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Ferrarelli L.K.,Science Signaling | Gough N.R.,Science Signaling
Science Signaling | Year: 2017

The proteins that regulate cell proliferation, metastatic potential, survival in circulation, and immune evasion represent most of the targets for therapeutic intervention in cancer. Furthermore, genomic profiling of just the cancer cells leaves critical information about the tumor microenvironment in the dark. The articles highlighted in this Focus Issue describe efforts to translate genomic data into knowledge of aberrant signaling that can be therapeutically targeted and strategies to explore not only the changes that occur in the protein landscape of the tumors but also in the protein profiles of the tumor microenvironment. © 2017 The Authors, some rights reserved.


News Article | May 19, 2017
Site: www.sciencedaily.com

Johns Hopkins researchers say they have identified a new way that cells in the brain alert the rest of the body to recruit immune cells when the brain is injured. The work was completed in mouse models that mimic infection, stroke or trauma in humans. Investigators already knew there was a communication highway between the brain and the immune system but have been unclear about how exactly how the brain sends signals to the immune system. While immune system cells' purpose is to defend and protect the body, ironically the brain's "call to arms" may cause more harm than good when it instructs immune cells to enter into the brain. The persistence of these cells can cause chronic inflammation and damage the brain. In their new study, described in Science Signaling April 13, Johns Hopkins researchers say there is evidence that vesicles or small (about the size of a virus), fat-like molecules and protein-filled sacks released from a type of immune cell in the brain called astrocytes travel through the bloodstream to the liver. The liver then instructs white blood cells to go to the site of injury in the brain. "This work describes an entirely new way that the brain talks with the body," says Norman Haughey, Ph.D., professor of neurology at the Johns Hopkins University School of Medicine. "Identifying this pathway has helped us pinpoint ways to impede this process and reduce brain damage brought on by the body's own excessive immune response." Because of the work of several other collaborators, Haughey says, his team knew that some sort of inflammation-promoting molecule was released from brain and targeted to the liver after brain injury to send immune system cells to the damaged area, but the identity of this go-between had been elusive for years. The questions remained of what the signal was, and how, exactly, the signal got all the way to the liver from the brain, particularly since the blood-brain barrier prevents many molecules in the brain from crossing over into the rest of the body, just as it prevents molecules from getting into the brain. The team focused on an enzyme called neutral sphingomyelinase, known as nSMase2, which they knew from a separate project was turned on by an immune system chemical messenger, a cytokine interleukin 1-beta (IL-1b) that promotes inflammation. Sphingomyelinases like nSMase2 play a normal role in the cell's metabolism by breaking down fatty molecules into smaller components that cells use for every day functions. To see if possibly nSMase2 was also involved in alerting the immune system during brain injury, the researchers mimicked brain injury in mice by injecting cytokine IL-1b into the striatum, a structure found in the deep center of the brain. As a comparison group, they injected saline (saltwater) in the same brain area of other mice. They also injected the mouse brains with both the cytokine IL-1b and a drug called altenusin that blocks the nSMase enzyme from working. Twenty-four hours after the injection, the researchers saw large numbers of immune system white blood cells in tissue samples of the rodent brains near the site of injury of those mice injected with the cytokine IL-1b, but not in the brain tissue of the control group of mice. In addition, they no longer saw the same large influx of white blood cells into the brain when they used the drug that inhibited nSMase, with the number of white blood cells in the brain dropping by about 90 percent. This finding told the researchers of nSMase2's involvement but still didn't tell them about the signal sent from the brain to activate the body's immune response. According to Haughey, after many failed experiments to determine the brain's messenger, he visited his colleague and collaborator Daniel Anthony at Oxford University, who introduced him to the concept of "exosomes" -- miniature vesicles released from cells. "That conversation was the 'Ah-ha' moment when it all began to make sense," says Haughey. He read earlier studies showing that the enzyme nSMase2 was required for forming and releasing exosomes. Exosomes form inside cell compartments and release outside the cell when these compartments fuse with the cell's surrounding membrane. Exosomes are surrounded by bits of cell membrane and filled with proteins and different types of the genetic material RNA. To test that exosomes were the source of this brain to body communication, Haughey's research team isolated exosomes from the blood of mice four hours after injecting the cytokine IL-1b into brain and then injected the exosomes into the tail veins of different mice that had the cytokine and the nSMase-blocking drug altenusin already in their brains. The researchers found that white blood cells in healthy mice who received exosomes from the blood of the mice with brain damage traveled to the site of brain injury, which the researchers say demonstrates that exosomes released from brain in response to damage alert the immune system to send the immune cell sentinels to the brain. When they stripped the vesicles of protein and their genetic cargo and injected them back into mice, the blood cells no longer went to the site of brain injury. Finally, the researchers analyzed the protein and genetic material contents of the exosomes in an effort to identify the molecules inside that alerted the immune system to brain damage. They found 10 unique proteins and 23 microRNAs -- short bits of RNA that don't code for genes -- at increased levels in the vesicles. Several of these components had connections to a specific mechanism used by the liver to activate inflammation. "Given the therapeutic potential of the nSMase target, we're now working closely with Drs. Barbara Slusher, Camilo Rojas, Ajit Thomas and colleagues at the Johns Hopkins Drug Discovery facility to identify potent inhibitors of the nSMase enzyme which can be developed for clinical use," says Haughey.


News Article | May 18, 2017
Site: www.eurekalert.org

Johns Hopkins researchers say they have identified a new way that cells in the brain alert the rest of the body to recruit immune cells when the brain is injured. The work was completed in mouse models that mimic infection, stroke or trauma in humans. Investigators already knew there was a communication highway between the brain and the immune system but have been unclear about how exactly how the brain sends signals to the immune system. While immune system cells' purpose is to defend and protect the body, ironically the brain's "call to arms" may cause more harm than good when it instructs immune cells to enter into the brain. The persistence of these cells can cause chronic inflammation and damage the brain. In their new study, described in Science Signaling April 13, Johns Hopkins researchers say there is evidence that vesicles or small (about the size of a virus), fat-like molecules and protein-filled sacks released from a type of immune cell in the brain called astrocytes travel through the bloodstream to the liver. The liver then instructs white blood cells to go to the site of injury in the brain. "This work describes an entirely new way that the brain talks with the body," says Norman Haughey, Ph.D., professor of neurology at the Johns Hopkins University School of Medicine. "Identifying this pathway has helped us pinpoint ways to impede this process and reduce brain damage brought on by the body's own excessive immune response." Because of the work of several other collaborators, Haughey says, his team knew that some sort of inflammation-promoting molecule was released from brain and targeted to the liver after brain injury to send immune system cells to the damaged area, but the identity of this go-between had been elusive for years. The questions remained of what the signal was, and how, exactly, the signal got all the way to the liver from the brain, particularly since the blood-brain barrier prevents many molecules in the brain from crossing over into the rest of the body, just as it prevents molecules from getting into the brain. The team focused on an enzyme called neutral sphingomyelinase, known as nSMase2, which they knew from a separate project was turned on by an immune system chemical messenger, a cytokine interleukin 1-beta (IL-1b) that promotes inflammation. Sphingomyelinases like nSMase2 play a normal role in the cell's metabolism by breaking down fatty molecules into smaller components that cells use for every day functions. To see if possibly nSMase2 was also involved in alerting the immune system during brain injury, the researchers mimicked brain injury in mice by injecting cytokine IL-1b into the striatum, a structure found in the deep center of the brain. As a comparison group, they injected saline (saltwater) in the same brain area of other mice. They also injected the mouse brains with both the cytokine IL-1b and a drug called altenusin that blocks the nSMase enzyme from working. Twenty-four hours after the injection, the researchers saw large numbers of immune system white blood cells in tissue samples of the rodent brains near the site of injury of those mice injected with the cytokine IL-1b, but not in the brain tissue of the control group of mice. In addition, they no longer saw the same large influx of white blood cells into the brain when they used the drug that inhibited nSMase, with the number of white blood cells in the brain dropping by about 90 percent. This finding told the researchers of nSMase2's involvement but still didn't tell them about the signal sent from the brain to activate the body's immune response. According to Haughey, after many failed experiments to determine the brain's messenger, he visited his colleague and collaborator Daniel Anthony at Oxford University, who introduced him to the concept of "exosomes" -- miniature vesicles released from cells. "That conversation was the 'Ah-ha' moment when it all began to make sense," says Haughey. He read earlier studies showing that the enzyme nSMase2 was required for forming and releasing exosomes. Exosomes form inside cell compartments and release outside the cell when these compartments fuse with the cell's surrounding membrane. Exosomes are surrounded by bits of cell membrane and filled with proteins and different types of the genetic material RNA. To test that exosomes were the source of this brain to body communication, Haughey's research team isolated exosomes from the blood of mice four hours after injecting the cytokine IL-1b into brain and then injected the exosomes into the tail veins of different mice that had the cytokine and the nSMase-blocking drug altenusin already in their brains. The researchers found that white blood cells in healthy mice who received exosomes from the blood of the mice with brain damage traveled to the site of brain injury, which the researchers say demonstrates that exosomes released from brain in response to damage alert the immune system to send the immune cell sentinels to the brain. When they stripped the vesicles of protein and their genetic cargo and injected them back into mice, the blood cells no longer went to the site of brain injury. Finally, the researchers analyzed the protein and genetic material contents of the exosomes in an effort to identify the molecules inside that alerted the immune system to brain damage. They found 10 unique proteins and 23 microRNAs -- short bits of RNA that don't code for genes -- at increased levels in the vesicles. Several of these components had connections to a specific mechanism used by the liver to activate inflammation. "Given the therapeutic potential of the nSMase target, we're now working closely with Drs. Barbara Slusher, Camilo Rojas, Ajit Thomas and colleagues at the Johns Hopkins Drug Discovery facility to identify potent inhibitors of the nSMase enzyme which can be developed for clinical use," says Haughey. To view the video that accompany this release please click here. Additional authors on the paper include Alex Dickens, Luis Tovar-y-Romo, Seung-Wan Yoo, Amanda Trout, Mihyun Bae, Marlene Kanmogne, Kenneth Witwer, Nino Tabatadze, and Robert Cole of Johns Hopkins Medicine; Bezawit Megra, Dionna Williams and Joan Berman of Albert Einstein College of Medicine; Mar Gacias and Patrizia Casaccia of Mount Sinai; and Daniel Anthony of University of Oxford. The study was supported by grants from the National Institute of Mental Health (R01 MH077542, R01 MH096636, R03 MH103985, P01 MH075673, R01 MH075679, R01 MH090958 and R21 MH102112).


News Article | May 18, 2017
Site: www.biosciencetechnology.com

Johns Hopkins researchers say they have identified a new way that cells in the brain alert the rest of the body to recruit immune cells when the brain is injured. The work was completed in mouse models that mimic infection, stroke or trauma in humans. Investigators already knew there was a communication highway between the brain and the immune system but have been unclear about how exactly how the brain sends signals to the immune system. While immune system cells’ purpose is to defend and protect the body, ironically the brain’s “call to arms” may cause more harm than good when it instructs immune cells to enter into the brain. The persistence of these cells can cause chronic inflammation and damage the brain. In their new study, described in Science Signaling April 13, Johns Hopkins researchers say there is evidence that vesicles or small (about the size of a virus), fat-like molecules and protein-filled sacks released from a type of immune cell in the brain called astrocytes travel through the bloodstream to the liver. The liver then instructs white blood cells to go to the site of injury in the brain. “This work describes an entirely new way that the brain talks with the body,” said Norman Haughey, Ph.D., professor of neurology at the Johns Hopkins University School of Medicine. “Identifying this pathway has helped us pinpoint ways to impede this process and reduce brain damage brought on by the body’s own excessive immune response.” Because of the work of several other collaborators, Haughey says, his team knew that some sort of inflammation-promoting molecule was released from brain and targeted to the liver after brain injury to send immune system cells to the damaged area, but the identity of this go-between had been elusive for years. The questions remained of what the signal was, and how, exactly, the signal got all the way to the liver from the brain, particularly since the blood-brain barrier prevents many molecules in the brain from crossing over into the rest of the body, just as it prevents molecules from getting into the brain. The team focused on an enzyme called neutral sphingomyelinase, known as nSMase2, which they knew from a separate project was turned on by an immune system chemical messenger, a cytokine interleukin 1-beta (IL-1b) that promotes inflammation. Sphingomyelinases like nSMase2 play a normal role in the cell’s metabolism by breaking down fatty molecules into smaller components that cells use for every day functions. To see if possibly nSMase2 was also involved in alerting the immune system during brain injury, the researchers mimicked brain injury in mice by injecting cytokine IL-1b into the striatum, a structure found in the deep center of the brain. As a comparison group, they injected saline (saltwater) in the same brain area of other mice. They also injected the mouse brains with both the cytokine IL-1b and a drug called altenusin that blocks the nSMase enzyme from working. Twenty-four hours after the injection, the researchers saw large numbers of immune system white blood cells in tissue samples of the rodent brains near the site of injury of those mice injected with the cytokine IL-1b, but not in the brain tissue of the control group of mice. In addition, they no longer saw the same large influx of white blood cells into the brain when they used the drug that inhibited nSMase, with the number of white blood cells in the brain dropping by about 90 percent. This finding told the researchers of nSMase2’s involvement but still didn’t tell them about the signal sent from the brain to activate the body’s immune response. According to Haughey, after many failed experiments to determine the brain’s messenger, he visited his colleague and collaborator Daniel Anthony at Oxford University, who introduced him to the concept of “exosomes” — miniature vesicles released from cells. “That conversation was the ‘Ah-ha’ moment when it all began to make sense,” said Haughey. He read earlier studies showing that the enzyme nSMase2 was required for forming and releasing exosomes. Exosomes form inside cell compartments and release outside the cell when these compartments fuse with the cell’s surrounding membrane. Exosomes are surrounded by bits of cell membrane and filled with proteins and different types of the genetic material RNA. To test that exosomes were the source of this brain to body communication, Haughey’s research team isolated exosomes from the blood of mice four hours after injecting the cytokine IL-1b into brain and then injected the exosomes into the tail veins of different mice that had the cytokine and the nSMase-blocking drug altenusin already in their brains. The researchers found that white blood cells in healthy mice who received exosomes from the blood of the mice with brain damage traveled to the site of brain injury, which the researchers say demonstrates that exosomes released from brain in response to damage alert the immune system to send the immune cell sentinels to the brain. When they stripped the vesicles of protein and their genetic cargo and injected them back into mice, the blood cells no longer went to the site of brain injury. Finally, the researchers analyzed the protein and genetic material contents of the exosomes in an effort to identify the molecules inside that alerted the immune system to brain damage. They found 10 unique proteins and 23 microRNAs — short bits of RNA that don’t code for genes — at increased levels in the vesicles. Several of these components had connections to a specific mechanism used by the liver to activate inflammation. “Given the therapeutic potential of the nSMase target, we’re now working closely with Drs. Barbara Slusher, Camilo Rojas, Ajit Thomas and colleagues at the Johns Hopkins Drug Discovery facility to identify potent inhibitors of the nSMase enzyme which can be developed for clinical use,” said Haughey.


News Article | May 23, 2017
Site: www.eurekalert.org

Inflammation is the process by which the body responds to injury or infection but when this process becomes out of control it can cause disease. Monash Biomedicine Discovery Institute (BDI) researchers, in collaboration with the Monash Institute of Pharmaceutical Sciences (MIPS), have shed light on a key aspect of the process. Their findings may help guide the development of new treatments of inflammatory diseases such as atherosclerosis, which can lead to heart attack or stroke, and type 2 diabetes. Published today in the journal Science Signaling, the research reveals how certain proteins cause the white blood cells that play a central role in inflammatory responses to behave in different ways. White blood cells are beneficial in helping to eliminate invading microorganisms or repair damaged tissue, but they can prolong the response and damage healthy tissues, leading to disease. The proteins, called chemokines, are secreted into blood vessels and activate chemokine receptors embedded in the outer membranes of the white blood cells. While it was previously thought that this occurred like an on-off switch, the scientists found that the chemokine receptor can behave more like a 'dimmer switch' with one chemokine giving a strong signal and another giving a weaker signal. They found that different responses can be caused by different chemokines activating the same receptor. This explained for the first time the mechanism by which white blood cells produced varying responses: a strong short-lived response (acute inflammation) or a steady, longer-lived response (chronic inflammation). "Until now, we did not understand how this was possible," said co-lead author Associate Professor Martin Stone. "Our work has identified the specific features of chemokines and receptors that are involved in their inflammatory activity," Associate Professor Stone said. "The ultimate goal is to develop anti-inflammatory drugs that target these molecules," he said. The findings, which Associate Professor Stone presented at an international conference on cell signalling last week, will have wide implications as the proteins involved are essential to all inflammatory diseases. Associate Professor Stone, who heads a laboratory in the Infection and Immunity Program at the Monash BDI collaborated closely with co-lead author Dr Meritxell Canals from MIPS. First author was PhD student Mrs Zil E. Huma. This research was supported by the Australian National Health and Medical Research Council, the Australian Research Council, Monash University and ANZ Trustees. Read the full paper titled Key determinants of selective binding and activation by the monocyte chemoattractant proteins at the chemokine receptor CCR2 Committed to making the discoveries that will relieve the future burden of disease, the newly established Monash Biomedicine Discovery Institute at Monash University brings together more than 120 internationally-renowned research teams. Our researchers are supported by world-class technology and infrastructure, and partner with industry, clinicians and researchers internationally to enhance lives through discovery.


News Article | May 24, 2017
Site: www.medicalnewstoday.com

Inflammation is the process by which the body responds to injury or infection but when this process becomes out of control it can cause disease. Monash Biomedicine Discovery Institute (BDI) researchers, in collaboration with the Monash Institute of Pharmaceutical Sciences (MIPS), have shed light on a key aspect of the process. Their findings may help guide the development of new treatments of inflammatory diseases such as atherosclerosis, which can lead to heart attack or stroke, and type 2 diabetes. Published in the journal Science Signaling, the research reveals how certain proteins cause the white blood cells that play a central role in inflammatory responses to behave in different ways. White blood cells are beneficial in helping to eliminate invading microorganisms or repair damaged tissue, but they can prolong the response and damage healthy tissues, leading to disease. The proteins, called chemokines, are secreted into blood vessels and activate chemokine receptors embedded in the outer membranes of the white blood cells. While it was previously thought that this occurred like an on-off switch, the scientists found that the chemokine receptor can behave more like a 'dimmer switch' with one chemokine giving a strong signal and another giving a weaker signal. They found that different responses can be caused by different chemokines activating the same receptor. This explained for the first time the mechanism by which white blood cells produced varying responses: a strong short-lived response (acute inflammation) or a steady, longer-lived response (chronic inflammation). "Until now, we did not understand how this was possible," said co-lead author Associate Professor Martin Stone. "Our work has identified the specific features of chemokines and receptors that are involved in their inflammatory activity," Associate Professor Stone said. "The ultimate goal is to develop anti-inflammatory drugs that target these molecules," he said. The findings, which Associate Professor Stone presented at an international conference on cell signalling last week, will have wide implications as the proteins involved are essential to all inflammatory diseases. Associate Professor Stone, who heads a laboratory in the Infection and Immunity Program at the Monash BDI collaborated closely with co-lead author Dr Meritxell Canals from MIPS. First author was PhD student Mrs Zil E. Huma. This research was supported by the Australian National Health and Medical Research Council, the Australian Research Council, Monash University and ANZ Trustees. Article: Key determinants of selective binding and activation by the monocyte chemoattractant proteins at the chemokine receptor CCR2, Martin J. Stone et al., Science Signaling, doi: 10.1126/scisignal.aai8529, published 23 May 2017.


News Article | May 3, 2017
Site: www.biosciencetechnology.com

Even though fragile X syndrome is the most common genetic cause of autism and intellectual disability, no treatments have been discovered to address the disorder. Akiko Hata, Ph.D., professor in the Department of Biochemistry & Biophysics in the Cardiovascular Research Institute at the University of California, San Francisco, and author of a new study, told Bioscience Technology that the difficulty of drug discovery for fragile X syndrome (FXS) stems from a lack of a drug screen platform to perform an unbiased screen of compounds that can improve intellectual and cognitive disabilities associated with FXS. FXS is caused by changes in the fragile X mental retardation 1 (FMR1) gene. The FMR1 gene usually makes a protein called fragile X mental retardation protein (FMRP), which is needed for normal brain development.  However, people with FXS don’t make this protein. Although FXS is a disease that’s caused by a single defective gene and FMR1 knock out mice and rats provide a decent animal model, the behavioral tests are variable and not suited for large scale screenings of compounds, Hata explained. Now, Hata and colleagues have developed a new crawling assay using mutated fruit fly larvae and an open-source application called LarvaTrack that they say provide a quick, reproducible and cost-effective way of uncovering potential treatments for FXS. Along with being an economical and fast assay, it is also adaptable to higher throughput screening, Hata said.  It allowed the researchers to monitor the effect of drugs on synaptic growth by examining highly accessible synapse at the neuromuscular junction (NMJ). The NMJ is a chemical synapse and is where a motor neuron is able to transmit a signal to the muscle fiber, causing muscle contraction. Patients with FXS have neuronal abnormalities, and in addition to developmental delays and learning disabilities, they often show symptoms of anxiety and hyperactivity. The disease, on average, affects 1 in 5,000 individuals. In the new study, scientists used fruit fly larvae with mutations in the FMR1 gene.  They showed that the flies exhibited hyperactivity similar to that presented in humans with FXS, by crawling at a faster speed and farther than control larvae. The fly models also had analogous neurological defects as seen in humans. With the researchers’ new application LarvaTrack, the team could track the crawling path in up to 15 flies at the same time, and calculate crawling distance and velocity using video recorded with an iPhone camera. Hata said the team estimates that the current system would make the screening of up to a few thousand compounds feasible. The tool was used to show that a new drug candidate reduced hyperactivity in mutant larvae and caused them to crawl at rates similar to control flies. “We previously identified that FMRP encoded by the FMR1 gene inhibits the translation of the receptor for bone morphogenetic protein family of cytokines,” Hata said. “Both in FXS patients and FMR1-null mouse brain, BMPR2 and the downstream signaling molecules, LIM domain kinase 1 (LIMK1) is aberrantly activated compared to healthy controls.” For this study, the team tested the effect of three different LIMK1 antagonists. In addition to reversing the crawling phenotype in the fly model of FXS, the team showed that the neuronal abnormalities at the NMJ could also be reversed by administering LIMK1 antagonists. In a mouse model of FXS, Hata and colleagues showed that one of the LIMK1 antagonists tested was able to improve the abnormality in the central nervous neuron morphology, as well as reverse hyperactivity and memory defects. The researchers believe coupled together, their fly assay and new application will aid drug discovery for FXS. When it comes to the biggest takeaway for this study, Hata said: “The molecular pathway underlying the development of neuronal abnormalities in FXS is conserved from insect to human. We could use Drosophila model of FXS as a primary screening platform to find a cure for the disease.” Up next, the researchers plan to adapt the fruit fly crawling assay to a high-throughput, fully automated small molecule library screen that combines feeding a compound to an individual larva and recording the crawling behavior individually. Hata noted that since 2008 there have been more than 20 clinical trials for the treatment of FXS, but many had to be halted prematurely either due to side effects or the inability to show efficacy. “There is a strong need of a large-scale unbiased screen of compounds instead of traditional approaches of identifying FMRP target gene first, followed by a generation of compounds that inhibit the FMRP target,” she said. The findings were reported May 2 in Science Signaling.


Foley J.F.,Science Signaling
Science Signaling | Year: 2013

This Focus Issue of Science Signaling, which complements the Science Special Issue on Inflammation, includes research that reveals regulators of a receptor implicated in an inflammatory bowel disease, as well as the contribution of a matrix metalloproteinase to skin inflammation. Perspectives discuss the role of proinflammatory cytokines in brain inflammatory disorders and the regulation of multiple types of cell death in tissues in response to proinflammatory factors. Together with content from the Science Signaling Archives, these articles underline the importance of understanding the basis of inflammatory responses that can both protect and harm the host. © 2013 American Association for the Advancement of Science.


Gough N.R.,Science Signaling
Science Signaling | Year: 2015

With contributions from the Board of Reviewing Editors and the Chief Scientific Editor, Science Signaling highlights some common concerns surrounding repro-ducibility and issues related to appropriate methodological considerations for accurately quantifying and then modeling regulatory phenomena. Specific topics include sources of error, understanding biological "n" and the application of appropriate statistical analyses, quantitative Western blotting, quantitative mass spectrometry-based proteomics, and parameterization for establishing quantitative models of cellular networks.


Adler E.M.,Science Signaling
Science Signaling | Year: 2010

Nominations for this year's signaling breakthroughs spanned physiology, therapeutics and drug development, neuroscience, and plant signaling. Among the most exciting advances in mammalian biology were therapeutic applications of research that are overturning the conventional boundaries of signaling pathways, unexpected mechanisms to prolong life and prevent aging, new insights into schizophrenia and memory, development of a transgenic primate model, and the discovery that the cells in the lungs can "taste" noxious substances. In plant signaling, the nominations converged on the identification of the elusive receptor for the plant stress hormone abscisic acid. Finally, methodological advances were also noted with new techniques in synthetic biology enabling the precise spatiotemporal control of signaling events and increasingly facile methods for creation and analysis of proteomic data yielding tremendous increases in raw data and insights into cellular regulation. Copyright 2008 by the American Association for the Advancement of Science; all rights reserved.

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