Researchers at the University of Maryland School of Medicine have found a "nose within the nose," a unique olfactory system within the noses of mice that is able to "smell" hormones involved in regulating water and salt balance in the body. This research may lead to new insights into the complex system of "chemical communication" between individuals. The findings are published in the Proceedings of the National Academy of Sciences, USA online early edition.
"The sense of smell provides an important way for humans and animals to interact with their environment, as well as with other members of their species," says Steven Munger, Ph.D., associate professor of anatomy and neurobiology at the University of Maryland School of Medicine and lead author on the paper. "It allows animals to detect food and determine that food's quality, it provides social information like sexual status about other animals, and it can warn an animal when a predator is present. Because of the great similarities between humans and animals when it comes to the sense of smell, the more we learn about the building blocks of the system, the more we will learn about how odors affect our lives."
The noses of mice and most other mammals contain both a main and accessory olfactory system. These two systems work together to detect general odors, including food odors, as well as pheromones, which carry important social information between members of the same species. However, previous work had suggested that a third group of olfactory cells in the nose, named "GC-D neurons" for their expression of the molecule GC-D, might play a unique role in sensing the odor environment.
To investigate these novel cells in the nose, Dr. Munger, graduate student Renee Cockerham, and their colleagues engineered a line of mice in which GC-D neurons were specifically labeled, making them easier to identify and characterize. In some mice, the GC-D gene was also "knocked out" completely, allowing the cells to be turned off. They then asked what odors might activate GC-D cells by exposing them to various compounds present in mouse urine.
"Urine contains a rich mixture of social signals for animals, including odors that communicate information about sex, dominance and genetic identity," says Dr. Munger. "We found that GC-D neurons responded to peptide hormones, such as uroguanylin and guanylin, found in the urine. These hormones are known to be involved in regulating fluid and salt balance in the body. Additionally, we found that the GC-D molecule itself is required for the neurons to respond to those hormones, which means that, in the absence of GC-D, these animals are 'blind' to these odors."
"This is evidence of an entirely different olfactory system mixed in with the main system in mice," says Dr. Munger. "It carries a very specific type of odor information that may communicate hormonal states between individuals. It's basically a 'nose within the nose.'"
According to Dr. Munger, animals may be able to detect the metabolic state of other animals by using this olfactory subsystem. "This system may tell a mouse that his brother needs a drink and that they must look for water or that another mouse has just had a big meal so food must be nearby," he says. "Throughout human evolution and for most wild animals today, food and water are scarce resources that need to be detected. This olfactory system is a mechanism by which these types of communication can occur."
The GC-D system is unlikely to be functional in humans because of a disruption in a necessary gene. "Even though this specific system may not be functional in humans, it is clear that a number of other ones involved in chemical communication between individuals are present and working," says Dr. Munger. "Having a better understanding of the complexity of chemical communication across all mammals will give us important insights into how humans use their sense of smell. Odors not only enrich the experience of tasting wine, for example, but enrich our interactions with each other."
The study was done in collaboration with Drs. Trese Leinders-Zufall and Frank Zufall of the University of Saarland in Germany, Drs. Stylianos Michalakis and Martin Biel of the Ludwig-Maximilians University in Germany, Dr. David Garbers of the University of Texas-Southwestern Medical Center and Dr. Randall Reed of Johns Hopkins University.
Source: Rebecca Ceraul
University of Maryland Medical Center
вторник, 30 августа 2011 г.
суббота, 27 августа 2011 г.
Research On Enzyme For Activating Promising Disease-Fighters Co-Authored By Middle School Students
Grown-ups aren't the only ones making exciting scientific discoveries these days. Two middle school students from Wisconsin joined a team of scientists who are reporting the first glimpse of the innermost structure of a key bacterial enzyme. It helps activate certain antibiotics and anti-cancer agents so that those substances do their job. Their study appears in ACS' weekly journal Biochemistry. The student co-authors of the study are from Edgewood Campus Middle School in Madison and participated in Project CRYSTAL, a special program that provides middle school students with hands-on laboratory experience.
In the report, study leader Hazel Holden and colleagues note intense scientific interest in a chemical process called methylation, which increases the activity of DNA, proteins, and other substances in the body by transferring methyl (CH3) groups to them. Special enzymes called methyltransferases make methylation possible, and these proteins are very important in a myriad of key biological processes.
Holden and colleagues studied a bacterial methyltransferase involved in the production of tetronitrose, a component of the promising anti-cancer agent, tetrocarcin, and the antibiotic kijanimicin. The methyltransferase seems to play a key role in activating these disease-fighters. The scientists identified the 3D structure of this methyltransferase, a key step in determining how it works and how it might be modified for potential use in medicine.
Article: "Molecular Architecture of a C-3'-Methyltransferase Involved in the Biosynthesis of D-Tetronitrose"
Source:
Michael Bernstein
American Chemical Society
In the report, study leader Hazel Holden and colleagues note intense scientific interest in a chemical process called methylation, which increases the activity of DNA, proteins, and other substances in the body by transferring methyl (CH3) groups to them. Special enzymes called methyltransferases make methylation possible, and these proteins are very important in a myriad of key biological processes.
Holden and colleagues studied a bacterial methyltransferase involved in the production of tetronitrose, a component of the promising anti-cancer agent, tetrocarcin, and the antibiotic kijanimicin. The methyltransferase seems to play a key role in activating these disease-fighters. The scientists identified the 3D structure of this methyltransferase, a key step in determining how it works and how it might be modified for potential use in medicine.
Article: "Molecular Architecture of a C-3'-Methyltransferase Involved in the Biosynthesis of D-Tetronitrose"
Source:
Michael Bernstein
American Chemical Society
среда, 24 августа 2011 г.
Stretch A DNA Loop, Turn Off Proteins
It may look like mistletoe wrapped around a flexible candy cane. But this molecular model shows how some proteins form loops in DNA when they chemically attach, or bind, at separate sites to the double-helical molecule that carries life's genetic blueprint.
Biologists have discovered that the physical manifestation of DNA loops are a consequence of many biochemical processes in the cell, such as the regulation of gene expression. In other words, these loops indicate the presence of enzymes or other proteins that are turned on. Now physicists at the University of California, San Diego have discovered that stretching the DNA molecule can also turn off the proteins known to cause loops in DNA
"We showed that certain enzymes acting on DNA could be switched off or on simply by applying a small amount of mechanical tension across the DNA molecule," said Douglas Smith, an assistant professor of physics at UCSD who headed the team that published the discovery in the December issue of the Biophysical Journal. "We showed this by mechanically manipulating and stretching single DNA molecules. This switching effect could provide a molecular mechanism for cells to be able to sense and respond to mechanical stresses that they may normally experience. Such stresses could be generated internally by the cells themselves, such as when the cell undergoes changes in shape during the cell cycle, or as external stresses from the environment."
The amount of tension or stretching that needs to be applied to the molecule is extremely small, Smith added, only one pico-Newton, or one-trillionth of the force generated by the weight of an apple.
Other members of the UCSD team were Gregory Gemmen, a physics graduate student, and Rachel Millin, a laboratory assistant. The study was supported by grants from the Burroughs Wellcome Fund, Kinship Foundation and Arnold and Mabel Beckman Foundation.
Contact: Kim McDonald
University of California - San Diego
Biologists have discovered that the physical manifestation of DNA loops are a consequence of many biochemical processes in the cell, such as the regulation of gene expression. In other words, these loops indicate the presence of enzymes or other proteins that are turned on. Now physicists at the University of California, San Diego have discovered that stretching the DNA molecule can also turn off the proteins known to cause loops in DNA
"We showed that certain enzymes acting on DNA could be switched off or on simply by applying a small amount of mechanical tension across the DNA molecule," said Douglas Smith, an assistant professor of physics at UCSD who headed the team that published the discovery in the December issue of the Biophysical Journal. "We showed this by mechanically manipulating and stretching single DNA molecules. This switching effect could provide a molecular mechanism for cells to be able to sense and respond to mechanical stresses that they may normally experience. Such stresses could be generated internally by the cells themselves, such as when the cell undergoes changes in shape during the cell cycle, or as external stresses from the environment."
The amount of tension or stretching that needs to be applied to the molecule is extremely small, Smith added, only one pico-Newton, or one-trillionth of the force generated by the weight of an apple.
Other members of the UCSD team were Gregory Gemmen, a physics graduate student, and Rachel Millin, a laboratory assistant. The study was supported by grants from the Burroughs Wellcome Fund, Kinship Foundation and Arnold and Mabel Beckman Foundation.
Contact: Kim McDonald
University of California - San Diego
воскресенье, 21 августа 2011 г.
RNA Binding Proteins At Heart Of Problem In Myotonic Dystrophy Type 1
A new mouse model for myotonic dystrophy -- the most common form of adult-onset muscular dystrophy -- helped Baylor College of Medicine researchers show that levels of CUGBP1, a protein that binds and controls the activity of the genetic material RNA, increase early in affected cells of the animals with the disease. This means CUGBP1 plays a key role in the disorder.
"We wanted to find out if this is a primary event associated with the disorder or if it is a secondary response to tissue injury," said Dr. Thomas A. Cooper, professor of pathology at BCM and senior author of the report that appears in the Journal of Clinical Investigation.
Myotonic dystrophy type 1 is associated with hundreds and even thousands of repeats of the nucleotides CTG within a gene called DM kinase protein gene or DMPK. [Cytosine (C), thymine (T), guanine (G) and adenine (A) are all nucleotides that make up DNA. C, G, A, and uracil (U) make up RNA.] In the mouse that Cooper and his colleagues specially bred, the repeats in the gene can be turned on in heart, skeletal muscle and brain tissue at any age.
The researchers found that within three hours of turning on the repeats, another RNA-binding protein called muscleblind like (MBNL) began to bind the genetic material in the nucleus of the cell. That mean the RNA was trapped in the nucleus and unable to take the genetic message about which proteins to make to the protein manufacturing areas in the cytoplasm of the cell.
Within six hours, levels of CUGBP1 begin to increase. The increased in CUGBP1 then alters how a number of other genes are regulated. At that point, the cascade of events that affect the heart starts.
"The heart doesn't even 'know' that it is sick yet," said Cooper. This finding shows that the increase levels of CUGBP1 is an early event and plays an important role in the development of the disease.
Others who took part in this research include Drs. Guey-Shin Wang, Debra L. Kearney, Mariella De Biasi and George Taffet, all of BCM. Funding for this research came from the National Institutes of Health and the Muscular Dystrophy Association.
Source: Graciela Gutierrez
Baylor College of Medicine
"We wanted to find out if this is a primary event associated with the disorder or if it is a secondary response to tissue injury," said Dr. Thomas A. Cooper, professor of pathology at BCM and senior author of the report that appears in the Journal of Clinical Investigation.
Myotonic dystrophy type 1 is associated with hundreds and even thousands of repeats of the nucleotides CTG within a gene called DM kinase protein gene or DMPK. [Cytosine (C), thymine (T), guanine (G) and adenine (A) are all nucleotides that make up DNA. C, G, A, and uracil (U) make up RNA.] In the mouse that Cooper and his colleagues specially bred, the repeats in the gene can be turned on in heart, skeletal muscle and brain tissue at any age.
The researchers found that within three hours of turning on the repeats, another RNA-binding protein called muscleblind like (MBNL) began to bind the genetic material in the nucleus of the cell. That mean the RNA was trapped in the nucleus and unable to take the genetic message about which proteins to make to the protein manufacturing areas in the cytoplasm of the cell.
Within six hours, levels of CUGBP1 begin to increase. The increased in CUGBP1 then alters how a number of other genes are regulated. At that point, the cascade of events that affect the heart starts.
"The heart doesn't even 'know' that it is sick yet," said Cooper. This finding shows that the increase levels of CUGBP1 is an early event and plays an important role in the development of the disease.
Others who took part in this research include Drs. Guey-Shin Wang, Debra L. Kearney, Mariella De Biasi and George Taffet, all of BCM. Funding for this research came from the National Institutes of Health and the Muscular Dystrophy Association.
Source: Graciela Gutierrez
Baylor College of Medicine
четверг, 18 августа 2011 г.
The Effect On Muscle Repair And Regeneration Of Cholesterol-Lowering Drugs
Statins are powerful drugs that reduce "bad" cholesterol and thus cut the risk of a heart attack. While these medications offer tremendous benefits to millions, they can carry side effects for some. The most frequently reported consequence is fatigue, and about nine percent of patients report statin-related pain. Both can be exacerbated when statin doses are increased, or physical activity is added. The results of a new study may offer another note of caution for high-dose statin patients. Working with primary human satellite cell cultures, researchers have found that statins at higher doses may affect the ability of the skeletal muscles - which allow the body to move - to repair and regenerate themselves.
The study is entitled "Simvastatin Reduces Human Primary Satellite Cell Proliferation in Culture." It was conducted by Anna Thalacker-Mercer, Melissa Baker, Chris Calderon and Marcas Bamman, University of Alabama at Birmingham. They will discuss their findings at the American Physiological Society (APS; The-APS) conference, The Integrative Biology of Exercise V. The meeting is being held September 24-27, 2008 in Hilton Head, SC.
The Study
Statins have been reported to have adverse effects on skeletal muscle in both human and animal models causing cramping and fatigue and potentially myopathy. Relatively little is known regarding the effect of statins on the muscle progenitor cells (i.e., satellite cells (SC)) which play a key role in skeletal muscle repair and regeneration following exercise or injury. SC remain in a quiescent state until stimulated to proliferate. Statins are known to have antiproliferative effects in other cell types and therefore may inhibit or effect this critical step in muscle repair. Thus it is important to understand the influence of statins on SC function which may further affect the overall health and physiology of human skeletal muscle..
The study examined the proliferative capacity of human satellite cells in culture, which were exposed, to a lipophilic statin: simvastatin. The aim of the study was to determine SC viability during proliferation when treated with statins which may be indicative of the ability of SCs to undergo mitosis (i.e. divide to make new cells).
The research team used primary cell lines isolated from quadriceps muscle biopsies. SC were mixed and grown for 48 hours with several concentrations of statin: 0.0, 0 plus the solvent DMSO (control), 0.05, 0.1, 1.0, 10, or 100ВµM. The MTS assay was utilized to measure cell viability/reproducibility.
Additionally the investigators determined the effects of varying concentrations of simvastatin on SCs in different states (i.e., undergoing differentiation or differentiated into myotubes).
Key Findings
The researchers found the following:
There was a dose dependent decrease in the viability of the satellite cells at 1.0, 10 and 100ВµM concentrations of simvastatin. At approximately 5.0 ВµM concentration the viability of the proliferating cells was reduced by 50% (equivalent to the availability of simvastatin in circulation from a 40 milligram dose per day used in some patients). Specifically, the higher end concentrations led to reduced SC proliferation, which would likely negatively affect the muscle's ability to heal and/or repair itself.
There was no change in the viability of satellite cells at concentrations of 0.05 or 0.1ВµM.
Cell viability was reduced by approximately half in differentiating cells and myotubes with concentrations of 1.0 and 5.0 ВµM, respectively.
Next Steps
According to Dr. Thalacker-Mercer, a member of the research team, "While these are preliminary data and more research is necessary, the results indicate serious adverse effects of statins that may alter the ability of skeletal muscle to repair and regenerate due to the anti-proliferative effects of statins."
Looking ahead, she added, "We are very interested in these effects in the older population. It is possible that older adults may not be able to distinguish between muscle pain related to a statin effect or an effect of aging and therefore adverse effects of statins in older adults may be under-reported. Therefore, our next step is to examine statins among older adults."
Physiology is the study of how molecules, cells, tissues and organs function to create health or disease. The American Physiological Society (APS; The-APS/press) has been an integral part of this discovery process since it was established in 1887.
The APS Conference, The Integrative Biology of Exercise V, is being held September 24-27, 2008 in Hilton Head, SC.
Source: Donna Krupa
American Physiological Society
The study is entitled "Simvastatin Reduces Human Primary Satellite Cell Proliferation in Culture." It was conducted by Anna Thalacker-Mercer, Melissa Baker, Chris Calderon and Marcas Bamman, University of Alabama at Birmingham. They will discuss their findings at the American Physiological Society (APS; The-APS) conference, The Integrative Biology of Exercise V. The meeting is being held September 24-27, 2008 in Hilton Head, SC.
The Study
Statins have been reported to have adverse effects on skeletal muscle in both human and animal models causing cramping and fatigue and potentially myopathy. Relatively little is known regarding the effect of statins on the muscle progenitor cells (i.e., satellite cells (SC)) which play a key role in skeletal muscle repair and regeneration following exercise or injury. SC remain in a quiescent state until stimulated to proliferate. Statins are known to have antiproliferative effects in other cell types and therefore may inhibit or effect this critical step in muscle repair. Thus it is important to understand the influence of statins on SC function which may further affect the overall health and physiology of human skeletal muscle..
The study examined the proliferative capacity of human satellite cells in culture, which were exposed, to a lipophilic statin: simvastatin. The aim of the study was to determine SC viability during proliferation when treated with statins which may be indicative of the ability of SCs to undergo mitosis (i.e. divide to make new cells).
The research team used primary cell lines isolated from quadriceps muscle biopsies. SC were mixed and grown for 48 hours with several concentrations of statin: 0.0, 0 plus the solvent DMSO (control), 0.05, 0.1, 1.0, 10, or 100ВµM. The MTS assay was utilized to measure cell viability/reproducibility.
Additionally the investigators determined the effects of varying concentrations of simvastatin on SCs in different states (i.e., undergoing differentiation or differentiated into myotubes).
Key Findings
The researchers found the following:
There was a dose dependent decrease in the viability of the satellite cells at 1.0, 10 and 100ВµM concentrations of simvastatin. At approximately 5.0 ВµM concentration the viability of the proliferating cells was reduced by 50% (equivalent to the availability of simvastatin in circulation from a 40 milligram dose per day used in some patients). Specifically, the higher end concentrations led to reduced SC proliferation, which would likely negatively affect the muscle's ability to heal and/or repair itself.
There was no change in the viability of satellite cells at concentrations of 0.05 or 0.1ВµM.
Cell viability was reduced by approximately half in differentiating cells and myotubes with concentrations of 1.0 and 5.0 ВµM, respectively.
Next Steps
According to Dr. Thalacker-Mercer, a member of the research team, "While these are preliminary data and more research is necessary, the results indicate serious adverse effects of statins that may alter the ability of skeletal muscle to repair and regenerate due to the anti-proliferative effects of statins."
Looking ahead, she added, "We are very interested in these effects in the older population. It is possible that older adults may not be able to distinguish between muscle pain related to a statin effect or an effect of aging and therefore adverse effects of statins in older adults may be under-reported. Therefore, our next step is to examine statins among older adults."
Physiology is the study of how molecules, cells, tissues and organs function to create health or disease. The American Physiological Society (APS; The-APS/press) has been an integral part of this discovery process since it was established in 1887.
The APS Conference, The Integrative Biology of Exercise V, is being held September 24-27, 2008 in Hilton Head, SC.
Source: Donna Krupa
American Physiological Society
понедельник, 15 августа 2011 г.
Liposome finding implies electrical effect on cell development
Experiments with liposomes - cell-like "water balloons" composed of artificially created phospholipid bilayers similar to
natural cell membranes - have revealed unexpected behavior in the presence of electrical fields that may provide a
paradigm-shifting change in science's understanding of biomembrane function in operating living systems.
Arizona State University chemists Mark Hayes and Michele Pysher have found that liposomes have a tendency to form tube-like
extensions in their membranes through the influence of local electrical fields. In particular, the surprising finding of such
electrically caused bionanotubule formation may reveal a previously unknown process involved in the development of structures
like axons and dendrites in nerve cells.
Hayes will present the results of the experiments at a 2 p.m. March 15 session entitled "Colloids in Complex Fluids" at the
American Chemical Society meeting in San Diego.
In the experiments, the researchers placed liposomes in a droplet of water and applied very low electric fields (5-10 volts
per centimeter), much lower than the fields present in operating neurons (a fraction of a volt but operating over a very
short distance--less than a micron--to produce a field up to one thousand times stronger). In images achieved through optical
and scanning electron microscopy, microtubules were observed to immediately form and extend from the phospholipid balloon,
like a seed putting forth a stalk or root.
Hayes believes that the phenomena may have significant implications for both cellular biology and for nanotechnology. "This
finding might not only be important in its application to understanding life processes, but it has a potentially exciting
practical application in the fabrication of bionanotubes," he said.
Source: Mark Hayes, 480-965-2566; 480-620-0193 (cell)
Images/video: bionanotubes.homestead
Contact: James Hathaway
hathawayasu
480-965-6375
Arizona State University
asu/asunews
natural cell membranes - have revealed unexpected behavior in the presence of electrical fields that may provide a
paradigm-shifting change in science's understanding of biomembrane function in operating living systems.
Arizona State University chemists Mark Hayes and Michele Pysher have found that liposomes have a tendency to form tube-like
extensions in their membranes through the influence of local electrical fields. In particular, the surprising finding of such
electrically caused bionanotubule formation may reveal a previously unknown process involved in the development of structures
like axons and dendrites in nerve cells.
Hayes will present the results of the experiments at a 2 p.m. March 15 session entitled "Colloids in Complex Fluids" at the
American Chemical Society meeting in San Diego.
In the experiments, the researchers placed liposomes in a droplet of water and applied very low electric fields (5-10 volts
per centimeter), much lower than the fields present in operating neurons (a fraction of a volt but operating over a very
short distance--less than a micron--to produce a field up to one thousand times stronger). In images achieved through optical
and scanning electron microscopy, microtubules were observed to immediately form and extend from the phospholipid balloon,
like a seed putting forth a stalk or root.
Hayes believes that the phenomena may have significant implications for both cellular biology and for nanotechnology. "This
finding might not only be important in its application to understanding life processes, but it has a potentially exciting
practical application in the fabrication of bionanotubes," he said.
Source: Mark Hayes, 480-965-2566; 480-620-0193 (cell)
Images/video: bionanotubes.homestead
Contact: James Hathaway
hathawayasu
480-965-6375
Arizona State University
asu/asunews
пятница, 12 августа 2011 г.
People Also Have Antiviral 'Plant Defences'
In addition to known antiviral agents such as antibodies and interferons, people also seem to have a similar immune system to that previously identified in plants. This is the result of research carried out by Esther Schnettler at Wageningen University. Together with the group of Professor Ben Berkhout of the Academic Medical Centre (AMC) in Amsterdam, Schnettler discovered that a protein used by plant viruses to bypass plant resistance can also impair the defence against HIV viruses in people. Schnettler's findings may open up new opportunities for improving health.
Plants defend themselves against viruses by attacking, deactivating and breaking down genetic material in a process called RNA silencing. Viruses try to bypass this defence by producing proteins that block it. Schnettler researched the functioning of these silencing suppressor proteins in plants, recognising that the improvement of plant defences would enable more sustainable cultivation by reducing the need for chemical pesticides to combat insects and pathogens.
Schnettler also studied whether the silencing suppressor proteins that allow plant viruses to bypass plant defences could also have an influence on our immunity systems. We know that antibodies can detect the protein shells of viruses, which allow them to be broken down. Our bodies also protect themselves against viruses by releasing interferons that give a sign to cells to die, preventing the viruses within those cells from multiplying or spreading.
In cooperation with a group of scientists from the AMC, Schnettler found that HIV mutants which are unable to produce a specific protein (making it almost impossible for them to multiply) can start multiplying up to wild type virus titer levels when a silencing suppressor protein from a plant virus is added. This seems to suggest that people also have the defence against viruses used by plants against intruders and which detects and deactivates the genetic material of the HIV virus.
"The research has helped us to understand that the process of RNA silencing seems to be a widely occurring antiviral defence," says Schnettler. "Our findings could offer new opportunities for developing antiviral medication. This is not yet certain, however, as the RNA silencing process in the human body has (additional) other functions that must not be impaired by medicines."
Sources: Wageningen University and Research Centre, AlphaGalileo Foundation.
Plants defend themselves against viruses by attacking, deactivating and breaking down genetic material in a process called RNA silencing. Viruses try to bypass this defence by producing proteins that block it. Schnettler researched the functioning of these silencing suppressor proteins in plants, recognising that the improvement of plant defences would enable more sustainable cultivation by reducing the need for chemical pesticides to combat insects and pathogens.
Schnettler also studied whether the silencing suppressor proteins that allow plant viruses to bypass plant defences could also have an influence on our immunity systems. We know that antibodies can detect the protein shells of viruses, which allow them to be broken down. Our bodies also protect themselves against viruses by releasing interferons that give a sign to cells to die, preventing the viruses within those cells from multiplying or spreading.
In cooperation with a group of scientists from the AMC, Schnettler found that HIV mutants which are unable to produce a specific protein (making it almost impossible for them to multiply) can start multiplying up to wild type virus titer levels when a silencing suppressor protein from a plant virus is added. This seems to suggest that people also have the defence against viruses used by plants against intruders and which detects and deactivates the genetic material of the HIV virus.
"The research has helped us to understand that the process of RNA silencing seems to be a widely occurring antiviral defence," says Schnettler. "Our findings could offer new opportunities for developing antiviral medication. This is not yet certain, however, as the RNA silencing process in the human body has (additional) other functions that must not be impaired by medicines."
Sources: Wageningen University and Research Centre, AlphaGalileo Foundation.
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