Human CO2 Emissions Could Avert the Next Ice Age, Study Says

By Rebecca Boyle

Glacier in the Alps Wikimedia Commons

Earth could be entering a new Ice Age within the next millennium, but it might not, the deep freeze averted by warming from increased carbon dioxide emissions. Humans could be thwarting the next glacial inception, a new study says.

Even in the comparatively long time scales of Earth history, we’re kind of overdue for another ice age — our current Holocene era has lasted about 11,600 years, roughly 600 years longer than the average interglacial (between-ice-age) periods of the past. If atmospheric CO2 levels were lower, the next ice age might have started sometime within the next 1,000 years, according to researchers from University College London and Cambridge University.

Their conclusion is based in part on abrupt temperature changes in the overall temperature contrast between Greenland and Antarctica, according to a Cambridge news release. The North Atlantic would cool rapidly while Antarctica warms, fluctuations that would only happen if expanding ice sheets were calving icebergs huge enough to impact ocean circulation. These temperature see-saws can therefore be used to pinpoint the activation of a new ice age, a “glacial inception.”

Chronis Tzedakis from UC London and colleagues examined our present conditions, including temperature averages and solar radiation strength, and found a close analogue to the present, an era called Marine Isotope Stage 19, or about 780,000 years ago. The eras have a similar astronomical configuration and climate, although their CO2 trajectories are pretty different (ours is on the rise).

A phenomenon called insolation was a key factor here. Insolation is the seasonal and latitudinal distribution of solar radiation, which changes a tiny bit over tens of thousands of years due to tiny variations in Earth’s orbit around the sun. These little differences are one of the factors that can help trigger a cooling event, cascading toward an ice age. The insolation minimum in the MIS19 era was similar to our own, so it’s a valid analogy, the researchers say.

The team applied their glacial inception fingerprinting method to MIS19, looking at ice core samples, plankton remains and debris that would have floated on the encroaching ice, and determined at what point the glacial inception would have started. Then they compared that time frame to the Holocene time frame.

“Taking the [current era] to MIS19c analogy to its logical conclusion implies that the current interglacial would be nearing its end,” the researchers write. If, that is, atmospheric CO2 levels were comparable to the MIS19 era. Which they aren't. This shows that while insolation is an important ingredient, apparently it’s not as potent an ice age determinant as CO2.

“The current insolation forcing and lack of new ice growth mean that orbital-scale variability will not be moderating the effects of anthropogenically induced global warming,” the authors conclude.

The paper is published in the early online version of Nature Geoscience.

Flatworm Flouts Fundamental Rule of Biology: Worm Regenerates Without Centrosome, a Structure Long Thought Necessary for Cell Division

The freshwater flatworm Schmidtea mediterranea lives in southern Europe and Northern Africa is the first animal ever discovered without a crucial structure inside its cells known as the centrosome. (Credit: UCSF/J. Azimzadeh)

Science Daily  — Reporting in the journal Science, researchers at the University of California, San Francisco (UCSF) and the Stowers Institute for Medical Research in Kansas City, MO, have discovered that the worm lacks a key cellular structure called a "centrosome," which scientists have considered essential for cell division.

Every animal ever examined, from the mightiest mammals to the lowliest insects, has these centrosomes in their cells.

"This is the first time we've found one that didn't," said Wallace Marshall, PhD, an associate professor in the Department of Biochemistry & Biophysics at UCSF, who led the research.

The fact that flatworms lack these centrosomes calls into question their purpose, Marshall added. "Clearly we have to rethink what centrosomes are actually doing," he said.

The Necessity of Even Division

A central component of all multicellular life is the ability of cells to divide -- and divide evenly. Before a cell divides, it has to assemble two exact copies of its DNA and then make sure that DNA sorts evenly into the two separate halves as they pinch off. Many health problems arise from cells losing this ability.

A hallmark of cancer, for instance, involves abnormalities in this division. Tumor cells often duplicate extra pieces of DNA. Certain forms of childhood mental retardation are also marked by abnormal divisions, which cause the loss of large pieces of DNA, leading to development problems in certain brain structures.

Centrosomes have been seen as animals' ultimate evolutionary fix for this problem. Plants and fungi don't have them, but animals have had centrosomes in their cells, as long as there have been animals. These structures were thought to play a central role in cell division -- laying down track-like spindles onto which the cells sort their dividing DNA. Centrosomes were seen as so important to cell division that all animals were assumed to have them.

The discovery that at least one animal doesn't came quite unexpectedly.

Interested in the basic mechanics of the centrosome, Marshall and UCSF postdoctoral researcher Juliette Azimzadeh, PhD, teamed up with Alejandro Sánchez Alvarado, PhD, a Howard Hughes Medical Institute and Stowers Institute investigator, who has worked with the flatworm Schmidtea mediterranea for several years.

Worm Regenerates Without Centrosomes

With a charming name that masks an otherwise humble appearance, this worm is a puddle wiggler just a few millimeters long at most. But its remarkable regenerative ability has made Schmidtea mediterranea a great scientific curiosity. When cut into tiny pieces, every piece will grow into a perfectly normal worm in a matter of days. Each offspring can then be segmented over and over again as well -- it's how the worm reproduces.

The original intention of the study Azimzadeh, Marshall and Sánchez Alvarado devised was to see what happened to the worm when it lost its centrosome.

Together they manipulated the flatworm to knock out genes needed to assemble these centrosomes. Without centrosomes the worms should have lost their ability to regenerate normally -- or so they thought.

They were amazed to find that losing these structures didn't affect the worms' ability to regenerate at all. Then they looked more carefully at the worms and discovered that they never had these centrosomes in the first place.

"It came as a surprise to all of us," said Sánchez Alvarado. What it means, he said, is that the evolutionary pressure that has maintained these structures in nearly all animals may have very little to do with cell division itself.

"There may be another function for centrosomes that is still obscured," he said.

The article, "Centrosome Loss in the Evolution of Planarians," by Juliette Azimzadeh, Mei Lie Wong, Diane Miller Downhour, Alejandro Sánchez Alvarado and Wallace F. Marshall, is published in Science Express on Jan. 5, 2012.

In addition to UCSF and the Stowers Institute, authors of this paper are affiliated with the University of Utah School of Medicine in Salt Lake City.

The work was supported in part by the Howard Hughes Medical Institute, the W.M. Keck Foundation and the National Institute of General Medical Sciences.

UCSF is a leading university dedicated to promoting health worldwide through advanced biomedical research, graduate-level education in the life sciences and health professions, and excellence in patient care.

Down to the Wire for Silicon: Researchers Create a Wire Four Atoms Wide, One Atom Tall

Wires just one atom tall have been created by inserting a string of phosphorus atoms in a silicon crystal by a team of researchers from the Univeristy of New South Wales, Melbourne Univeristy and Purdue University. This image from a computational simulation run of the wires shows electron density as electrons flow from left to right. The wires are 20 times smaller than the smallest wires now available and measure just four atoms wide by one phosphorus atom tall. (Credit: Purdue University image/Sunhee Lee, Hoon Ryu and Gerhard Klimeck)

Science Daily — The smallest wires ever developed in silicon -- just one atom tall and four atoms wide -- have been shown by a team of researchers from the University of New South Wales, Melbourne University and Purdue University to have the same current-carrying capability as copper wires.

Experiments and atom-by-atom supercomputer models of the wires have found that the wires maintain a low capacity for resistance despite being more than 20 times thinner than conventional copper wires in microprocessors.

The discovery, which was published in this week's journal Science, has several implications, including:

• For engineers it could provide a roadmap to future nanoscale computational devices where atomic sizes are at the end of Moore's law. The theory shows that a single dense row of phosphorus atoms embedded in silicon will be the ultimate limit of downscaling.
• For computer scientists, it places donor-atom based silicon quantum computing closer to realization.
• And for physicists, the results show that Ohm's Law, which demonstrates the relationship between electrical current, resistance and voltage, continues to apply all the way down to an atomic-scale wire.

Bent Weber, the paper's lead author and a graduate student in the Centre of Excellence for Quantum Computation and Communication Technology at the University of New South Wales, was thrilled with the finding.

"It's extraordinary to show that Ohm's Law, such a basic law, still holds even when constructing a wire from the fundamental building blocks of nature -- atoms," he says.

The innovation of the Australian group was to build the circuits up atom by atom, instead of the current method of building microprocessors, in which material is stripped away, says Gerhard Klimeck, a Purdue professor of electrical and computer engineering and director of the Network for Computational Nanotechnology.

"Typically we chip or etch material away, which can be very expensive, difficult and inaccurate," Klimeck says. "Once you get to 20 atoms wide you have atomic flucuations that make scaling difficult. But this experimental group built devices by placing atomically thin layers of phosphorus in silicon and found that with densely doped phosphorus wires just four atoms wide it acts like a wire that conducts just as well as metal."

The goal of the research is to develop future quantum computers in which single atoms are used for the computation, says Michelle Simmons, director of the Centre of Excellence for Quantum Computation and Communication Technology at the University of New South Wales and the project's principal investigator.

"We are on the threshold of making transistors out of individual atoms," Simmons says. "But to build a practical quantum computer we have recognized that the interconnecting wiring and circuitry also needs to shrink to the atomic scale."

Hoon Ryu, a Purdue graduate who is now a senior researcher with the Korea Institute of Science and Technology's Supercomputing Center, said the practicality of the research is exciting.

"The metallic wire is in principle quite difficult to be scaled into one- to two-nanometer pitch, but in both experimental and modeling views, the research result is quite remarkable," Ryu says. "For the first time, this demonstrates the possibility that densely doping wire is a viable alternative for the next-gerenation, ultra-scale metallic interconnect in silicon chips."

To assist the Australian researchers, Klimeck's research team ran hundreds of simulations to study the variability of these nanoscale structures.

"Having the throughput capability for a highly scalable code is important for doing that, and we have that capability here at Purdue with http://nanoHUB.org," Klimeck says. "We ran hundreds of cases to understand the potential landscape of these devices, so this was computationally intensive work."

Klimeck says that in addition to the project's scientific and engineering implications, he found the collaboration the most rewarding aspect.

"It is an exciting collaboration," he says. "We were doing simulations of experimental work, which was based on a theoretical model. So we were bringing the three legs of modern science together in one project. Plus, our graduate students are able to stay in contact and work with each other despite working in various locations around the world. It's hard to think of a better example of how science is done today."

Men and Women Have Major Personality Differences: New Report Suggests Previous Measurements Have Underestimated Variation Between the Sexes

 A new test has found that men and women have large differences in personality. (Credit: iStockphoto/David Marchal)

Science Daily  — Men and women have large differences in personality, according to a new study published Jan. 4 in the online journal PLoS ONE.

The researchers used personality measurements from more than 10,000 people, approximately half men and half women. The personality test included 15 personality scales, including such traits as warmth, sensitivity, and perfectionism. When comparing men's and women's overall personality profiles, which take multiple traits into account, very large differences between the sexes became apparent, even though differences look much smaller when each trait is considered separately.The existence of such differences, and their extent, has been a subject of much debate, but the authors of the new report, led by Marco Del Giudice of the University of Turin in Italy, describe a new method for measuring and analyzing personality differences that they argue is more accurate than previous methods.

However, the study indicates that previous methods to measure such differences have been inadequate, both because they focused on one trait at a time and because they failed to correct for measurement error.

The authors conclude that the true extent of sex differences in human personality has therefore been consistently underestimated.

Hybrid Silkworms Spin Stronger Spider Silk

Silk made with spider silk sequences. (Credit: Image courtesy of University of Notre Dame)                                                 Science Daily  — Research was published this week showing that silk produced by transgenically engineered silkworms in the laboratory of Malcolm Fraser Jr., professor of biological sciences at University of Notre Dame, exhibits the highly sought-after strength and elasticity of spider silk. This stronger silk could possibly be used to make sutures, artificial limbs and parachutes.

"It's something nobody has done before," Fraser says. The project, which used Fraser's piggyBac vectors to create transgenic silkworms with both silkworm and spider silk proteins, was a collaboration of his laboratory with Donald Jarvis and Randolph Lewis at the University of Wyoming. Jarvis' lab made the transgene plasmids, while Fraser's lab made the transgenic silkworms and Lewis' lab analyzed the fiber from the silkworms. Results showed that the fibers were tougher than typical silkworm silk and as tough as dragline silk fibers produced by spiders, demonstrating that silkworms can be engineered to produce such improved fibers.The findings were published in theProceedings of the National Academy of Sciences and highlighted for their breakthrough in the long search for silk with such mechanical properties. The manuscript was published after an in-depth peer review process, and was deemed by the publishers as a newsworthy article of the issue in which it appears, further indicating its relative importance to science and technology.

Commercial production of spider silk from spiders is impractical because spiders are too cannibalistic and territorial for farming. Researchers have experimented with producing the stronger material in other organisms, including bacteria, insects, mammals and plants, but those proteins require mechanical spinning -- a task the silkworms perform naturally. The stronger fiber could find application in sutures, where some natural silkworm silk is used, as well as wound dressings, artificial ligaments, tendons, tissue scaffolds, microcapsules, cosmetics and textiles.

This work is the culmination of a research effort begun more than 10 years ago with an internal award from Notre Dame to Fraser to develop silkworm transgenics capabilities; a two-year NIH R21 grant awarded to Jarvis, Lewis and Fraser; and several years of supplemental funding from Kraig BioCraft Laboratories. The success of this research would have been impossible without the ability to carry out silkworm transgenesis, mastered by Bong-hee Sohn and Young-soo Kim in the Fraser lab at Notre Dame.

Kraig Biocraft Laboratories Inc., with Fraser, Lewis and Jarvis on its scientific board, is currently evaluating several business opportunities for this first generation fiber for both textile and non-textile use. The researchers ultimately expect to improve on the first-generation product to make even stronger fibers.

Researchers have discovered the existence of neutrophils in the spleen

 by Biomechanism 

These neutrophils are there without there being any infection and play an immunoregulating role

For the first time, it has been discovered that neutrophils exist in the spleen without there being an infection. This important finding made by the research group on the Biology of B Cells of IMIM (Hospital del Mar Research Institute) in collaboration with researchers from Mount Sinai in New York, has also made it possible to determine that these neutrophils have an immunoregulating role.

Image of B lymphocytes (in blue) surrounded by neutrophils (in green) and endothelial cells (in red) of a human spleen. The image on the left side corresponds to a normal spleen and on the right side to a spleen of a patient with neutropenia, where the presence of neutrophils is much lower. Credit: IMIM (Hospital del Mar Research Institute)

Neutrophils are the so-called cleaning cells, since they are the first cells to migrate to a place with an infection and inflammation to destroy the pathogens. Until now, scientific literature had considered neutrophils essentially as lowly qualified soldiers that simply limited the expansion of an infection, as a first action to pave the way for other cells of the immune system in charge of eradicating the infection permanently.

“This study has revealed that neutrophils are found in the spleen without there being an infection, contributing totally new knowledge in the field of biology” explains Andrea Cerutti, the coordinator of the research group on the Biology of B Cells of IMIM, a professor at ICREA and the last signatory of the article.

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Researchers noticed that the existence of neutrophils in the spleen started when the fetus is developing, even when there is no infectious process involved; this was not known in scientific literature. The study was expanded to people of different ages and other mammals. Detecting the presence of neutrophils in the spleen suggested that these played a different role in the spleen to the one usually given to them.

The neutrophils in the spleen are located around B lymphocytes to help their activation and offer a first rapid response when there are pathogens. “through several different experimental approaches we have proven that neutrophils in the spleen acquire the ability to interact with B cells or B lymphocytes, inducing the production of antibodies, a role that lymphocytes circulating in blood are not able to do” states Irene Puga, researcher of the IMIM and a signatory of this article.

This finding improves the understanding of the mechanisms with which our immune system protects us against an infection, an essential requirement to better control all pathologies linked to it. Also, when faced with certain diseases, such as neutropenia (or a numeric deficiency of neutrophils), it will become necessary to study not only the deficiency of neturophils, but also how this affects the production of antibodies.

This work opens the door to therapies which are geared at, and more affective against, different pathogens, for example, to develop vaccines to increase the capacity of neutrophils in the spleen so as to have an incidence on the production of antibodies by type B lymphocytes.

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This study has been made possible thanks to the simples gathered mainly in different Catalan hospitals such as Hospital del Mar, Hospital Clínic, Hospital de la Vall d’Hebron and Hospital Sant Joan de Déu, together with other centres in the USA and Europe.

Reference article

“B–helper neutrophils stimulate immunoglobulin diversification and production in the marginal zone of the spleen” Irene Puga, Montserrat Cols, Carolina Barra, Bing He, Linda Cassis, Maurizio Gentile, Laura Comerma, Alejo Chorny, Meimei Shan, Weifeng Xu, Giuliana Magri, Daniel M.Knowles, Wayne Tam, April Chiu, James B Bussel, Sergi Serrano, José Antonio Lorente,Beatriz Bellosillo, Josep Lloreta, Nuria Juanpere, Francesc Alameda, Teresa Baró, Cristina Díaz de Heredia, Núria Torán, Albert Català, Montserrat Torrebadell, Claudia Fortuny,Victoria Cusi, Carmen Carreras, George A. Diaz, J. Magarian Blander, Claire-Michèle Farber, Guido Silvestri, Charlotte Cunningham-Rundles, Michaela Calvillo, Carlo Dufour, Lucia Dora Notarangelo, Vassilios Lougaris, Alessandro Plebani, Jean-Laurent Casanova, Stephanie C. Ganal, Andreas Diefenbach, Juan Ignacio Aróstegui, Manel Juan, Jordi Yagüe, Nizar Mahlaoui, Jean Donadieu, Kang Chen & Andrea Cerutti. Nature Immunology 2011

For further information

Rosa Manaut, head of communications at IMIM, Tel: +34 618 509 885 or Marta Calsina, Communication service at IMIM, Tel: +34 933 16 06 80.

A shot of young stem cells made rapidly aging mice live longer and healthier

 by Biomechanism 

Mice bred to age too quickly seemed to have sipped from the fountain of youth after scientists at the University of Pittsburgh School of Medicine injected them with stem cell-like progenitor cells derived from the muscle of young, healthy animals. Instead of becoming infirm and dying early as untreated mice did, animals that got the stem/progenitor cells improved their health and lived two to three times longer than expected, according to findings published in the Jan. 3 edition of Nature Communications.

Previous research has revealed stem cell dysfunction, such as poor replication and differentiation, in a variety of tissues in old age, but it’s not been clear whether that loss of function contributed to the aging process or was a result of it, explained senior investigators Johnny Huard, Ph.D., and Laura Niedernhofer, M.D., Ph.D. Dr. Huard is professor in the Departments of Orthopaedic Surgery and of Microbiology and Molecular Genetics, Pitt School of Medicine, and director of the Stem Cell Research Center at Pitt and Children’s Hospital of PIttsburgh of UPMC. Dr. Niedernhofer is associate professor in Pitt’s Department of Microbiology and Molecular Genetics and the University of Pittsburgh Cancer Institute (UPCI).

“Our experiments showed that mice that have progeria, a disorder of premature aging, were healthier and lived longer after an injection of stem cells from young, healthy animals,” Dr. Niedernhofer said. “That tells us that stem cell dysfunction is a cause of the changes we see with aging.” Continue reading below…

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Their team examined a stem/progenitor cell population derived from the muscle of progeria mice and found that compared to those from normal rodents, the cells were fewer in number, did not replicate as often, didn’t differentiate as readily into specialized cells and were impaired in their ability to regenerate damaged muscle. The same defects were discovered in the stem/progenitor cells isolated from very old mice.

“We wanted to see if we could rescue these rapidly aging animals, so we injected stem/progenitor cells from young, healthy mice into the abdomens of 17-day-old progeria mice,” Dr. Huard said. “Typically the progeria mice die at around 21 to 28 days of age, but the treated animals lived far longer – some even lived beyond 66 days. They also were in better general health.”

As the progeria mice age, they lose muscle mass in their hind limbs, hunch over, tremble, and move slowly and awkwardly. Affected mice that got a shot of stem cells just before showing the first signs of aging were more like normal mice, and they grew almost as large. Closer examination showed new blood vessel growth in the brain and muscle, even though the stem/progenitor cells weren’t detected in those tissues.

In fact, the cells didn’t migrate to any particular tissue after injection into the abdomen.

“This leads us to think that healthy cells secrete factors to create an environment that help correct the dysfunction present in the native stem cell population and aged tissue,” Dr. Niedernhofer said. “In a culture dish experiment, we put young stem cells close to, but not touching, progeria stem cells, and the unhealthy cells functionally improved.”

Animals that age normally were not treated with stem/progenitor cells, but the provocative findings urge further research, she added. They hint that it might be possible one day to forestall the biological declines associated with aging by delivering a shot of youthful vigor, particularly if specific rejuvenating proteins or molecules produced by the stem cells could be identified and isolated.

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Co-authors from the University of Pittsburgh include Mitra Lavasani, Ph.D., Aiping Lu, M.D., and Minjung Song, Ph.D., all of the Stem Cell Research Center and the Department of Orthopaedics; Andria Robinson, of UPCI and Pitt’s Graduate School of Public Health; Joseph M. Feduska and Bahar Ahani of the Stem Cell Research Center; Jeremy S. Tilstra, Ph.D., and Chelsea H. Feldman of Pitt’s Department of Microbiology and Molecular Genetics; and Paul D. Robbins, Ph.D., of the departments of Orthopaedic Surgery and Microbiology and Molecular Genetics, and UPCI.

The project was funded by grants ES016114, AG033907 and AR051456 from the National Institutes of Health and additional support from The Ellison Medical Foundation, the Henry J. Mankin Endowed Chair at the University of Pittsburgh, and the William F. and Jean W. Donaldson endowed chair at Children’s Hospital of Pittsburgh of UPMC.

Researchers discovers what triggers breast cancer to spread to other body parts

 by Biomechanism 

Research led by Shyamal Desai, PhD, Assistant Professor of Biochemistry and Molecular Biology at LSU Health Sciences Center New Orleans, has discovered a key change in the body’s defense system that increases the potential for breast cancer to spread to other parts of the body. The results, reported for the first time, are featured in the January 2012 issue of Experimental Biology and Medicine.

For cancer cells shape matters. All cells contain a protein cytoskeleton that acts as a scaffold determining overall shape and function, the position of the cell within an organ or tissue, and the ability of the cell to communicate with its neighbors to prevent the uncontrolled growth typical of cancer cells. However, cell transformations that result in cancer disrupt the genetic programs of the cell and alter the cytoskeleton, leading to changes in shape, function, and cell communication that produce uncontrolled growth and metastatic spreading of the tumor. Understanding these changes to the normal genetic program of a cell and the consequences that ultimately lead to cancer have been major challenges to cancer biologists.

This research, funded by the National Institutes of Health, found that a cellular defense system called the ISG15 pathway, which is normally involved in fighting bacterial and viral infection, is triggered in breast cancer to disrupt normal cytoskeletal function and increase the possibility that the cancer cells will metastasize, or spread.

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“Our findings, for the first time, causally link an alteration in the ISG15 pathway during transformation with metastatic potential,” notes Dr. Shyamal Desai, Assistant Professor of Biochemistry and Molecular Biology at LSU Health Sciences Center New Orleans, “thus providing a novel therapeutic target for future drug discovery.”

Cells contain a protein quality control pathway termed the Proteasome that breaks down damaged and unneeded proteins to their component amino acids for recycling. Such proteins are marked for degradation by flagging them with a small protein called Ubiquitin, which is then recognized by the Proteasome. Alterations in the genetic program that controls the Ubiquitin/Proteasome system have been known for some time to cause cell transformation and cancer. More recently, Dr. Desai and her colleagues have demonstrated that, unlike normal cells, transformed cancer cells produce increased amounts of a related control system that marks proteins with another small protein called ISG15.

Previous research reports that the amount of ISG15 is increased in high-grade compared with low-grade cancers. The ISG15 system is normally activated by interferon and is part of an ancient cellular immune response designed to counter bacterial and viral infection. By a still unidentified mechanism, cancer cell transformation activates the ISG15 pathway. Dr. Desai and colleagues have previously reported that activation of the ISG15 system interferes with function of the Ubiquitin/Proteasome pathway. In their latest work, Dr. Desai and colleagues show that several key proteins that regulate cell movement, invasion, and metastasis are blocked from Proteasome degradation by the ISG15 system and that genetic manipulation to inhibit this pathway reverses cancer cell transformation, suggesting an approach to blocking cancer progression.

Arthur Haas, PhD, the Roland Coulson Professor and Chairman of Biochemistry and Molecular Biology at LSU Health Sciences Center New Orleans, discovered the ISG15 pathway and co-discovered the Ubiquitin/Proteasome system that was awarded the 2004 Nobel Prize in Chemistry. “These results provide a functional link between the Ubiquitin and ISG15 pathways that reveals how small cell alterations can yield large overall consequences for cell transformation.”

The research team also included Arthur Haas, PhD, and Dr. Desai’s lab members Ryan Reed, Surendran Sankar, PhD, and Julian Burks in the LSUHSC Department of Biochemistry and Molecular Biology, Jerome Breslin, PhD, in the LSUHSC Department of Physiology, and Ashok Pullikuth, PhD, in the LSUHSC Department Pharmacology, as well as scientists at the UMDNJ-Robert Wood Johnson Medical School in New Jersey, and the University of Pennsylvania School of Medicine in Philadelphia.

“Although this current project focused on breast cancer, ISG15 is also elevated in a variety of cancers,” concludes Dr. Desai. “Therefore, this discovery has important implications in other cancers as well.”

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Courtesy LSU Health Sciences Center, New Orleans