Medical.Net

Mitochondria are organelles found within most cells, best known for generating the chemical energy required to power cellular functions. Increasingly, however, researchers are discovering how mitochondrial function -; and dysfunction -; play critical roles in numerous diseases, and even aging.

In a new study published in the August 4, 2022 online issue of Immunity, scientists at University of California San Diego School of Medicine and Salk Institute for Biological Studies report a surprising link between mitochondria, inflammation and DNMT3A and TET2, a pair of genes that normally help regulate blood cell growth, but when mutated, are associated with an increased risk of atherosclerosis.

We found that the genes DNMT3A and TET2, in addition to their normal job of altering chemical tags to regulate DNA, directly activate expression of a gene involved in mitochondrial inflammatory pathways, which hints as a new molecular target for atherosclerosis therapeutics. They also interact with mitochondrial inflammatory pathways, which hints at a new molecular target for atherosclerosis therapeutics."

Gerald Shadel, PhD, co-senior study author and director of the San Diego Nathan Shock Center of Excellence in the Basic Biology of Aging at Salk Institute

While studying the roles of DNMT3A and TET2 mutations in clonal hematopoiesis, which happens when stem cells begin making new blood cells with the same genetic mutation, co-senior study author Christopher Glass, MD, PhD, professor in the departments of Medicine and Cellular and Molecular Medicine at UC San Diego School of Medicine, and colleagues noted that abnormal inflammatory signaling related to DNMT3A and TET2 deficiency in blood cells played a major role in the inflammation response that promotes development of atherosclerosis.

But the question remained how DNMT3A and TET2 genes were involved in inflammation and atherosclerosis -; the buildup of fatty plaques in arteries and the primary underlying cause of cardiovascular disease. It is estimated approximately half of Americans between the ages of 45 and 84 have atherosclerosis, which is the single leading cause of death in the United States and westernized nations.

"The problem was we couldn't work out how DNMT3A and TET2 were involved because the proteins they code seemingly do opposite things regarding DNA regulation," said Glass. "Their antagonistic activity led us to believe there may be other mechanisms at play, which prompted us to take a different approach and contact Shadel, who had uncovered the same inflammatory pathway years earlier while examining responses to mitochondrial DNA stress."

Inside mitochondria resides a unique subset of the cell's DNA that must be organized and condensed correctly to sustain normal function. Shadel's team had previously investigated the effects of mitochondrial DNA stress by removing TFAM, a gene that helps ensure mitochondrial DNA is packaged correctly.

Shadel and colleagues determined that when TFAM levels are reduced, mitochondrial DNA is expelled from mitochondria into the cell's interior, setting off the same molecular alarms that alert cells to a bacterial or viral invader and trigger a defensive molecular pathway that prompts an inflammatory response.

Glass' and Shadel's labs worked together to better understand why DNMT3A and TET2 mutations led to inflammatory responses similar to those observed during mitochondrial DNA stress. The teams applied genetic engineering tools and cell imaging to examine cells from people with normal cells, those with loss of function mutations in DNMT3A or TET2 expression and those with atherosclerosis.

They discovered that experimentally reducing the expression of DNMT3A or TET2 in normal blood cells produced similar results to blood cells that had loss of function mutations and to blood cells from atherosclerosis patients. In all three cases, there was an increased inflammatory response.

They also observed that low levels of DNMT3A and TET2 expression in blood cells led to reduced TFAM expression, which in turn led to abnormal mitochondria DNA packaging, instigating inflammation due to released mitochondrial DNA.

"We discovered that DNMT3A and TET2 mutations prevent their ability to bind and activate the TFAM gene," said first author Isidoro Cobo, PhD, a postdoctoral scholar in Glass' lab. "Missing or reducing this binding activity leads to mitochondrial DNA release and an overactive mitochondrial inflammation response. We believe this may exacerbate plaque buildup in atherosclerosis."

Shadel said the findings broaden and deepen understanding of mitochondrial function and their role in disease.

"It's very exciting to see our discovery on TFAM depletion causing mitochondrial DNA stress and inflammation now have direct relevance for a disease like atherosclerosis," said Shadel. "Ever since we revealed this pathway, there has been an explosion of interest in mitochondria being involved in inflammation and many reports linking mitochondrial DNA release to other clinical contexts."

Therapeutics that target inflammation signaling pathways already exist for many other diseases. Glass and Shadel believe that blocking pathways that exacerbate atherosclerosis in patients with TET2A and DNMT3A mutations could form the basis for new treatments.

Source:

Journal reference:

Cobo, I.,et al.(2022) DNA methyltransferase 3 alpha and TET methylcytosine dioxygenase 2 restrain mitochondrial DNA-mediated interferon signaling in macrophages.Immunity.doi.org/10.1016/j.immuni.2022.06.022.

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Mitochondrial DNA mutations are associated with an increased risk of atherosclerosis - News-Medical.Net

Cell Biology

Fully reduced form of vitamin K found to efficiently inhibit ferroptotic cell death – News-Medical.Net

A team of researchers at Tohoku University has reported on a novel function of vitamin K, which is generally known for its importance in blood clotting. The researchers discovered that the fully reduced form of vitamin K acts as an antioxidant efficiently inhibiting ferroptotic cell death. Ferroptosis is a natural form of cell death that is characterized by extensive lipid peroxidation in cellular membranes. In addition, the team identified FSP1 as the warfarin-insensitive enzyme reducing vitamin K, the identity of which had been postulated but remained unknown for more than half a century. Recently, ferroptosis has been implicated as a driver of Alzheimer's disease and acute organ injuries among many other diseases. The findings suggest that vitamin K treatment might be a new powerful strategy to ameliorate these ferroptosis-related diseases.

Since ferroptosis prevention is considered a highly promising approach for the therapy of many degenerative diseases, new mechanisms and compounds regulating ferroptosis are extensively being explored. To identify these new molecules, a team of researchers led by Dr Eikan Mishima (Tohoku University) and Dr Marcus Conrad (Helmholtz Munich), systematically studied several naturally occurring vitamins, as well as their derivatives. "Surprisingly, we identified that vitamin K, including phylloquinone (vitamin K1) and menaquinone-4 (vitamin K2), are able to efficiently rescue cells and tissues from undergoing ferroptosis" Dr Mishima explained.

In 2019 a team of researchers, led by Dr Conrad, identified an enzyme as a novel and strong inhibitor of ferroptosis: ferroptosis suppressor protein-1, short FSP1. The current research team has now found that the fully reduced form of vitamin K (i.e., vitamin K hydroquinone) acts as a strong lipophilic antioxidant and prevents ferroptosis by trapping oxygen radicals in lipid bilayers. In addition, they identified that FSP1 is the enzyme that efficiently reduces vitamin K to vitamin K hydroquinone, thereby driving a novel non-canonical vitamin K cycle. Since vitamin K is critically involved in blood clotting processes, the team additionally showed that FSP1 is responsible for the vitamin K-reduction pathway insensitive against warfarin, which is one of the most prescribed anticoagulants.

Unraveling the identity of this enzyme solved the last riddle of vitamin K metabolism in blood clotting and elucidated the molecular mechanism of why vitamin K constitutes the antidote for warfarin overdosing. Dr Mishima and Dr Conrad have indicated that "our results have the potential to connect the two worlds of ferroptosis research and vitamin K biology. They will serve as a stepping stone for the development of novel therapeutic strategies for diseases where ferroptosis has been implicated." In addition, since ferroptosis most likely constitutes one of the oldest types of cell death, the researchers hypothesize that vitamin K might be one of the most primitive types of naturally occurring antioxidants. "Thus, new aspects of the role of vitamin K throughout the evolution of life are expected to be unveiled."

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Fully reduced form of vitamin K found to efficiently inhibit ferroptotic cell death - News-Medical.Net

Cell Biology

RoslinCT and Lykan Bioscience Combine to Create Leading Advanced Cell Therapy CDMO – GlobeNewswire

RoslinCT and Lykan Bioscience Combine to Create Leading Advanced Cell Therapy CDMO

EDINBURGH, UK AND HOPKINTON, MA, 4 August 2022 RoslinCT, a cell and gene therapy Contract Development and Manufacturing Organisation (CDMO) developing life-changing therapies in Edinburghs BioQuarter, and Lykan Bioscience (Lykan), an innovative CDMO focused on cell-based therapies, today announce that they have entered into a business combination agreement to form a global leading innovative advanced therapies CDMO.

The combined group will offer process development expertise and cGMP manufacturing for a broad range of autologous and allogeneic cell therapies, with unparalleled expertise in gene editing and industry-leading induced Pluripotent Stem Cell (iPSC) capabilities.

The group will benefit from significantly expanded capacity, with process and analytical development laboratories and cGMP manufacturing facilities in Edinburgh, Scotland, and in Hopkinton, Massachusetts. Lykan has a 64,000 sq. ft. state-of-the-art cell therapy manufacturing facility and innovation/development laboratories with 16 cGMP processing suites running by the end of 2022. Further laboratory and cGMP capacity expansion in Scotland is planned to build on RoslinCTs existing 40,000 sq. ft facilities, including 8 cGMP suites.

With demand for high-quality development and manufacturing capacity increasing across the world, this complementary pairing of RoslinCT and Lykan will shorten development and manufacturing timelines for advanced therapy sponsors, facilitating clinical and commercial GMP product release on both sides of the Atlantic.

Earlier in 2022, Global Healthcare Opportunities, or GHO Capital Partners LLP (GHO), the European specialist investor in global healthcare, announced its investment in RoslinCT. As part of the new agreement, GHO is making a majority investment in Lykan and is backing the funding of the combined entity. WindRose Health Investors, previously the majority owner of Lykan Bioscience, have reinvested in the new combined group along with Lykan Management.

RoslinCT CEO Peter Coleman and Lykan President & CEO Patrick Lucy will remain in their current roles. Together, the new entity will have a global headcount of ~300 employees.

Peter Coleman, Chief Executive Officer of RoslinCT said: This combination puts us in a strong position as a leading global CDMO in the process development and manufacturing of advanced cell therapies, and we look forward to working with our new colleagues at Lykan to fuel future growth and meet the increasing demand for innovative therapies.

Patrick Lucy, President & Chief Executive Officer of Lykan Bioscience, commented: We are delighted to combine with RoslinCT to better serve the growing demand for manufacturing capacity and expand the range of innovative services we can provide our partners to support the development of advanced cell and gene therapies.

The Partners at GHO Capital, said, This is a significant step towards the realisation of our shared ambition for RoslinCT and Lykan to build a leading global CDMO in the development and manufacture of advanced cell therapies. The collaboration represents an important step in the continued growth and internationalisation of the two businesses and we look forward to partnering with the combined Management teams and WindRose Health Investors to realise this vision.

CJ Burnes, Partner at WindRose Health Investors, said, Lykan has grown tremendously during our ownership, including completion of their state-of-the art facility and the subsequent doubling of cGMP manufacturing capacity. The combination of RoslinCT and Lykan will further accelerate this growth as it creates a unique platform providing key value-added services to the highly complex segment of advanced cell therapies and we look forward to partnering with GHO, RoslinCT and Lykan Management through this next phase.

Advisors

Ropes & Gray and Slaughter & May acted as legal advisors to GHO, Alvarez & Marsal as financial and tax advisor, Dark Horse Consulting Group as technical advisor and ERM as ESG advisor. McDermott Will & Emery LLP acted as legal advisor to Lykan, and William Blair & Company served as financial advisor.

ENDS

About RoslinCT

RoslinCT is a leading UK Cell Therapy Contract Development and Manufacturing Organisation (CDMO) focused on providing services for companies developing cell-based therapeutic products. Originally founded in 2006 as a spin-out from the Roslin Institute, we built on the broad range of scientific expertise available in the field of cell biology. Based at the Edinburgh BioQuarter, we operate fully licensed GMP manufacturing facilities and have a proven track record in the delivery of cell-based products. For further information, please visit http://www.roslinct.com.

About Lykan Bioscience

Lykan Bioscience is an innovative contract development and manufacturing services organization (CDMO) focused on cell-based therapies. With decades of biopharmaceutical industry experience, Lykan offers a full range of development and manufacturing services. The state-of-the-art, purpose-built facility offering eight independent manufacturing suites is uniquely designed to fully integrate cGMP principles and advanced software solutions to enable real-time testing and release of product. Located in Hopkinton, Massachusetts, 25 miles southwest of downtown Boston and in the proximity of four international airports, Lykan Bioscience is ideally situated to deliver life-saving cell therapy treatments to patients on behalf of their partners. Visit http://www.lykanbio.com

About GHO Capital

Global Healthcare Opportunities, or GHO Capital Partners LLP, is a leading specialist healthcare investment advisor based in London. We apply global capabilities and perspectives to unlock high growth healthcare opportunities, targeting Pan-European and transatlantic internationalisation to build market leading businesses of strategic global value. Our proven investment track record reflects the unrivalled depth of our industry expertise and network. We partner with strong management teams to generate long-term sustainable value, improving the efficiency of healthcare delivery to enable better, faster, more accessible healthcare. For further information, please visit http://www.ghocapital.com

About WindRose Health Investors

WindRose makes equity investments in companies that operate within the services sectors of the healthcare industry. The firm focuses on companies with profitable business models and a demonstrated ability to deliver cost-effective solutions. WindRose manages over $2.6 billion in investments. WindRose is based in New York City. For more information, please email us at info@windrose.com.

Tel: +44 (0) 20 3709 5700ghocapital@consilium-comms.com

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RoslinCT and Lykan Bioscience Combine to Create Leading Advanced Cell Therapy CDMO - GlobeNewswire

Cell Biology

Beyond the Books at AU: Biology Major Follows Passion for Research With Internship at Avera Health – Augie

Augustana University student Vedant Thakkar 24, of Vadodara, India, is majoring in biology with concentrations in cell & molecular biology as well as minoring in chemistry. This summer, Thakkar is interning with Avera Health at Avera McKennan Hospital & University Health Center in Sioux Falls. There, he is responsible for testing a therapy consisting of two novel drugs in breast cancer cell models observing their effects on the cancer cells individually and in a combination at various concentrations. Following his time at AU, Thakkar plans to earn a Ph.D. in cell & molecular biology and eventually become a research scientist.

Q: What extracurricular activities are you involved in?

A: Currently, I am serving as the co-president of the Cancer Awareness Club and involved as a volunteer with the Augustana Garden. Moreover, this year, I will be helping out incoming international students as an ACE ambassador!

Q: Where or how did you hear about Augustana?

A: I got an email from Wade Gemar 08, my admission counselor and one of the most amazing people I know!

Q: What is/are the reason(s) you chose to come to Augustana?

A: Three things made me choose Augie. Firstly, my admission counselor, Wade, was amazingly helpful and he answered all of my queries about Augustana and life as an international student in the United States. Also, I had reached out to the biology department with questions and I got a really good response. These two things strengthened my belief that at Augie, I would be able to access the resources I need and have support from a strong community. Lastly, I had a lengthy conversation with Kirtana Krishna Kumar 20. Her insight into the community around Sioux Falls, and the tremendous amount of opportunities this city has to offer in the biomedical industry, cemented my decision to attend Augustana.

Q: How did you get the internship? Did anyone help you? What did that journey look like?

A: I applied to this internship through the job search portal on Avera Healths website, based on the recommendation of my sister, Barsha Shah 23. I managed to successfully clear two interviews with the translational oncology department and was offered the position of student intern for Summer 2022. Ann Kolbrek, my career & academic planning (CAP) specialist, helped me in preparation for the interview by providing me with amazing tips and tools that highlighted my skills better. Also, I had constant support and advice from the faculty in the biology department, especially Dr. Jennifer A.A. Gubbels, my academic advisor.

Q: What do you like most about your internship?

A: There are a multitude of things that I absolutely love about my internship. I get the first-hand experience of seeing the bench-to-bed process of drug discovery and distribution. In addition to that, my internship is designed with several workshops that allow me to learn tools and access resources for academic and professional development. Finally, I am able to connect with some of the best scientific minds in the Midwest like my principal investigator, Pradip De, and fellow scientists, such as Nandini Dey, Jennifer Aske, Xiaoqian Lin and Adam Dale 19.

Q: What do you hope to learn/gain from the internship?

A: My previous experiences have prepared me for the professional corporate world. However, I want to utilize this internship to apply and refine the tools I have gained previously. Also, this internship is very hands-on and I bear the majority of the responsibility for my project. Hence, I will learn how to be more independent and accountable. Furthermore, the internship has pushed me to learn more in-depth about the concepts that I have learned in my classes at Augie. As a result, I am more intrigued by cell biology and I want to explore cancer biology a lot more!

Q: Why is experiential learning important for your future endeavors?

A: I believe that experiential learning is crucial for individual growth and success. My experiential learning experiences have allowed me to strengthen my core concepts which has yielded a stronger academic foundation on which I can grow and build my career. Moreover, I have learned a rare skill the ability to transfer academic knowledge into the practical world. Finally, this internship is allowing me to explore my interests in scientific research and discern what field of study in biology I want to pursue in my future education.

Overall, I believe that experiential learning will give me access to a unique portfolio of skills and experiences that will convert in the future into, hopefully, a lucrative career.

Q: How important is building relationships/connections?

A: To succeed in the corporate world, I strongly believe that networking and establishing solid connections is very crucial. Many of my past and current internship opportunities were results of connections with various health care professionals, especially in the scientific research realm, around Sioux Falls, and at Augustana. Also, having ample connections creates the possibility of wonderful collaborations, which can accelerate ones career goals.

Learn about the 2,000+ jobs and internships posted annually by the Augustana University Student Success Center at Augie Opportunities.

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Beyond the Books at AU: Biology Major Follows Passion for Research With Internship at Avera Health - Augie