Discovery Of New Proteasome Regulatory Mechanism May Have Implications For Neurodegenerative Diseases And Cancer

Main Category: Alzheimer's / Dementia
Also Included In: Cancer / Oncology;??Parkinson's Disease
Article Date: 03 Jul 2013 - 1:00 PDT Current ratings for:
Discovery Of New Proteasome Regulatory Mechanism May Have Implications For Neurodegenerative Diseases And Cancer

Dysfunction of the ubiquitin-proteasome system is related to many severe neurodegenerative diseases, such as Alzheimer's and Parkinson's diseases, and certain types of cancer. Such dysfunction is also believed to be related to some degenerative muscle diseases.

The proteasome is a large protein complex that maintains cellular protein balance by degrading and destroying damaged or expired proteins. The ubiquitin is a small protein that labels proteins for destruction for the proteasome. If the system does not work effectively enough, expired and damaged proteins accumulate in the cell. If the system is overly active, it destroys necessary proteins in addition to unnecessary ones. In both cases, cell function is disturbed, and the cell may even die.

Proteasome activity is believed to decrease with ageing. However, not much is yet known about how proteasome activity is regulated in an aging multicellular organism. The research team of Academy Research Fellow, Docent Carina Holmberg-Still has discovered an important proteasome regulatory mechanism. The study was published in Cell Reports , a highly esteemed scientific journal.

"We examined whether proteasome activity is affected by insulin/IGF-1 signalling [IIS], which regulates aging in many organisms. The results show that decreased IIS increases proteasome activity," says Holmberg-Still.

Proteasome activity was studied in C. elegans, a free-living roundworm. Decreased IIS increases proteasome activity through the FOXO transcription factor DAF-16 and the UBH-4 enzyme. DAF-16 represses the expression of ubh-4 in certain cell types. The ubh-4 enzyme slows proteasome activity, which means that its repression accelerates proteasome activity.

"Using a cell culture model, we proved that the same mechanism works in human cells," says Holmberg-Still. When the expression of the uchl5 enzyme - the human equivalent of ubh-4 - was decreased, proteasome activity and the degradation of harmful proteins increased.

"Our study shows that the effect of ageing and the related signalling pathway on proteasome activity is tissue-specific. This was a new and interesting discovery that bears great significance in terms of treatment opportunities," says researcher Olli Matilainen, who prepared his dissertation in Holmberg-Still's research team.

The identification of proteins that regulate proteasome activity and an understanding of the regulatory mechanism offer new opportunities in treating diseases that involve proteasome dysfunction. According to Holmberg-Still, proteins that regulate proteasome activity are particularly interesting in terms of medicine development.

"An ability to accelerate proteasome activity could be beneficial in the treatment of neurodegenerative diseases. Targeted proteasome inhibitors would be useful in the treatment of cancer - general proteasome inhibitors are already used as cancer medication to some extent, but they often have harmful side effects, because they cannot be targeted to a specific tissue."

Holmberg-Still's team continues to investigate tissue-specific mechanisms that regulate proteasome activity. The team collaborates with clinical researchers to confirm whether its research results can be refined for clinical use.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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Study Findings Could Lead To Treatments In Cancer, Neurological Diseases

Main Category: Cancer / Oncology
Also Included In: Parkinson's Disease;??Huntingtons Disease
Article Date: 08 May 2013 - 0:00 PDT Current ratings for:
Study Findings Could Lead To Treatments In Cancer, Neurological Diseases

Kansas State University scientists helped discover new details about an intricate process in cells. Their finding may advance treatments for cancer and neurological diseases.

Kansas State University researchers Jeroen Roelofs, assistant professor, and Chingakham Ranjit Singh, research assistant professor -- both in the Division of Biology -- led part of the study. Both also are research affiliates with the university's Johnson Cancer Research Center. They worked with colleagues at Harvard Medical School, the University of California-San Francisco and the University of Kansas. The scientific journal Nature recently published the team's observations, titled "Reconfiguration of the proteasome during chaperone-mediated assembly."

The research focused on proteasomes, protein complexes inside the cells of humans and other organisms that help keep the cells healthy.

"The proteasome is a large, molecular machine in the cell that degrades other proteins," Roelofs said. "It's important for protein quality control as well as for the cell's ability quickly remove specific proteins, thereby ensuring the cell's health and proper function."

The goal was to better understand how the various particles inside proteasomes work together to make the proteasomes function -- think the gears and components needed, and in what order, to build a working machine. Scientists believe that disruption of two key particles -- and consequently a proteasome's ability to work correctly -- has implications for cancers as well as various neurological degenerative diseases, such as Parkinson's and Huntington's diseases.

The Nature study built on research that Roelofs made as a postdoctoral research fellow at Harvard Medical School in 2009. He found that proteins called chaperones play a key role in the assembly process of two particles that when connected, gives proteasomes the ability to scrub unwanted proteins from cells. Chaperones act as a foreman for the two particles.

One of the findings in the new study is that in addition to acting as a molecular foreman for the two particles, chaperones also control when those two particles come together. Similarly, the scientists found more about the two particles.

The core particle has seven pockets while the regulatory particle has six tails that tuck into those pockets. When docked together, they turn on the proteasome's functionality.

"In the assembly process there is only one tail that actually determines how the core particle and regulatory particle bind together," Roelofs said. "That's surprising because there are six tails, but only one is needed to give specificity, and the docking into the pocket is controlled by the chaperone."

Roelofs believes that the findings may reveal new targets for anticancer drugs, as a chaperone in the human genes is involved in liver cancer. The proteasome inhibitor Bortezomib is used in the treatment of current cancers. Additionally, the information may advance cancer and neurological research by giving scientists new pathways to study and manipulate.

"This is pretty basic research," Roelofs said. "Understanding the basic mechanics can often lead to new pathways for improvement, which is essential when it comes to human health."

Scientists made the findings through a combination of techniques, including Cryo-electron microscopy, X-ray crystallography, yeast genetics, biochemical reconstitution assays and proteasome activity measurements. These techniques helped researchers observe the submicroscopic tails and complex tail-to-pocket binding process, as well as study the role of the chaperones in the core and regulatory particle process.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our cancer / oncology section for the latest news on this subject. The study was largely funded by the Centers of Biomedical Research Excellence Protein Structure and Function, or COBRE-psf, support center at the University of Kansas -- a multidisciplinary, biomedical research program funded by the National Institute of Health; the Johnson Cancer Research Center at Kansas State University; and the Kansas IDeA Network of Biomedical Research Excellence, or K-INBRE.

Kansas State University

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posted by Gabriel on 8 May 2013 at 8:06 am

On behalf of those who endure Huntington's disease, we give infinite graces to the investigators and to which favor the investigation. Thank you and they continue investigating, we beg it.

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'Study Findings Could Lead To Treatments In Cancer, Neurological Diseases'

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Understanding of complex diseases likely to improve following the unexpected discovery of the ways Cells Move

Main category: Cancer / Oncology
Also included in: respiratory / asthma;??Biology / biochemistry
Article Date: June 25, 2013 - 1:00 PDT current ratings for:
Understanding of complex diseases likely to improve following the unexpected discovery of the ways Cells Move

A new discovery about how cells move within the organization can provide scientists with crucial information about the mechanisms of diseases such as the spreading of the cancer or constriction of the Airways caused by asthma. Led by researchers from the Harvard School of Public Health (HSPH) and the Institute for bioengineering of Catalonia (IBEC), investigators found that the epithelial cells - the type that form a barrier between the inside and the outside of the body, such as skin cells - move group, powered by forces both of in and from neighbouring cells - to fill the empty spaces that they encounter.

The study appears in Nature Materials advanced online edition.

"We have tried to understand the fundamental relationship between cellular movements collective and collective forces of cell phones, which may occur during the invasion of the cancer cells, for example. But, in so doing, we are fallen on a phenomenon that was totally unexpected, "said lead author Jeffrey Fredberg, Professor of Bioengineering and physiology to the investigator HSPH Department of Environmental Health and co-Minister of HSPH molecular laboratory and integrative cellular dynamics.

Biologists, engineers and physicists at HSPH and IBEC worked together to shed light on the collective cell movement because it plays a key role in functions such as the healing of wounds, organ development and tumor growth. Using a technique called stress monolayer microscopy--which they invented themselves - they have measured the forces affecting a single layer of epithelial cells in motion. They examined cells speed and direction as traction - how certain cells either pull or push themselves and thus force the collective movement.

As they expected, the researchers found that when an obstacle was placed in the path of a layer of advanced cell - in this case, a gel that provided no traction - cells settled around him, closely hugging the sides of the gel as they passed. However, the researchers also found something amazing - cells, in addition to moving forward, continued to collectively back to frost, as if the desire to fill the space empty. Researchers have dubbed this movement "kenotaxis", Greek words "keno" (empty) and "taxi" (arrangement), because it seemed that cells are trying to fill a void.

This new discovery could help researchers to better understand the behaviour of the cell - and evaluate the potential influence that behavior - in a variety of complex diseases, such as cancer, asthma, cardiovascular diseases, developmental anomalies and glaucoma. The findings could also help with regenerative medicine and tissue engineering, which rely on cell migration.

In carcinomas, for example - who represent 90% of all cancers and involve epithelial cells - new information on cell movement could improve understanding of how cancer cells migrate through the body. Research on asthma could also get a boost, because scientists believe the migration of epithelial cells damaged in the lungs are involved in narrowing of the Airways caused by the disease.

"Kenotaxis is a property of the cell collective, not the individual cell," said Jae Hun Kim, first author of the study. "It was amazing to us that the collective cell can organize itself draw systematically in one direction while moving consistently in a quite different direction. ''

Article adapted by Medical News Today press release original. Click on "references" tab above for the source.
Visit our cancer / Oncology section for the latest news on this subject. Other authors HSPH included James Butler, senior lecturer on physiology in the Department of health environmental and investigator co-Minister of the laboratory; and researchers Dhananjay Tambe, Enhua Zhou Chan Young Park, Monirosadat Sadati, Park Jin-Ah, Bomi Gweon and Emil Millet.

Support for the study came from the Spanish Ministry of Science and Innovation (BFU2012-38146 FPU fellowship XS) and the Swiss National Science Foundation (PBEZP2-140047), the National Research Foundation of Korea (2012R1A6A3A03040450), the European Research Council (Grant Agreement 242993) Parker B. Francis (RK Fellowship), American Heart Association (13SDG14320004) and the National Institutes of Health (R01HL102373, R01HL107561).

"Propulsion and navigation within the advanced single layer sheet," Jae Hun Kim, Xavier Serra-Picamal, Dhananjay T. Tambe, Enhua H. Zhou, Chan Young Park, Monirosadat Sadati, Park Jin-Ah, Krishnan Ramaswamy, Bomi Gweon, Emil Millet, James P. Butler, Xavier Trepat, Jeffrey J. Fredberg, Nature of materials, online, June 23, 2013

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How Nerve Wiring Self-Destructs Has Relevance To Diseases Of Peripheral And Central Nervous Systems

Main Category: Neurology / Neuroscience
Also Included In: Lymphoma / Leukemia / Myeloma;??Cancer / Oncology
Article Date: 13 May 2013 - 0:00 PDT Current ratings for:
How Nerve Wiring Self-Destructs Has Relevance To Diseases Of Peripheral And Central Nervous Systems

Many medical issues affect nerves, from injuries in car accidents and side effects of chemotherapy to glaucoma and multiple sclerosis. The common theme in these scenarios is destruction of nerve axons, the long wires that transmit signals to other parts of the body, allowing movement, sight and sense of touch, among other vital functions.

Now, researchers at Washington University School of Medicine in St. Louis have found a way the body can remove injured axons, identifying a potential target for new drugs that could prevent the inappropriate loss of axons and maintain nerve function.

"Treating axonal degeneration could potentially help a lot of patients because there are so many diseases and conditions where axons are inappropriately lost," says Aaron DiAntonio, MD, PhD, professor of developmental biology. "While this would not be a cure for any of them, the hope is that we could slow the progression of a whole range of diseases by keeping axons healthy."

DiAntonio is senior author of the study that appears online in the journal Cell Reports.

While axonal degeneration appears to be a major culprit in diseases like multiple sclerosis, it also paradoxically plays an important role in properly wiring the nervous systems of developing embryos.

"When an embryo is building its nervous system, there can be inappropriate or excessive axonal sprouts, or axons that are only needed at one time in development and not later," DiAntonio says. "These axons degenerate, and that's very important for wiring the nervous system. And in adult organisms, it might be useful to have a clean and quick way to remove a damaged axon from a healthy nerve, instead of letting it decay and potentially damage its neighboring axons."

DiAntonio compares the process to programmed cell death, or apoptosis, which is also important in embryonic development. Apoptosis culls unnecessary or damaged cells from the body. If cell death programs become overactive, they can kill healthy cells that should remain. And if apoptosis fails to destroy damaged cells in adults, it can lead to cancer.

The new discovery also underscores the relatively recent understanding that loss of axons is not a passive decay process resulting from injury. Just as apoptosis actively destroys cells, axonal degeneration results from a cellular program that actively removes the damaged axon. In certain diseases, the program may be inappropriately triggered.

"We want to understand axonal degeneration at the same level that we understand programmed cell death, in the hopes of developing drugs to block the process when it becomes overactive," DiAntonio says.

DiAntonio's major collaborators in this project include Jeffrey D. Milbrandt, MD, PhD, the James S. McDonnell Professor and head of the Department of Genetics, and first author Elisabetta Babetto, PhD, postdoctoral research scholar.

Studying mice, the researchers found that a gene called Phr1 plays a major role in governing the self-destruction of injured axons. When they removed Phr1 from adult mice, the severed portion of the axons remained intact for much longer than in genetically normal mice.

In the normal mice, a severed axon degenerated entirely after two days. In mice without Phr1, they found that about 75 percent of the severed axons remained at five days, with a quarter persisting at least 10 days after being cut. The mice showed no side effects and suffered no obvious problems due to the missing Phr1.

The findings raise the possibility that blocking the Phr1 protein with a drug could keep damaged axons alive and functional when the body would normally cause the axons to self-destruct.

DiAntonio emphasizes that he is not trying to save axons that have no connection to the rest of the nerve. The paradigm is simply a good way to model nerve injury. In many instances, such as a crush injury or disease processes in which the axon is not severed, blocking the Phr1 protein could potentially preserve an attached axon that would otherwise self-destruct.

Importantly, the research team also looked at optic nerves of the central nervous system, which are damaged in glaucoma, and found similar protective effects from the loss of Phr1.

"This is not the first gene identified whose loss protects mammalian axons from degeneration," DiAntonio says. "But it is the first one that shows evidence of working in the central nervous system. So it could be important in conditions like glaucoma, multiple sclerosis and other neurodegenerative diseases where the central nervous system is the primary problem."

DiAntonio also points out possible ways to help cancer patients. Many chemotherapy drugs cause damage to peripheral axons, which may limit the doses a patient can tolerate.

As part of the new study, the researchers showed that intact axons without Phr1 were protected from the damage caused by vincristine, a chemotherapy drug used to treat leukemia, neuroblastoma, Hodgkin's disease and non-Hodgkin's lymphoma, among other cancers.

"In this case, the loss of axons is not caused by disease," DiAntonio says. "It's caused by the drug doctors are giving. You know the date it will start. You know the date it will stop. This is probably where I am most optimistic that we could make an impact."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our neurology / neuroscience section for the latest news on this subject. This work was supported by the American-Italian Cancer Foundation, the European Molecular Biology Organization, the Muscular Dystrophy Association and the National Institutes of Health (NIH) grant numbers DA020812, NS065053 and NS078007.
Babetto E, Beirowski B, Russler EV, Milbrandt J, DiAntonio A. The Phr1 ubiquitin ligase promotes injury-induced axon self-destruction. Cell Reports. May 9, 2013.
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Gene-Silencing Activity Discovery Could Lead To Treatment For Viral Infections, Cancers And Other Diseases

Main Category: Infectious Diseases / Bacteria / Viruses
Also Included In: Cancer / Oncology;??Genetics
Article Date: 13 May 2013 - 0:00 PDT Current ratings for:
Gene-Silencing Activity Discovery Could Lead To Treatment For Viral Infections, Cancers And Other Diseases

A team led by scientists at The Scripps Research Institute (TSRI) has found how to boost or inhibit a gene-silencing mechanism that normally serves as a major controller of cells' activities. The discovery could lead to a powerful new class of drugs against viral infections, cancers and other diseases.

"Learning to control natural gene silencing processes will allow an entirely new approach to treating human disease," said Ian J. MacRae, assistant professor in TSRI's Department of Integrative Structural and Computational Biology and principal investigator for the study, which appears as the cover story in the May 9, 2013 issue of the journal Molecular Cell.

A Scientific Mystery and Technical Conundrum

The gene-silencer in question is Argonaute 2, a molecular machine in cells that can grab and destroy the RNA transcripts of specific genes, preventing them from being translated into proteins. Argonaute 2 and other Argonaute proteins regulate the influence of about a third of the genes found in humans and other mammals - and thus are among the most important modulators of our cells' day-to-day activities. Argonautes' gene-silencing functions also help cells cope with rogue genetic activity from invading viruses or cancer-promoting DNA mutations.

Yet Argonautes' workings are complex and not yet entirely understood. For example, before it starts a search-and-destroy mission against a specific type of target RNA, an Argonaute 2 protein takes on board a target-recognition device: a short length of "guide RNA," also known as a microRNA (miRNA). The miRNA's sequence is mostly complementary to the target RNA's - a sort of chemical mirror-image - so that it can stick tightly to it.

But how do an Argonaute protein and its miRNA guide, having formed their partnership, manage to part company? It has been a scientific mystery and technical conundrum for researchers, who have found it hard to separate Argonaute proteins from miRNAs in the lab dish.

"That problem led us to look for a way to get Argonautes to unload these miRNAs," said Nabanita De, a postdoctoral fellow in MacRae's laboratory who was first author of the new study.

Matches and Mismatches

In an initial set of experiments, the team demonstrated that when an miRNA hooks up with an Argonaute 2, the pair do remain locked together and functioning for an exceptionally long time: days to weeks, whereas solo miRNA normally is degraded within minutes.

Yet prior studies by other laboratories have hinted at the existence of mechanisms that can hasten the separation of miRNAs from Argonautes. Some viruses, for example, produce decoy target RNAs that virtually nullify the activity of the corresponding miRNAs, seemingly by destabilizing the miRNA-Argonaute pairing. A key feature of these decoy target RNAs is that they make an almost perfect complementary match to the miRNAs - especially at one end of the miRNAs, known as the three-prime or 3' end. In this respect, they match the miRNAs much better than the natural gene transcripts that the miRNAs evolved to target.

De confirmed that decoy RNAs designed to match miRNAs this way can greatly hasten the miRNAs' "unloading" from Argonautes, thus effectively dialing down these miRNAs' normal gene-silencing activities. By contrast, mismatches at the 3' end delayed unloading, enhancing the gene-silencing activity.

Why do these matches and mismatches have such effects on the miRNA-Argonaute pairing? The mechanisms aren't obvious. But De noted that mismatches at the opposite end of miRNAs - the 5' end - have the opposite effect. "Targets with 5'-end mismatches are actually better at unloading miRNAs from Argonaute," she said.

"The next thing we're trying to figure out is how all that works," said MacRae. "We have some guesses but no clear answer."

In a study reported last year, MacRae's laboratory used X-ray crystallography to determine the first high-resolution atomic structure of an Argonaute 2-miRNA complex. Now the team is working on a structural study of the complex as it grabs a target RNA. "When we can see the structural details of that interaction, then I think we'll have a much better handle on this loading and unloading process," said MacRae.

Many Potential Applications

Scientists already have begun developing gene-silencing drugs that work like miRNAs; they are taken up by Argonaute proteins as guide RNAs and lead to the silencing of targeted gene transcripts. Pharmaceutical companies also are developing drugs that bind directly to miRNAs to inhibit their activity. The findings here suggest a new and, in principle, more powerful class of miRNA inhibitors/enhancers, aimed at destabilizing or stabilizing the miRNA-Argonaute complex.

"I can think of many applications for these," said MacRae. "One of the most obvious would be against hepatitis C virus, which requires a certain miRNA in liver cells for efficient replication; an RNA-based drug that speeds up the unloading of this virus-enhancing miRNA would be a powerful approach for shutting down the virus."

A better understanding of the miRNA loading and unloading process also should lead to better miRNA-type drugs, he added.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our infectious diseases / bacteria / viruses section for the latest news on this subject. Other contributors to the study, "Highly Complementary Target RNAs Promote Release of Guide RNAs from Human Argonaute 2," were Lisa Young, Nicole-Claudia Meisner and David V. Morrissey of the Novartis Institutes for Biomedical Research, and Pick-Wei Lau of the MacRae laboratory at TSRI.
The study was funded by the National Institutes for Health (grant R01 GM086701).
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