ALBERT

Description: Yemaya No. 63, dated May 2021, features articles from US, The Netherlands, Myanmar, Senegal, and an article on women in fisheries and human rights. The article from the US by Linda Behnken argues that a growing coalition of small-scale, community-based fishers is calling for the recognition and protection of Alaska’s invaluable coastal fisheries during COVID-19. The article from the Netherlands by Cornelie Quist looks at the challenges facing women engaged in small-scale fishing and supplying fish through retailers and how they found new ways to directly reach consumers. The conversation between Miranda Bout and Cornelie Quist focuses on how they combined new product development with the use of social media to contact their customer base during the pandemic-induced disruption of traditional marketing chains. The article by Elena Finkbeiner, Juno Fitzpatrick and Whitney Yadao-Evans looks at recent media revelations and scientific research that have brought increased attention to human-rights violations and the myriad social issues facing fisheries, but with a disproportionate focus on labour-rights violations at sea and in industrial fishing operations. The systemic inequalities combined with the effects of COVID-19 exacerbated vulnerabilities of women to health risks, food and livelihood security. The article from Senegal by Aby Dia from Lumière Synergie pour le Développement (LSD), in collaboration with WoMin African Alliance, South Africa, narrates the story of traditional women fish processors from the Bargny who have been, for more than a decade, struggling against development projects that jeopardise their environment, health and livelihoods. In order to preserve their livelihoods, women processors in Senegal have come together to oppose the Tosyali steel project. The European Network of Women in Fisheries and Aquaculture in Europe (AKTEA) urges the Office of the Commissioner for the Environment, Oceans and Fisheries to integrate gender into all aspects of European fishing policy. The Profile column looks at how Linda Behnken became a fisher in Alaska and how fishing has shaped her individuality and work. Natalie Sattler says that fishing for halibut, sablefish and salmon from the sparkling waters of the Pacific along with her children and at the same time passion for working with the Alaska Longline Fishermen’s Association and the Alaska Sustainable Fisheries Trust is an immense challenge.

Description: Published

Description: Refereed

Description: Las pesquerías basadas en las agregaciones reproductivas pueden amenazar a especies como los pargos que tienen conductas gregarias durante el período reproductivo. Esta nota ofrece elementos que sugieren la existencia de sitios de agregación no registrados previamente y no protegidos en el Parque Nacional Cayos de San Felipe (PNCSF), región suroccidental de Cuba. La información tradicional obtenida de pescadores locales y trabajadores del parque se corroboró con muestreos cualitativos y cuantitativos de peces de arrecifes y datos de pesquerías locales del 2014. En la época de reproducción de pargos (mayo a julio) se observaron grupos de entre 40-100 ejemplares de Lutjanus cyanopterus, Lutjanus synagris y Lutjanus jocu en los arrecifes de la zona occidental del PNCSF (camellones entre 15-30 m de profundidad cerca del borde de la plataforma). Dentro de esa área, se señalan dos sitios que parecen ser utilizados para agregaciones de predesove, por lo que requieren protección y ser estudiados. Los censos cuantitativos confirmaron que en mayo y junio la zona occidental tiene densidad alta de pargos adultos. También, el pico de captura de estas especies ocurrió en la época reproductiva. Se comprobó que las pesquerías se realizaron durante las migraciones de peces hacia el borde de la plataforma en áreas de la zona occidental del PNCSF, y que más del 60% de los individuos tuvieron gónadas maduras (antes de desovar). Esta información debe incentivar el estudio de las agregaciones de desove en esta región de Cuba, la protección de especies amenazadas y áreas de alta significación ecológica y la implementación de pesquerías sostenibles.

Description: Fisheries based on reproductive aggregations can threaten species such as snappers that have gregarious behavior during the reproductive period. This note provides evidence to support the existence of aggregation sites, not previously registered and unprotected, in the National Park San Felipe Keys (NPSFK), southwestern region of Cuba. Traditionalinformation obtained from local fishermen and from the park staff was complemented with qualitative and quantitative fish reef censuses and local fisheries data in 2014. In the reproductive season of snappers (May to July) groups of between 40-100 specimens of Lutjanus cyanopterus, Lutja- nus synagris and Lutjanus jocu were observed in the western area of the NPSFK on the reefs (spoor and grove between 20-30 m deep close to the platform edge). Within that area two sites are indicated that can be used for prespawning aggregation, so they require protection and study. Quanti- tative censuses confirmed that in May and June the western zone has high density of adult snappers. Also, the peak of capture of these snapper species occurred in the reproduc- tive season. It was found that fisheries carried out during fish migrations to the edge of the shelf in areas of the western area of the NPSFK and more than 60% of the individuals had mature gonads (before spawning). This information should promote the study of spawning aggregations in this region of Cuba, the protection of threatened species and areas of high ecological significance and the implementation of sustainable fisheries.

Description: Published

Description: Refereed

Description: The ICES Workshop on ICES reference points (WKREF2) was tasked review the WKREF1 report and based on the outcome develop updated guidelines for the ICES reference points system and recommendations for ACOM consideration. The WKREF1 report has suggested 5 key recom- mendations to simplify and harmonise the ICES reference points framework representing a ma- jor change to the current guidelines. At WKREF2, we detailed discussions and four key concerns were raised about the proposed approach. The first related to the simplification of rules to define Blim. Around two thirds of category 1 stocks would end up as WKREF1 “Blim Type 2” where Blim would be set as a fraction of B0. The Allee effect or “depensation” maybe more important than previously thought and should be furthered explored for ICES stocks since it has important consequences for Blim. A number of challenges and issues around defining Blim using the current guidelines were documented. Some suggestions on improvement criteria were discussed including using classifiers to define spas- modic stocks and using change point algorithms to address non-stationary productivity regimes. However, further work is need to make these approaches operational and there was no consen- sus that the WKREF1 Blim types should replace the current guidelines. WKREF1 recommended that the FMSY proxy should be based on a biological proxies and should be less than the deterministic FMSY. It was pointed out that the stochastic FMSY estimated in EqSim for example, is lower than the deterministic FMSY and that the current guidelines ensure that the FMSY should not pose a more than 5% risk to Blim. A large amount of work described in WD 1 was carried out to develop an MSE framework to consistency and robustness test a candidate refer- ence point system for North East Atlantic stocks. However, WKREF2 recommended that further work needs to be carried out to condition and test the simulation framework before the conclu- sions could be adopted by ICES and incorporated into the guidelines. A number of considerations for defining MSY related reference points were discussed including using model validation and prediction skill to ensure that ICES provide robust and credible ad- vice. There is evidence that density dependence (DD) is important in the majority of ICES stocks (68% in recruitment and 54% in growth). The correct prediction of the shape and strength of density-dependence in productivity is key to predicting future stock development and providing the best possible long-term fisheries management advice. A suggested approach to use surplus production models (SPMs) to account for DD in FMSY was suggested and discussed but there was no consensus on whether that approach was appropriate. There was consensus that the FECO approach as a means of adapting target fishing mortality to medium-term changes in productiv- ity should be included in the guidelines subject to a benchmark and ACOM approval. While WKREF1 and 2 focused mainly on Category 1 stocks ToR c) called for a “simplified and harmonised set of guidelines for estimating MSY and precautionary reference points applicable in the advice framework across various ICES stock categories.” Ideally the ICES assessment cat- egories should provide equivalent risk across all stocks. This issue was discussed but no recom- mendations emerged. There was no consensus a revised reference point framework was proposed at WKREF2. How- ever, it was agreed that it should be presented here for further discussion at ACOM and other fora. The key feature of the suggested approach is that the stock status evaluation is treated in- dependent of the Advice Rule (AR). The main feature of the system is that the biomass trigger is not linked to a stock status evaluation, it is linked to the expected biomass when fishing at the target fishing mortality, in contrast to the current ICES approach. It also entailed that FMSY would also become an upper limit of fishing mortality and that the advised fishing mortality would be set at or lower than that level. WKREF2 did not discuss what to do in situations where SSB〈 Blim or alternative forms of HCR for the advice rule. Building community understanding and con- sensus around simplified and harmonised guidelines has yet to be achieved. A further workshop WKREF3 will be required to achieve that aim. The report includes 6 recommendations for ACOM consideration.

Description: ICES

Description: The main objective of the workshop was to review the recommendations of WKREF1 and con- sider how these might feed into a new reference points framework and guidelines for ICES. There were a number of presentations on the wider issues of best practice for reference points, the Allee effect, density dependence and the WKIRISH approach. The starting point was to try and develop a set of simplified and harmonised guidelines based on the WKREF1 report rather than evolving the current guidelines to include the WKREF1 conclusions. A key aspect of the meeting was to allow for discussions in order to build a shared understanding of the strengths and weakness of the current framework and of the new framework emerging from WKREF1.

Description: Published

Description: Non Refereed

Description: © The Author(s), 2022. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in Dowd, S., Chapman, M., Koehn, L., & Hoagland, P. The economic tradeoffs and ecological impacts associated with a potential mesopelagic fishery in the California Current. Ecological Applications, 32(4), (2022): e2578, https://doi.org/10.1002/eap.2578.

Description: The ocean's mesopelagic zone (200–1000 m) remains one of the most understudied parts of the ocean despite knowledge that mesopelagic fishes are highly abundant. Apex predators from the surface waters are known to consume these fishes, constituting an important ecological interaction. Some countries have begun exploring the potential harvest of mesopelagic fishes to supply fishmeal and fish oil markets due to the high fish abundance in the mesopelagic zone compared with overfished surface waters. This study explored the economic and ecological implications of a moratorium on the harvest of mesopelagic fishes such as lanternfish off the US West Coast, one of the few areas where such resources are managed. We adapted a bioeconomic decision model to examine the tradeoffs between the values gained from a hypothetical mesopelagic fishery with the potential values lost from declines in predators of mesopelagic fishes facing a reduced prey resource. The economic rationale for a moratorium on harvesting mesopelagics was sensitive both to ecological relationships and the scale of the nonmarket values attributed to noncommercial predators. Using a California Current-based ecological simulation model, we found that most modeled predators of mesopelagic fishes increased in biomass even under high mesopelagic harvest rates, but the changes (either increases or decreases) were small, with relatively few predators responding with more than a 10% change in their biomass. While the ecological simulations implied that a commercial mesopelagic fishery might not have large biomass impacts for many species in the California Current system, there is still a need to further explore the various roles of the mesopelagic zone in the ocean.

Description: Sally Dowd acknowledges sponsorship from the WHOI Summer Student Fellowship and the Rausser College of Natural Resources Honors Program at UC Berkeley. This project would not have been possible without the guidance provided by Kama Thieler and Carl Boettiger. Porter Hoagland acknowledges funding from the Audacious Project, a collaborative endeavor, housed at TED and the J. Seward Johnson Fund in support of the Marine Policy Center at WHOI.

Description: Buesseler, K., Jin, D., Kourantidou, M., Levin, D., Ramakrishna, K., Renaud, P., Ausubel, J., Baltes, K., Gjerde, K., Holland, M., Kostel, K., LaCapra, V., Martin, A., Sosik, H., Thorrold, S., Tierney, T., Joyce, K., Renier, N., Taylor, E. (2022). The Ocean Twilight Zone’s Role in Climate Change. Woods Hole Oceanographic Institution, 32 pp.

Description: The ocean twilight zone (more formally known as the mesopelagic zone) plays a fundamental role in global climate. It is the mid-ocean region roughly 100 to 1000 meters below the surface, encompassing a half-mile deep belt of water that spans more than two-thirds of our planet. The top of the ocean twilight zone only receives 1% of incident sunlight and the bottom level is void of sunlight. Life in the ocean twilight zone helps to transport billions of metric tons (gigatonnes) of carbon annually from the upper ocean into the deep sea, due in part to processes known as the biological carbon pump. Once carbon moves below roughly 1000 meters depth in the ocean, it can remain out of the atmosphere for centuries to millennia. Without the benefits of the biological carbon pump, the atmospheric CO 2 concentration would increase by approximately 200 ppm 1 which would significantly amplify the negative effects of climate change that the world is currently trying to curtail and reverse. Unfortunately, existing scientific knowledge about this vast zone of the ocean, such as how chemical elements flow through its living systems and the physical environment, is extremely limited, jeopardizing the efforts to improve climate predictions and to inform fisheries management and ocean policy development.

Description: Funding is: The Audacious Project housed at TED

Description: © The Author(s), 2021. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in Kourantidou, M., Hoagland, P., Dale, A., & Bailey, M. Equitable allocations in northern fisheries: bridging the divide for Labrador Inuit. Frontiers in Marine Science, 8, (2021): 590213, https://doi.org/10.3389/fmars.2021.590213.

Description: Canada has undertaken commitments to recognize the rights of Indigenous Peoples in fisheries through policies and agreements, including Integrated Fishery Management Plans, the Reconciliation Strategy, and Land Claim Agreements (LCAs). In addition to recognizing rights, these commitments were intended to respect geographic adjacency principles, to enhance the economic viability of Indigenous communities, and to be reflective of community dependence on marine resources. We examined the determinants of quota allocations in commercial fisheries involving Nunatsiavut, Northern Labrador, the first self-governing region for the Inuit peoples in Canada. It has been argued that current fishery allocations for Nunatsiavut Inuit have not satisfied federal commitments to recognize Indigenous rights. Indicators that measure equity in commercial allocations for the turbot or Greenland halibut (Reinhardtius hippoglossoides) and northern shrimp (Pandalus borealis) fisheries were identified and assessed. In these two cases, historical allocations continue to predominate for allocations based upon equity or other social or economic considerations. We illustrate equity-enhancing changes in the quota distribution under scenarios of different levels of inequality aversion, and we make qualitative assessments of the effects of these allocations to Nunatsiavut for socioeconomic welfare. This approach could benefit fisheries governance in Northern Labrador, where federal commitments to equity objectives continue to be endorsed but have not yet been integrated fully into quota allocations.

Description: This research was undertaken with funding from the Canada First Research Excellence Fund through the Ocean Frontier Institute (MK and MB) and the Johnson Endowment of the Woods Hole Oceanographic Institution’s (WHOI) Marine Policy Center (PH).

Description: This paper summarizes the results of the experiments on the induced breeding and larval rearing of milkfish (Chanos chanos) during the 1979 season. Milkfish larvae could be reared successfully without the use of trochophore larvae of oysters as feed during the first few days. In order to induce the ovulation of wild adult milkfish a higher dose of human chorionic gonadotropin hormone is required.

Description: An outline is given of aquaculture and fisheries in Asia, providing information of use to students whose work can influence laws, rules, policy and regulations on aquaculture and fisheries, with the view in mind to sustainable aquaculture. In this issue, the following countries are examined: China, Indonesia, and Bangladesh.

Description: Round scad exploration by purse seine in the waters of western Philippines was conducted from April 22 to May 7, 1998 for a period of five (5) fishing days with a total catch of 7.3 tons and an average of 1.5 tons per setting. Dominant species caught were Decapterus spp. having 70.09% of the total catch, followed by Selar spp. at 12.66% and Rastrelliger spp. 10.70%. Among the Decapterus spp. caught, D. macrosoma attained the highest total catch composition by species having 68.81% followed by D. kurroides and D.russelli with 0.31% and 1.14% respectively. The round scad fishery stock was composed mainly of juvenile fish (less than 13 cm) and Age group II (13 cm to 14 cm). Few large round scad at Age group IV and V (20 cm to 28 cm) stayed at the fishery. Other fishes caught were: Auxis rochei (0.85%), A. thazard (0.12%), Caranx spp. (0.45%), Emmilichthys nitidus (0.58%), Euthynnus affinis (0.42%), Leiognathus ruconius (0.58%), Loligo sp. (0.31%), Megalaspis cordyla (0.09%), Rastrelliger spp. (10.70%), Sardinella longiceps (0.03%), Scomberoides lysan (0.24%), Selar spp. (12.66%), Sphyraena spp. (0.90%), Thunnus albacares (0.96%) and others (1.02%). Tuna and tuna like fishes such as yellowfin tuna, eastern little tuna, bullet tuna, frigate tuna and oceanic squid are distributed in the upper latitudes of the survey area. On the other hand, round scads, big-eyed scads and Indian mackerels are dominantly present in the lower latitudes of the survey area.

Description: Presented in this paper is the status of the fishery industry in Brunei Darussalam. Specifically, it discussed the following topics: fishery management strategies, zonation scheme, licencing, the use of poisons and explosives, the minimum cod-end mesh size for trawlers, closed areas, enhancement of fishing grounds, and the enforcement activities.

Description: An exploratory tuna longline fishing survey was conducted using the research and training vessels of the Southeast Asian Fisheries Development Center, the 1,178 GT MV SEAFDEC and the Bureau of Fisheries and Aquatic Resources, the 165 GT MV MAYA-MAYA in the South China Sea Waters, West of the Philippines from April to May, 1998. A total of 3,796 hooks was set in sixteen (16) fishing stations. There were no tuna caught during the entire survey but only minor and irrelevant species like the Pacific lancetfish, sharks and an opah species, Lampris guttatus. The important fishing and oceanographic factors during the survey and other research results on longline are described and analyzed. Additional longline studies within and near the Philippines territorial waters are also presented to substantiate the research results of the joint SEAFDEC/BFAR resource exploratory.

Description: Presented in the paper is the standard procedure in the determination of K value which is an index to measure the enzymatic freshness of fish and squid. Specifically, reagents, apparatus and the analytical procedures needed and the calculations are presented.

Description: Presented in the paper is the standard procedure in measuring K value in fish meat by means of the freshness testing paper technique.

Description: Presented in the paper is the standard procedure in the measurement of pH in the fresh fish meat. Specifically, the procedures in sampling and sample preparation, apparatus and reagents required, and the analytical procedures are presented.

Description: Starch is commonly used in the production of fish jelly products as an extender and as binding agent. The paper provides the methodology in the determination of starch in fish jelly products. Instructions for sample preparation and the reagents needed are presented. Detailed procedures in the determination of the starch in a sample are provided.

Description: Monitoring and investigative work undertaken in the Philippines regarding dinoflagellate blooms are described. Chronological observations of the occurrence of red tides, aerial surveys, spatial distribution of the dinoflagellate and the physical environment are discussed. Fishing and the examination of gut content of fish and mussels and bioassay tests are detailed. Incidents of paralytic shellfish poisoning in the Philippines are considered briefly.

Description: A report is made of the first incidence occurring of paralytic shellfish poisoning in Thailand in May 1983, following an extensive bloom of Trichodesmium erythraeum. Investigations undertaken regarding the source of the toxicity are outlined.

Description: A brief account is given of recent cases of paralytic shellfish poisoning in Sabah, Malaysia, and toxicological studies undertaken. Hydrography surveys, underwater observations after the occurrence of the red tides and plankton studies and monitoring of red tides are discussed.

Description: Cholera is an acute specific infection caused by the organism, Vibrio cholera. Diagnosis may be confirmed by the presence of large numbers of the comma-shaped bacilli on direct microscopic examination of a fecal or vomitus smear, and by the isolation of the organism on culture. Fish and shellfish have been identified as vehicles of cholera. Large numbers of V. cholera must usually be ingested to cause cholera. Thus problems often occur when poor handling and inadequate refrigeration have allowed the organism to multiply. Presented in the paper is the methodology of determining the presence of Vibrio cholera in fish and fishery products.

Description: Fishery statistics in Brunei Darussalam have been collected by the Department of Fisheries since the 1940s. In the early 1980s, a number of statistics were collected, such as catch and effort data of artisanal fishermen, aquaculture statistics, processing statistics as well as data from major wet markets focusing on the amount, prices of marketed fish either from the local fishermen or imported. In 1984, the collection of statistics on commercial fishing was started. The statistics have been used in the formulation of fishery management and development policies as well as for sectoral development. Following a brief account of the responsibility and statistic collections of the Department of Fisheries, an examination is made of employment in the fishery sector, fisheries production, fish marketed and the GDP for the fishery industry. Fisheries in Brunei Darussalam is a very healthy industry, where production is well below the maximum allowable harvestable limit of 20,000 tons at 30%. The Department is embarking to increase production from the capture fishery to reduce the country's dependence on imported fish; the same applies for aquaculture, in order to complement production from the capture fisheries. The processing sector is also increasing in importance, especially with the increase in the number of capture fishery licenses, and the demand for quality and value-added products.

Description: Sodium chloride is an important additive for the production of fish jelly products. It extracts the salt soluble protein to give the gel strength of the final product. The paper provides the methodology in the determination of the amount of sodium chloride in fish jelly products. Instructions for sample preparation and the reagents needed are presented. Detailed procedures in the determination of the salt in a sample are provided.

Description: Food poisoning due to Vibrio parahaemolyticus is a food-borne infection resulting from the ingestion of a large number of this organism (about 106-109 viable cells). The major symptoms are diarrhea and abdominal pain with headache, fever, and vomiting also occurring. The organisms are excreted during the acute stage of the illness after which they decrease rapidly. The differentiation of V. parahaemolyticus from other pathogenic species of Vibrio is based mainly on salt tolerance, Voges-Proskauer reaction, fermentation of sucrose, and growth at 43°C. Presented in the paper is the methodology of determining the presence of Vibrio cholera in fish and fishery products.

Description: The first meeting of the South West Indian Ocean EAF Regional Task Group (RTG) was held in Mombasa, Kenya, from 27 to 30 January 2009, together with an ecological risk assessment methodology workshop. It was attended by 20 partic ipants from the South West Indian Ocean (SWIO) countries, the South West Indian Ocean Fisheries Project (SWIOFP), the Agulhas and Somali Currents Large Marine Ecosystems (ASCLME) project, the Scientific Committee of the South West Indian Ocean Fisheries Commission, the United Nations Environment Programme (UNEP)/Nairobi Convention Implementation Unit, the African Union Commission and FAO. The RTG is an implementation structure under the EAF-Nansen project GCP/INT/003/NOR and serves as the forum for training in ecological risk assessment that is the methodology used for the identification and prioritization of issues requiring management attention. The main objectives of the meeting and workshop we re to discuss and facilitate key processes and activities for the implementation of the ecosystem approach to fisheries management in the South West Indian Ocean region including the modalities for the formation and functioning of the RTG and National Task Groups (NTGs). It was explained that, to be able to achieve the objectives of implementing an ecosystem approach to fisheries at the national level, certain key structures have to be in place including the NTG with representatives of key stakeholders in a given fishery and that would take the lead in the process. An overview of the key concepts and process of the ecological risk assessment methodology were clarified. Participants were also introduced to the preparation of EAF baseline reports to be used as initial input for the work on ecosystems approach to fisheries. It was explained that the preparation of the report is to be led by national and regional experts and overseen by the NTG. For the exercises the participants worked in three subgroups formed during the meeting with each group selecting a chairman who moderate d the discussions and a rapporteur. The participants expressed satisfaction with the development of a communication strategy for the project and especially with the participatory approach used.

Description: FAO, NORAD, Institute of Marine Research

Description: Published

Description: National task groups

Description: Regional task groups

Description: Ecosystem Approach to Fisheries

Description: Published

Description: Fisheries newsletter

Description: Published

Description: Fisheries newsletter

Description: Published

Description: Fisheries newsletter

Description: Published

Description: Fisheries newsletter

Description: The balance between stem cell self-renewal and differentiation is controlled by intrinsic factors and niche signals. In the Drosophila melanogaster ovary, some intrinsic factors promote germline stem cell (GSC) self-renewal, whereas others stimulate differentiation. However, it remains poorly understood how the balance between self-renewal and differentiation is controlled. Here we use D. melanogaster ovarian GSCs to demonstrate that the differentiation factor Bam controls the functional switch of the COP9 complex from self-renewal to differentiation via protein competition. The COP9 complex is composed of eight Csn subunits, Csn1-8, and removes Nedd8 modifications from target proteins. Genetic results indicated that the COP9 complex is required intrinsically for GSC self-renewal, whereas other Csn proteins, with the exception of Csn4, were also required for GSC progeny differentiation. Bam-mediated Csn4 sequestration from the COP9 complex via protein competition inactivated the self-renewing function of COP9 and allowed other Csn proteins to promote GSC differentiation. Therefore, this study reveals a protein-competition-based mechanism for controlling the balance between stem cell self-renewal and differentiation. Because numerous self-renewal factors are ubiquitously expressed throughout the stem cell lineage in various systems, protein competition may function as an important mechanism for controlling the self-renewal-to-differentiation switch.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pan, Lei -- Wang, Su -- Lu, Tinglin -- Weng, Changjiang -- Song, Xiaoqing -- Park, Joseph K -- Sun, Jin -- Yang, Zhi-Hao -- Yu, Junjing -- Tang, Hong -- McKearin, Dennis M -- Chamovitz, Daniel A -- Ni, Jianquan -- Xie, Ting -- GM64428/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 Oct 9;514(7521):233-6. doi: 10.1038/nature13562.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Stowers Institute for Medical Research, 1000 East 50th Street, Kansas City, Missouri 64110, USA [2] Chinese Academy of Sciences Key Laboratory of Infection and Immunity, Institute of Biophysics, 15 Da Tun Road, Beijing 100101, China [3]. ; 1] Stowers Institute for Medical Research, 1000 East 50th Street, Kansas City, Missouri 64110, USA [2] Department of Cell Biology and Anatomy, University of Kansas School of Medicine, 3901 Rainbow Boulevard, Kansas City, Kansas 66160, USA [3]. ; 1] Center for Life Sciences, School of Medicine, Tsinghua University, Beijing 100084, China [2]. ; Stowers Institute for Medical Research, 1000 East 50th Street, Kansas City, Missouri 64110, USA. ; 1] Department of Molecular Biology and Graduate School of Biomedical Sciences, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9148, USA [2] Howard Hughes Medical Institute, Chevy Chase, Maryland 20815-6789, USA. ; Center for Life Sciences, School of Medicine, Tsinghua University, Beijing 100084, China. ; 1] Stowers Institute for Medical Research, 1000 East 50th Street, Kansas City, Missouri 64110, USA [2] Chinese Academy of Sciences Key Laboratory of Infection and Immunity, Institute of Biophysics, 15 Da Tun Road, Beijing 100101, China. ; Chinese Academy of Sciences Key Laboratory of Infection and Immunity, Institute of Biophysics, 15 Da Tun Road, Beijing 100101, China. ; Department of Plant Sciences, Tel Aviv University, Tel Aviv 69978, Israel. ; 1] Stowers Institute for Medical Research, 1000 East 50th Street, Kansas City, Missouri 64110, USA [2] Department of Cell Biology and Anatomy, University of Kansas School of Medicine, 3901 Rainbow Boulevard, Kansas City, Kansas 66160, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25119050" target="_blank"〉PubMed〈/a〉

Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4469351/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4469351/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Geisbert, Thomas W -- UC7 AI070083/AI/NIAID NIH HHS/ -- England -- Nature. 2014 Oct 2;514(7520):41-3. doi: 10.1038/nature13746. Epub 2014 Aug 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Texas Medical Branch at Galveston, Galveston National Laboratory, Galveston, Texas 77550-0610, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25171470" target="_blank"〉PubMed〈/a〉

Description: The neutralizing antibody response to influenza virus is dominated by antibodies that bind to the globular head of haemagglutinin, which undergoes a continuous antigenic drift, necessitating the re-formulation of influenza vaccines on an annual basis. Recently, several laboratories have described a new class of rare influenza-neutralizing antibodies that target a conserved site in the haemagglutinin stem. Most of these antibodies use the heavy-chain variable region VH1-69 gene, and structural data demonstrate that they bind to the haemagglutinin stem through conserved heavy-chain complementarity determining region (HCDR) residues. However, the VH1-69 antibodies are highly mutated and are produced by some but not all individuals, suggesting that several somatic mutations may be required for their development. To address this, here we characterize 197 anti-stem antibodies from a single donor, reconstruct the developmental pathways of several VH1-69 clones and identify two key elements that are required for the initial development of most VH1-69 antibodies: a polymorphic germline-encoded phenylalanine at position 54 and a conserved tyrosine at position 98 in HCDR3. Strikingly, in most cases a single proline to alanine mutation at position 52a in HCDR2 is sufficient to confer high affinity binding to the selecting H1 antigen, consistent with rapid affinity maturation. Surprisingly, additional favourable mutations continue to accumulate, increasing the breadth of reactivity and making both the initial mutations and phenylalanine at position 54 functionally redundant. These results define VH1-69 allele polymorphism, rearrangement of the VDJ gene segments and single somatic mutations as the three requirements for generating broadly neutralizing VH1-69 antibodies and reveal an unexpected redundancy in the affinity maturation process.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pappas, Leontios -- Foglierini, Mathilde -- Piccoli, Luca -- Kallewaard, Nicole L -- Turrini, Filippo -- Silacci, Chiara -- Fernandez-Rodriguez, Blanca -- Agatic, Gloria -- Giacchetto-Sasselli, Isabella -- Pellicciotta, Gabriele -- Sallusto, Federica -- Zhu, Qing -- Vicenzi, Elisa -- Corti, Davide -- Lanzavecchia, Antonio -- U19 AI-057266/AI/NIAID NIH HHS/ -- England -- Nature. 2014 Dec 18;516(7531):418-22. doi: 10.1038/nature13764. Epub 2014 Oct 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Insitute for Research in Biomedicine, Universita della Svizzera Italiana, Via Vincenzo Vela 6, 6500 Bellinzona, Switzerland. ; Department of Infectious Diseases and Vaccines MedImmune LLC, One MedImmune Way, Gaithersburg, Maryland 20878, USA. ; Viral Pathogens and Biosafety Unit, San Raffaele Scientific Institute, Via Olgettina 58, 20132 Milan, Italy. ; Humabs BioMed SA, Via Mirasole 1, 6500 Bellinzona, Switzerland. ; Unit of Preventive Medicine, San Raffaele Scientific Institute, Via Olgettina 58, 20132 Milan, Italy. ; 1] Insitute for Research in Biomedicine, Universita della Svizzera Italiana, Via Vincenzo Vela 6, 6500 Bellinzona, Switzerland [2] Humabs BioMed SA, Via Mirasole 1, 6500 Bellinzona, Switzerland [3]. ; 1] Insitute for Research in Biomedicine, Universita della Svizzera Italiana, Via Vincenzo Vela 6, 6500 Bellinzona, Switzerland [2] Insitute for Microbiology, ETH Zurich, Wolfgang-Pauli-Strasse 10, 8093 Zurich, Switzerland [3].〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25296253" target="_blank"〉PubMed〈/a〉

Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉England -- Nature. 2014 Oct 9;514(7521):140. doi: 10.1038/514140a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25297398" target="_blank"〉PubMed〈/a〉

Description: The TRIM37 (also known as MUL) gene is located in the 17q23 chromosomal region, which is amplified in up to approximately 40% of breast cancers. TRIM37 contains a RING finger domain, a hallmark of E3 ubiquitin ligases, but its protein substrate(s) is unknown. Here we report that TRIM37 mono-ubiquitinates histone H2A, a chromatin modification associated with transcriptional repression. We find that in human breast cancer cell lines containing amplified 17q23, TRIM37 is upregulated and, reciprocally, the major H2A ubiquitin ligase RNF2 (also known as RING1B) is downregulated. Genome-wide chromatin immunoprecipitation (ChIP)-chip experiments in 17q23-amplified breast cancer cells identified many genes, including multiple tumour suppressors, whose promoters were bound by TRIM37 and enriched for ubiquitinated H2A. However, unlike RNF2, which is a subunit of polycomb repressive complex 1 (PRC1), we find that TRIM37 associates with polycomb repressive complex 2 (PRC2). TRIM37, PRC2 and PRC1 are co-bound to specific target genes, resulting in their transcriptional silencing. RNA-interference-mediated knockdown of TRIM37 results in loss of ubiquitinated H2A, dissociation of PRC1 and PRC2 from target promoters, and transcriptional reactivation of silenced genes. Knockdown of TRIM37 in human breast cancer cells containing amplified 17q23 substantially decreases tumour growth in mouse xenografts. Conversely, ectopic expression of TRIM37 renders non-transformed cells tumorigenic. Collectively, our results reveal TRIM37 as an oncogenic H2A ubiquitin ligase that is overexpressed in a subset of breast cancers and promotes transformation by facilitating silencing of tumour suppressors and other genes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4269325/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4269325/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bhatnagar, Sanchita -- Gazin, Claude -- Chamberlain, Lynn -- Ou, Jianhong -- Zhu, Xiaochun -- Tushir, Jogender S -- Virbasius, Ching-Man -- Lin, Ling -- Zhu, Lihua J -- Wajapeyee, Narendra -- Green, Michael R -- R01 GM033977/GM/NIGMS NIH HHS/ -- R01GM033977/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 Dec 4;516(7529):116-20. doi: 10.1038/nature13955. Epub 2014 Nov 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Howard Hughes Medical Institute, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA [2] Programs in Gene Function and Expression and Molecular Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA. ; CEA/DSV/iRCM/LEFG, Genopole G2, and Universite Paris Diderot, 91057 Evry, France. ; Programs in Gene Function and Expression and Molecular Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA. ; Boehringer Ingelheim Pharmaceuticals, Inc., Ridgefield, Connecticut 06877, USA. ; 1] Programs in Gene Function and Expression and Molecular Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA [2] Program in Bioinformatics and Integrative Biology, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA. ; Department of Pathology, Yale University School of Medicine, New Haven, Connecticut 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25470042" target="_blank"〉PubMed〈/a〉

Description: Sensory regions of the brain integrate environmental cues with copies of motor-related signals important for imminent and ongoing movements. In mammals, signals propagating from the motor cortex to the auditory cortex are thought to have a critical role in normal hearing and behaviour, yet the synaptic and circuit mechanisms by which these motor-related signals influence auditory cortical activity remain poorly understood. Using in vivo intracellular recordings in behaving mice, we find that excitatory neurons in the auditory cortex are suppressed before and during movement, owing in part to increased activity of local parvalbumin-positive interneurons. Electrophysiology and optogenetic gain- and loss-of-function experiments reveal that motor-related changes in auditory cortical dynamics are driven by a subset of neurons in the secondary motor cortex that innervate the auditory cortex and are active during movement. These findings provide a synaptic and circuit basis for the motor-related corollary discharge hypothesized to facilitate hearing and auditory-guided behaviours.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4248668/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4248668/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schneider, David M -- Nelson, Anders -- Mooney, Richard -- NS079929/NS/NINDS NIH HHS/ -- R01 DC013826/DC/NIDCD NIH HHS/ -- R21 NS079929/NS/NINDS NIH HHS/ -- T32 GM008441/GM/NIGMS NIH HHS/ -- England -- Nature. 2014 Sep 11;513(7517):189-94. doi: 10.1038/nature13724. Epub 2014 Aug 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Neurobiology, Duke University School of Medicine, Durham, North Carolina 27710, USA [2]. ; Department of Neurobiology, Duke University School of Medicine, Durham, North Carolina 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25162524" target="_blank"〉PubMed〈/a〉

Description: Fertilization occurs when sperm and egg recognize each other and fuse to form a new, genetically distinct organism. The molecular basis of sperm-egg recognition is unknown, but is likely to require interactions between receptor proteins displayed on their surface. Izumo1 is an essential sperm cell-surface protein, but its receptor on the egg has not been described. Here we identify folate receptor 4 (Folr4) as the receptor for Izumo1 on the mouse egg, and propose to rename it Juno. We show that the Izumo1-Juno interaction is conserved within several mammalian species, including humans. Female mice lacking Juno are infertile and Juno-deficient eggs do not fuse with normal sperm. Rapid shedding of Juno from the oolemma after fertilization suggests a mechanism for the membrane block to polyspermy, ensuring eggs normally fuse with just a single sperm. Our discovery of an essential receptor pair at the nexus of conception provides opportunities for the rational development of new fertility treatments and contraceptives.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3998876/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3998876/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bianchi, Enrica -- Doe, Brendan -- Goulding, David -- Wright, Gavin J -- 098051/Wellcome Trust/United Kingdom -- England -- Nature. 2014 Apr 24;508(7497):483-7. doi: 10.1038/nature13203. Epub 2014 Apr 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell Surface Signalling Laboratory, Wellcome Trust Sanger Institute, Hinxton, Cambridge, CB10 1SA, UK. ; Mouse Production Team, Wellcome Trust Sanger Institute, Hinxton, Cambridge, CB10 1SA, UK. ; Electron and Advanced Light Microscopy Suite, Wellcome Trust Sanger Institute, Hinxton, Cambridge, CB10 1SA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24739963" target="_blank"〉PubMed〈/a〉

Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Biller-Andorno, Nikola -- England -- Nature. 2014 Jul 10;511(7508):155. doi: 10.1038/511155a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25008510" target="_blank"〉PubMed〈/a〉

Description: T-helper type 17 (TH17) cells that produce the cytokines interleukin-17A (IL-17A) and IL-17F are implicated in the pathogenesis of several autoimmune diseases. The differentiation of TH17 cells is regulated by transcription factors such as RORgammat, but post-translational mechanisms preventing the rampant production of pro-inflammatory IL-17A have received less attention. Here we show that the deubiquitylating enzyme DUBA is a negative regulator of IL-17A production in T cells. Mice with DUBA-deficient T cells developed exacerbated inflammation in the small intestine after challenge with anti-CD3 antibodies. DUBA interacted with the ubiquitin ligase UBR5, which suppressed DUBA abundance in naive T cells. DUBA accumulated in activated T cells and stabilized UBR5, which then ubiquitylated RORgammat in response to TGF-beta signalling. Our data identify DUBA as a cell-intrinsic suppressor of IL-17 production.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rutz, Sascha -- Kayagaki, Nobuhiko -- Phung, Qui T -- Eidenschenk, Celine -- Noubade, Rajkumar -- Wang, Xiaoting -- Lesch, Justin -- Lu, Rongze -- Newton, Kim -- Huang, Oscar W -- Cochran, Andrea G -- Vasser, Mark -- Fauber, Benjamin P -- DeVoss, Jason -- Webster, Joshua -- Diehl, Lauri -- Modrusan, Zora -- Kirkpatrick, Donald S -- Lill, Jennie R -- Ouyang, Wenjun -- Dixit, Vishva M -- England -- Nature. 2015 Feb 19;518(7539):417-21. doi: 10.1038/nature13979. Epub 2014 Dec 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Genentech, 1 DNA Way, South San Francisco, California 94080, USA. ; Department of Physiological Chemistry, Genentech, 1 DNA Way, South San Francisco, California 94080, USA. ; Department of Protein Chemistry, Genentech, 1 DNA Way, South San Francisco, California 94080, USA. ; Department of Early Discovery Biochemistry, Genentech, 1 DNA Way, South San Francisco, California 94080, USA. ; Discovery Chemistry, Genentech, 1 DNA Way, South San Francisco, California 94080, USA. ; Department of Pathology, Genentech, 1 DNA Way, South San Francisco, California 94080, USA. ; Department of Molecular Biology, Genentech, 1 DNA Way, South San Francisco, California 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25470037" target="_blank"〉PubMed〈/a〉

Description: The kinetochore is the crucial apparatus regulating chromosome segregation in mitosis and meiosis. Particularly in meiosis I, unlike in mitosis, sister kinetochores are captured by microtubules emanating from the same spindle pole (mono-orientation) and centromeric cohesion mediated by cohesin is protected in the following anaphase. Although meiotic kinetochore factors have been identified only in budding and fission yeasts, these molecules and their functions are thought to have diverged earlier. Therefore, a conserved mechanism for meiotic kinetochore regulation remains elusive. Here we have identified in mouse a meiosis-specific kinetochore factor that we termed MEIKIN, which functions in meiosis I but not in meiosis II or mitosis. MEIKIN plays a crucial role in both mono-orientation and centromeric cohesion protection, partly by stabilizing the localization of the cohesin protector shugoshin. These functions are mediated mainly by the activity of Polo-like kinase PLK1, which is enriched to kinetochores in a MEIKIN-dependent manner. Our integrative analysis indicates that the long-awaited key regulator of meiotic kinetochore function is Meikin, which is conserved from yeasts to humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Jihye -- Ishiguro, Kei-ichiro -- Nambu, Aya -- Akiyoshi, Bungo -- Yokobayashi, Shihori -- Kagami, Ayano -- Ishiguro, Tadashi -- Pendas, Alberto M -- Takeda, Naoki -- Sakakibara, Yogo -- Kitajima, Tomoya S -- Tanno, Yuji -- Sakuno, Takeshi -- Watanabe, Yoshinori -- England -- Nature. 2015 Jan 22;517(7535):466-71. doi: 10.1038/nature14097. Epub 2014 Dec 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Chromosome Dynamics, Institute of Molecular and Cellular Biosciences, University of Tokyo, 1-1-1Yayoi, Tokyo 113-0032, Japan. ; Instituto de Biologia Molecular y Celular del Cancer (CSIC-USAL), 37007 Salamanca, Spain. ; Center for Animal Resources and Development, Kumamoto University, 2-2-1 Honjo, Kumamoto 860-0811 Japan. ; Laboratory for Chromosome Segregation, RIKEN Center for Developmental Biology, 2-2-3 Minatojima-Minamimachi, Chuo-ku, Kobe 650-0047, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25533956" target="_blank"〉PubMed〈/a〉

Description: The gastrointestinal tracts of mammals are colonized by hundreds of microbial species that contribute to health, including colonization resistance against intestinal pathogens. Many antibiotics destroy intestinal microbial communities and increase susceptibility to intestinal pathogens. Among these, Clostridium difficile, a major cause of antibiotic-induced diarrhoea, greatly increases morbidity and mortality in hospitalized patients. Which intestinal bacteria provide resistance to C. difficile infection and their in vivo inhibitory mechanisms remain unclear. Here we correlate loss of specific bacterial taxa with development of infection, by treating mice with different antibiotics that result in distinct microbiota changes and lead to varied susceptibility to C. difficile. Mathematical modelling augmented by analyses of the microbiota of hospitalized patients identifies resistance-associated bacteria common to mice and humans. Using these platforms, we determine that Clostridium scindens, a bile acid 7alpha-dehydroxylating intestinal bacterium, is associated with resistance to C. difficile infection and, upon administration, enhances resistance to infection in a secondary bile acid dependent fashion. Using a workflow involving mouse models, clinical studies, metagenomic analyses, and mathematical modelling, we identify a probiotic candidate that corrects a clinically relevant microbiome deficiency. These findings have implications for the rational design of targeted antimicrobials as well as microbiome-based diagnostics and therapeutics for individuals at risk of C. difficile infection.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4354891/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4354891/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Buffie, Charlie G -- Bucci, Vanni -- Stein, Richard R -- McKenney, Peter T -- Ling, Lilan -- Gobourne, Asia -- No, Daniel -- Liu, Hui -- Kinnebrew, Melissa -- Viale, Agnes -- Littmann, Eric -- van den Brink, Marcel R M -- Jenq, Robert R -- Taur, Ying -- Sander, Chris -- Cross, Justin R -- Toussaint, Nora C -- Xavier, Joao B -- Pamer, Eric G -- AI95706/AI/NIAID NIH HHS/ -- DP2 OD008440/OD/NIH HHS/ -- DP2OD008440/OD/NIH HHS/ -- K23 AI095398/AI/NIAID NIH HHS/ -- P01 CA023766/CA/NCI NIH HHS/ -- P30 CA008748/CA/NCI NIH HHS/ -- R01 AI042135/AI/NIAID NIH HHS/ -- R01 AI095706/AI/NIAID NIH HHS/ -- R01 AI42135/AI/NIAID NIH HHS/ -- T32 CA009149/CA/NCI NIH HHS/ -- T32 GM007739/GM/NIGMS NIH HHS/ -- T32GM07739/GM/NIGMS NIH HHS/ -- U54 CA148967/CA/NCI NIH HHS/ -- England -- Nature. 2015 Jan 8;517(7533):205-8. doi: 10.1038/nature13828. Epub 2014 Oct 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Infectious Diseases Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA [2] Lucille Castori Center for Microbes, Inflammation and Cancer, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA. ; 1] Computational Biology Program, Sloan-Kettering Institute, New York, New York 10065, USA [2] Department of Biology, University of Massachusetts Dartmouth, North Dartmouth, Massachusetts 02747, USA. ; Computational Biology Program, Sloan-Kettering Institute, New York, New York 10065, USA. ; Lucille Castori Center for Microbes, Inflammation and Cancer, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA. ; Donald B. and Catherine C. Marron Cancer Metabolism Center, Sloan-Kettering Institute, New York, New York 10065, USA. ; Genomics Core Laboratory, Sloan-Kettering Institute, New York, New York 10065, USA. ; 1] Bone Marrow Transplant Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA [2] Immunology Program, Sloan-Kettering Institute, New York, New York 10065, USA. ; Bone Marrow Transplant Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA. ; 1] Lucille Castori Center for Microbes, Inflammation and Cancer, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA [2] Computational Biology Program, Sloan-Kettering Institute, New York, New York 10065, USA. ; 1] Infectious Diseases Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA [2] Lucille Castori Center for Microbes, Inflammation and Cancer, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA [3] Immunology Program, Sloan-Kettering Institute, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25337874" target="_blank"〉PubMed〈/a〉

Description: Intracellular ISG15 is an interferon (IFN)-alpha/beta-inducible ubiquitin-like modifier which can covalently bind other proteins in a process called ISGylation; it is an effector of IFN-alpha/beta-dependent antiviral immunity in mice. We previously published a study describing humans with inherited ISG15 deficiency but without unusually severe viral diseases. We showed that these patients were prone to mycobacterial disease and that human ISG15 was non-redundant as an extracellular IFN-gamma-inducing molecule. We show here that ISG15-deficient patients also display unanticipated cellular, immunological and clinical signs of enhanced IFN-alpha/beta immunity, reminiscent of the Mendelian autoinflammatory interferonopathies Aicardi-Goutieres syndrome and spondyloenchondrodysplasia. We further show that an absence of intracellular ISG15 in the patients' cells prevents the accumulation of USP18, a potent negative regulator of IFN-alpha/beta signalling, resulting in the enhancement and amplification of IFN-alpha/beta responses. Human ISG15, therefore, is not only redundant for antiviral immunity, but is a key negative regulator of IFN-alpha/beta immunity. In humans, intracellular ISG15 is IFN-alpha/beta-inducible not to serve as a substrate for ISGylation-dependent antiviral immunity, but to ensure USP18-dependent regulation of IFN-alpha/beta and prevention of IFN-alpha/beta-dependent autoinflammation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4303590/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4303590/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Xianqin -- Bogunovic, Dusan -- Payelle-Brogard, Beatrice -- Francois-Newton, Veronique -- Speer, Scott D -- Yuan, Chao -- Volpi, Stefano -- Li, Zhi -- Sanal, Ozden -- Mansouri, Davood -- Tezcan, Ilhan -- Rice, Gillian I -- Chen, Chunyuan -- Mansouri, Nahal -- Mahdaviani, Seyed Alireza -- Itan, Yuval -- Boisson, Bertrand -- Okada, Satoshi -- Zeng, Lu -- Wang, Xing -- Jiang, Hui -- Liu, Wenqiang -- Han, Tiantian -- Liu, Delin -- Ma, Tao -- Wang, Bo -- Liu, Mugen -- Liu, Jing-Yu -- Wang, Qing K -- Yalnizoglu, Dilek -- Radoshevich, Lilliana -- Uze, Gilles -- Gros, Philippe -- Rozenberg, Flore -- Zhang, Shen-Ying -- Jouanguy, Emmanuelle -- Bustamante, Jacinta -- Garcia-Sastre, Adolfo -- Abel, Laurent -- Lebon, Pierre -- Notarangelo, Luigi D -- Crow, Yanick J -- Boisson-Dupuis, Stephanie -- Casanova, Jean-Laurent -- Pellegrini, Sandra -- 1P01AI076210-01A1/AI/NIAID NIH HHS/ -- 309449/European Research Council/International -- 8UL1TR000043/TR/NCATS NIH HHS/ -- P01 AI076210/AI/NIAID NIH HHS/ -- P01 AI090935/AI/NIAID NIH HHS/ -- P01AI090935/AI/NIAID NIH HHS/ -- R00 AI106942/AI/NIAID NIH HHS/ -- R00AI106942-02/AI/NIAID NIH HHS/ -- R01 AI035237/AI/NIAID NIH HHS/ -- R37 AI095983/AI/NIAID NIH HHS/ -- R37AI095983/AI/NIAID NIH HHS/ -- U19 AI083025/AI/NIAID NIH HHS/ -- U19AI083025/AI/NIAID NIH HHS/ -- UL1 TR000043/TR/NCATS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2015 Jan 1;517(7532):89-93. doi: 10.1038/nature13801. Epub 2014 Oct 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Key Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan 430074, China. ; 1] St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, New York 10065, USA [2] Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA. ; Institut Pasteur, Cytokine Signaling Unit, CNRS URA 1961, 75724 Paris, France. ; 1] Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA [2] Global Health and Emerging Pathogens Institute, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA [3] Microbiology Training Area, Graduate School of Biomedical Sciences of Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA. ; 1] Division of Immunology, Children's Hospital Boston, Boston, Massachusetts 02115, USA [2] Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genoa, 16132 Genoa, Italy. ; Immunology Division and Pediatric Neurology Department, Hacettepe University Children's Hospital, 06100 Ankara, Turkey. ; Division of Infectious Diseases and Clinical Immunology, Pediatric Respiratory Diseases Research Center, National Research Institute of Tuberculosis and Lung Diseases, Shahid Beheshti University of Medical Sciences, 4739 Teheran, Iran. ; Manchester Academic Health Science Centre, University of Manchester, Genetic Medicine, Manchester, M13 9NT, UK. ; Department of Pediatrics, Third Xiangya Hospital, Central South University, Changsha 410013, China. ; St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, New York 10065, USA. ; BGI-Shenzhen, Shenzhen 518083, China. ; Sangzhi County People's Hospital, Sangzhi 427100, China. ; Genetics Laboratory, Hubei Maternal and Child Health Hospital, Wuhan, Hubei 430070, China. ; 1] Key Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan 430074, China [2] Center for Cardiovascular Genetics, Department of Molecular Cardiology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio 44195, USA. ; Institut Pasteur, Bacteria-Cell Interactions Unit, 75724 Paris, France. ; CNRS UMR5235, Montpellier II University, Place Eugene Bataillon, 34095 Montpellier, France. ; Department of Biochemistry, McGill University, Montreal, QC H3A 0G4, Canada. ; Paris Descartes University, 75006 Paris, France. ; 1] Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM U1163, Necker Hospital for Sick Children, 75015 Paris, France [2] Paris Descartes University, Imagine Institute, 75015 Paris, France. ; 1] Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM U1163, Necker Hospital for Sick Children, 75015 Paris, France [2] Paris Descartes University, Imagine Institute, 75015 Paris, France [3] Center for the Study of Primary Immunodeficiencies, Necker Hospital for Sick Children, 75015 Paris, France. ; 1] Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA [2] Global Health and Emerging Pathogens Institute, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA [3] Department of Medicine, Division of Infectious Diseases, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA. ; 1] St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, New York 10065, USA [2] Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM U1163, Necker Hospital for Sick Children, 75015 Paris, France [3] Paris Descartes University, Imagine Institute, 75015 Paris, France. ; Division of Immunology, Children's Hospital Boston, Boston, Massachusetts 02115, USA. ; 1] Manchester Academic Health Science Centre, University of Manchester, Genetic Medicine, Manchester, M13 9NT, UK [2] Paris Descartes University, Imagine Institute, 75015 Paris, France [3] INSERM UMR 1163, Laboratory of Neurogenetics and Neuroinflammation, Imagine Institute, 75006 Paris, France. ; 1] Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM U1163, Necker Hospital for Sick Children, 75015 Paris, France [2] Paris Descartes University, Imagine Institute, 75015 Paris, France [3] Howard Hughes Medical Institute, New York, New York 10065, USA [4] Pediatric Hematology-Immunology Unit, Necker Hospital for Sick Children, 75015 Paris, France [5]. ; 1] Institut Pasteur, Cytokine Signaling Unit, CNRS URA 1961, 75724 Paris, France [2].〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25307056" target="_blank"〉PubMed〈/a〉

Description: Broadly, tissue regeneration is achieved in two ways: by proliferation of common differentiated cells and/or by deployment of specialized stem/progenitor cells. Which of these pathways applies is both organ- and injury-specific. Current models in the lung posit that epithelial repair can be attributed to cells expressing mature lineage markers. By contrast, here we define the regenerative role of previously uncharacterized, rare lineage-negative epithelial stem/progenitor (LNEP) cells present within normal distal lung. Quiescent LNEPs activate a DeltaNp63 (a p63 splice variant) and cytokeratin 5 remodelling program after influenza or bleomycin injury in mice. Activated cells proliferate and migrate widely to occupy heavily injured areas depleted of mature lineages, at which point they differentiate towards mature epithelium. Lineage tracing revealed scant contribution of pre-existing mature epithelial cells in such repair, whereas orthotopic transplantation of LNEPs, isolated by a definitive surface profile identified through single-cell sequencing, directly demonstrated the proliferative capacity and multipotency of this population. LNEPs require Notch signalling to activate the DeltaNp63 and cytokeratin 5 program, and subsequent Notch blockade promotes an alveolar cell fate. Persistent Notch signalling after injury led to parenchymal 'micro-honeycombing' (alveolar cysts), indicative of failed regeneration. Lungs from patients with fibrosis show analogous honeycomb cysts with evidence of hyperactive Notch signalling. Our findings indicate that distinct stem/progenitor cell pools repopulate injured tissue depending on the extent of the injury, and the outcomes of regeneration or fibrosis may depend in part on the dynamics of LNEP Notch signalling.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4312207/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4312207/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vaughan, Andrew E -- Brumwell, Alexis N -- Xi, Ying -- Gotts, Jeffrey E -- Brownfield, Doug G -- Treutlein, Barbara -- Tan, Kevin -- Tan, Victor -- Liu, Feng Chun -- Looney, Mark R -- Matthay, Michael A -- Rock, Jason R -- Chapman, Harold A -- F32 HL117600-01/HL/NHLBI NIH HHS/ -- R01 HL44712/HL/NHLBI NIH HHS/ -- U01 HL099995/HL/NHLBI NIH HHS/ -- U01 HL099999/HL/NHLBI NIH HHS/ -- U01 HL111054/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2015 Jan 29;517(7536):621-5. doi: 10.1038/nature14112. Epub 2014 Dec 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Cardiovascular Research Institute, University of California, San Francisco (UCSF), San Francisco, California 94143, USA. ; Department of Biochemistry, Stanford University School of Medicine and Howard Hughes Medical Institute, Stanford, California 94305, USA. ; Max Planck Institute for Evolutionary Anthropology, Department of Evolutionary Genetics, Deutscher Platz 6, 04103 Leipzig, Germany. ; Department of Anatomy, School of Medicine, University of California, San Francisco (UCSF), San Francisco, California 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25533958" target="_blank"〉PubMed〈/a〉

Description: Despite three decades of successful, predominantly phenotype-driven discovery of the genetic causes of monogenic disorders, up to half of children with severe developmental disorders of probable genetic origin remain without a genetic diagnosis. Particularly challenging are those disorders rare enough to have eluded recognition as a discrete clinical entity, those with highly variable clinical manifestations, and those that are difficult to distinguish from other, very similar, disorders. Here we demonstrate the power of using an unbiased genotype-driven approach to identify subsets of patients with similar disorders. By studying 1,133 children with severe, undiagnosed developmental disorders, and their parents, using a combination of exome sequencing and array-based detection of chromosomal rearrangements, we discovered 12 novel genes associated with developmental disorders. These newly implicated genes increase by 10% (from 28% to 31%) the proportion of children that could be diagnosed. Clustering of missense mutations in six of these newly implicated genes suggests that normal development is being perturbed by an activating or dominant-negative mechanism. Our findings demonstrate the value of adopting a comprehensive strategy, both genome-wide and nationwide, to elucidate the underlying causes of rare genetic disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Deciphering Developmental Disorders Study -- 098395/Wellcome Trust/United Kingdom -- 100140/Wellcome Trust/United Kingdom -- CZD/16/6/Chief Scientist Office/United Kingdom -- WT098051/Wellcome Trust/United Kingdom -- Department of Health/United Kingdom -- England -- Nature. 2015 Mar 12;519(7542):223-8. doi: 10.1038/nature14135. Epub 2014 Dec 24.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25533962" target="_blank"〉PubMed〈/a〉

Description: Myocardial infarction (MI), a leading cause of death around the world, displays a complex pattern of inheritance. When MI occurs early in life, genetic inheritance is a major component to risk. Previously, rare mutations in low-density lipoprotein (LDL) genes have been shown to contribute to MI risk in individual families, whereas common variants at more than 45 loci have been associated with MI risk in the population. Here we evaluate how rare mutations contribute to early-onset MI risk in the population. We sequenced the protein-coding regions of 9,793 genomes from patients with MI at an early age (〈/=50 years in males and 〈/=60 years in females) along with MI-free controls. We identified two genes in which rare coding-sequence mutations were more frequent in MI cases versus controls at exome-wide significance. At low-density lipoprotein receptor (LDLR), carriers of rare non-synonymous mutations were at 4.2-fold increased risk for MI; carriers of null alleles at LDLR were at even higher risk (13-fold difference). Approximately 2% of early MI cases harbour a rare, damaging mutation in LDLR; this estimate is similar to one made more than 40 years ago using an analysis of total cholesterol. Among controls, about 1 in 217 carried an LDLR coding-sequence mutation and had plasma LDL cholesterol 〉 190 mg dl(-1). At apolipoprotein A-V (APOA5), carriers of rare non-synonymous mutations were at 2.2-fold increased risk for MI. When compared with non-carriers, LDLR mutation carriers had higher plasma LDL cholesterol, whereas APOA5 mutation carriers had higher plasma triglycerides. Recent evidence has connected MI risk with coding-sequence mutations at two genes functionally related to APOA5, namely lipoprotein lipase and apolipoprotein C-III (refs 18, 19). Combined, these observations suggest that, as well as LDL cholesterol, disordered metabolism of triglyceride-rich lipoproteins contributes to MI risk.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4319990/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4319990/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Do, Ron -- Stitziel, Nathan O -- Won, Hong-Hee -- Jorgensen, Anders Berg -- Duga, Stefano -- Angelica Merlini, Pier -- Kiezun, Adam -- Farrall, Martin -- Goel, Anuj -- Zuk, Or -- Guella, Illaria -- Asselta, Rosanna -- Lange, Leslie A -- Peloso, Gina M -- Auer, Paul L -- NHLBI Exome Sequencing Project -- Girelli, Domenico -- Martinelli, Nicola -- Farlow, Deborah N -- DePristo, Mark A -- Roberts, Robert -- Stewart, Alexander F R -- Saleheen, Danish -- Danesh, John -- Epstein, Stephen E -- Sivapalaratnam, Suthesh -- Hovingh, G Kees -- Kastelein, John J -- Samani, Nilesh J -- Schunkert, Heribert -- Erdmann, Jeanette -- Shah, Svati H -- Kraus, William E -- Davies, Robert -- Nikpay, Majid -- Johansen, Christopher T -- Wang, Jian -- Hegele, Robert A -- Hechter, Eliana -- Marz, Winfried -- Kleber, Marcus E -- Huang, Jie -- Johnson, Andrew D -- Li, Mingyao -- Burke, Greg L -- Gross, Myron -- Liu, Yongmei -- Assimes, Themistocles L -- Heiss, Gerardo -- Lange, Ethan M -- Folsom, Aaron R -- Taylor, Herman A -- Olivieri, Oliviero -- Hamsten, Anders -- Clarke, Robert -- Reilly, Dermot F -- Yin, Wu -- Rivas, Manuel A -- Donnelly, Peter -- Rossouw, Jacques E -- Psaty, Bruce M -- Herrington, David M -- Wilson, James G -- Rich, Stephen S -- Bamshad, Michael J -- Tracy, Russell P -- Cupples, L Adrienne -- Rader, Daniel J -- Reilly, Muredach P -- Spertus, John A -- Cresci, Sharon -- Hartiala, Jaana -- Tang, W H Wilson -- Hazen, Stanley L -- Allayee, Hooman -- Reiner, Alex P -- Carlson, Christopher S -- Kooperberg, Charles -- Jackson, Rebecca D -- Boerwinkle, Eric -- Lander, Eric S -- Schwartz, Stephen M -- Siscovick, David S -- McPherson, Ruth -- Tybjaerg-Hansen, Anne -- Abecasis, Goncalo R -- Watkins, Hugh -- Nickerson, Deborah A -- Ardissino, Diego -- Sunyaev, Shamil R -- O'Donnell, Christopher J -- Altshuler, David -- Gabriel, Stacey -- Kathiresan, Sekar -- 090532/Wellcome Trust/United Kingdom -- 095552/Wellcome Trust/United Kingdom -- 5U54HG003067-11/HG/NHGRI NIH HHS/ -- G-0907/Parkinson's UK/United Kingdom -- K08 HL114642/HL/NHLBI NIH HHS/ -- K08HL114642/HL/NHLBI NIH HHS/ -- P01 HL076491/HL/NHLBI NIH HHS/ -- P01 HL098055/HL/NHLBI NIH HHS/ -- R01 HL107816/HL/NHLBI NIH HHS/ -- R01HL107816/HL/NHLBI NIH HHS/ -- RC2 HL-102923/HL/NHLBI NIH HHS/ -- RC2 HL-102924/HL/NHLBI NIH HHS/ -- RC2 HL-102925/HL/NHLBI NIH HHS/ -- RC2 HL-102926/HL/NHLBI NIH HHS/ -- RC2 HL-103010/HL/NHLBI NIH HHS/ -- T32 HL007208/HL/NHLBI NIH HHS/ -- T32HL00720/HL/NHLBI NIH HHS/ -- T32HL007604/HL/NHLBI NIH HHS/ -- UL1 TR000439/TR/NCATS NIH HHS/ -- Canadian Institutes of Health Research/Canada -- England -- Nature. 2015 Feb 5;518(7537):102-6. doi: 10.1038/nature13917. Epub 2014 Dec 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Center for Human Genetic Research, Massachusetts General Hospital, Boston, Massachusetts 02114, USA. [2] Cardiovascular Research Center, Massachusetts General Hospital, Boston, Massachusetts 02114, USA. [3] Department of Medicine, Harvard Medical School, Boston, Massachusetts 02114, USA. [4] Program in Medical and Population Genetics, Broad Institute, 7 Cambridge Center, Cambridge, Massachusetts 02142, USA. ; 1] Cardiovascular Division, Department of Medicine, Washington University School of Medicine, St Louis, Missouri 63110, USA. [2] Division of Statistical Genomics, Washington University School of Medicine, St Louis, Missouri 63110, USA. ; Department of Clinical Biochemistry KB3011, Section for Molecular Genetics, Rigshospitalet, Copenhagen University Hospitals and Faculty of Health Sciences, University of Copenhagen, Copenhagen 1165, Denmark. ; Dipartimento di Biotecnologie Mediche e Medicina Traslazionale, Universita degli Studi di Milano, Milano 20122, Italy. ; Division of Cardiology, Ospedale Niguarda, Milano 20162, Italy. ; Program in Medical and Population Genetics, Broad Institute, 7 Cambridge Center, Cambridge, Massachusetts 02142, USA. ; Department of Cardiovascular Medicine, The Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford OX1 2J, UK. ; Department of Genetics, University of North Carolina, Chapel Hill, North Carolina 27599, USA. ; Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA. ; University of Verona School of Medicine, Department of Medicine, Verona 37129, Italy. ; John &Jennifer Ruddy Canadian Cardiovascular Genetics Centre, University of Ottawa Heart Institute, Ottawa, Ontario K1Y 4W7, Canada. ; Department of Public Health and Primary Care, University of Cambridge, Cambridge CB2 1TN, UK. ; MedStar Health Research Institute, Cardiovascular Research Institute, Hyattsville, Maryland 20782, USA. ; Department of Vascular Medicine, Academic Medical Center, Amsterdam 1105 AZ, The Netherlands. ; Department of Cardiovascular Sciences, University of Leicester, and Leicester NIHR Biomedical Research Unit in Cardiovascular Disease, Glenfield Hospital, Leicester LE3 9QP, UK. ; DZHK (German Research Centre for Cardiovascular Research), Munich Heart Alliance, Deutsches Herzzentrum Munchen, Technische Universitat Munchen, Berlin 13347, Germany. ; Medizinische Klinik II, University of Lubeck, Lubeck 23562, Germany. ; 1] Center for Human Genetics, Duke University, Durham, North Carolina 27708, USA. [2] Department of Cardiology and Center for Genomic Medicine, Duke University School of Medicine, Durham, North Carolina 27708, USA. ; Department of Cardiology and Center for Genomic Medicine, Duke University School of Medicine, Durham, North Carolina 27708, USA. ; Division of Cardiology, University of Ottawa Heart Institute, Ottawa, Ontario K1Y 4W7, Canada. ; Department of Biochemistry, Schulich School of Medicine and Dentistry, Robarts Research Institute, University of Western Ontario, London, Ontario N6A 3K7, Canada. ; 1] Department of Biochemistry, Schulich School of Medicine and Dentistry, Robarts Research Institute, University of Western Ontario, London, Ontario N6A 3K7, Canada. [2] Department of Medicine, Schulich School of Medicine and Dentistry, Robarts Research Institute, University of Western Ontario, London, Ontario N6A 3K7, Canada. ; 1] Medical Faculty Mannheim, Mannheim Institute of Public Health, Social and Preventive Medicine, Heidelberg University, Ludolf Krehl Strasse 7-11, Mannheim D-68167, Germany. [2] Clinical Institute of Medical and Chemical Laboratory Diagnostics, Medical University of Graz, Graz 8036, Austria. [3] Synlab Academy, Mannheim 68259, Germany. ; Medical Faculty Mannheim, Mannheim Institute of Public Health, Social and Preventive Medicine, Heidelberg University, Ludolf Krehl Strasse 7-11, Mannheim D-68167, Germany. ; The National Heart, Lung, Blood Institute's Framingham Heart Study, Framingham, Massachusetts 01702, USA. ; National Heart, Lung, and Blood Institute Center for Population Studies, The Framingham Heart Study, Framingham, Massachusetts 01702, USA. ; Department of Biostatistics and Epidemiology, School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA. ; Department of Epidemiology, University of Alabama-Birmingham, Birmingham, Alabama 35233, USA. ; Department of Laboratory Medicine and Pathology, School of Medicine, University of Minnesota, Minneapolis, Minnesota 55455, USA. ; School of Medicine, Wake Forest University, Winston-Salem, North Carolina 27106, USA. ; Department of Medicine, Stanford University School of Medicine, Stanford, California 94305, USA. ; Department of Epidemiology, University of North Carolina, Chapel Hill, North Carolina 27599, USA. ; 1] Department of Genetics, University of North Carolina, Chapel Hill, North Carolina 27599, USA. [2] Carolina Center for Genome Sciences, University of North Carolina, Chapel Hill, North Carolina 27599, USA. ; Division of Epidemiology and Community Health, University of Minnesota School of Public Health, Minneapolis, Minnesota 55455, USA. ; University of Mississippi Medical Center, Jackson, Mississippi 39216, USA. ; Atherosclerosis Research Unit, Department of Medicine, and Center for Molecular Medicine, Karolinska Institutet, Stockholm 171 77, Sweden. ; Clinical Trial Service Unit and Epidemiological Studies Unit, University of Oxford, Oxford OX1 2JD, UK. ; Merck Sharp &Dohme Corporation, Rahway, New Jersey 08889, USA. ; The Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford OX1 2JD, UK. ; 1] The Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford OX1 2JD, UK. [2] Department of Statistics, University of Oxford, Oxford OX1 2JD, UK. ; National Heart, Lung, and Blood Institute, Bethesda, Maryland 20824, USA. ; 1] Cardiovascular Health Research Unit, Departments of Medicine, Epidemiology, and Health Services, University of Washington, Seattle, Washington 98195, USA. [2] Group Health Research Institute, Group Health Cooperative, Seattle, Washington 98101, USA. ; Section on Cardiology, and Public Health Sciences, Wake Forest School of Medicine, Winston-Salem, North Carolina 27106, USA. ; Jackson Heart Study, University of Mississippi Medical Center, Jackson State University, Jackson, Mississippi 39217, USA. ; Center for Public Health Genomics, University of Virginia, Charlottesville, Virginia 22904, USA. ; 1] Division of Genetic Medicine, Department of Pediatrics, University of Washington, Seattle, Washington 98195, USA. [2] Seattle Children's Hospital, Seattle, Washington 98105, USA. [3] Department of Genome Sciences, University of Washington, Seattle, Washington 98195, USA. ; Department of Biochemistry, University of Vermont, Burlington, Vermont 05405, USA. ; Department of Biostatistics, Boston University School of Public Health, Boston, Massachusetts 02118, USA. ; Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA. ; Cardiovascular Institute, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA. ; St Luke's Mid America Heart Institute, University of Missouri-Kansas City, Kansas City, Missouri 64111, USA. ; 1] Cardiovascular Division, Department of Medicine, Washington University School of Medicine, St Louis, Missouri 63110, USA. [2] Department of Genetics, Washington University in St Louis, Missouri 63130, USA. ; Department of Preventive Medicine and Institute for Genetic Medicine, University of Southern California Keck School of Medicine, Los Angeles, California 90033, USA. ; Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio 44195, USA. ; 1] Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA. [2] Department of Epidemiology, University of Washington, Seattle, Washington 98195, USA. ; Ohio State University, Columbus, Ohio 43210, USA. ; Human Genetics Center, The University of Texas Health Science Center at Houston, Houston, Texas 77030, USA. ; 1] Department of Epidemiology, University of Washington, Seattle, Washington 98195, USA. [2] Department of Medicine, School of Medicine, University of Washington, Seattle, Washington 98195, USA. ; 1] Department of Clinical Biochemistry KB3011, Section for Molecular Genetics, Rigshospitalet, Copenhagen University Hospitals and Faculty of Health Sciences, University of Copenhagen, Copenhagen 1165, Denmark. [2] Faculty of Health and Medical Sciences, University of Copenhagen, Blegdamsvej 3B, 2200 Kobenhavn N, Denmark. ; Center for Statistical Genetics, Department of Biostatistics, University of Michigan, Ann Arbor, Missouri 48109, USA. ; 1] Department of Cardiovascular Medicine, The Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford OX1 2J, UK. [2] The Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford OX1 2JD, UK. ; Department of Genome Sciences, University of Washington, Seattle, Washington 98195, USA. ; Department of Cardiology, Parma Hospital, Parma 43100, Italy. ; 1] Program in Medical and Population Genetics, Broad Institute, 7 Cambridge Center, Cambridge, Massachusetts 02142, USA. [2] Division of Genetics, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA. ; 1] Center for Human Genetic Research, Massachusetts General Hospital, Boston, Massachusetts 02114, USA. [2] Program in Medical and Population Genetics, Broad Institute, 7 Cambridge Center, Cambridge, Massachusetts 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25487149" target="_blank"〉PubMed〈/a〉

Description: TP53 is commonly altered in human cancer, and Tp53 reactivation suppresses tumours in vivo in mice (TP53 and Tp53 are also known as p53). This strategy has proven difficult to implement therapeutically, and here we examine an alternative strategy by manipulating the p53 family members, Tp63 and Tp73 (also known as p63 and p73, respectively). The acidic transactivation-domain-bearing (TA) isoforms of p63 and p73 structurally and functionally resemble p53, whereas the DeltaN isoforms (lacking the acidic transactivation domain) of p63 and p73 are frequently overexpressed in cancer and act primarily in a dominant-negative fashion against p53, TAp63 and TAp73 to inhibit their tumour-suppressive functions. The p53 family interacts extensively in cellular processes that promote tumour suppression, such as apoptosis and autophagy, thus a clear understanding of this interplay in cancer is needed to treat tumours with alterations in the p53 pathway. Here we show that deletion of the DeltaN isoforms of p63 or p73 leads to metabolic reprogramming and regression of p53-deficient tumours through upregulation of IAPP, the gene that encodes amylin, a 37-amino-acid peptide co-secreted with insulin by the beta cells of the pancreas. We found that IAPP is causally involved in this tumour regression and that amylin functions through the calcitonin receptor (CalcR) and receptor activity modifying protein 3 (RAMP3) to inhibit glycolysis and induce reactive oxygen species and apoptosis. Pramlintide, a synthetic analogue of amylin that is currently used to treat type 1 and type 2 diabetes, caused rapid tumour regression in p53-deficient thymic lymphomas, representing a novel strategy to target p53-deficient cancers.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4312210/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4312210/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Venkatanarayan, Avinashnarayan -- Raulji, Payal -- Norton, William -- Chakravarti, Deepavali -- Coarfa, Cristian -- Su, Xiaohua -- Sandur, Santosh K -- Ramirez, Marc S -- Lee, Jaehuk -- Kingsley, Charles V -- Sananikone, Eliot F -- Rajapakshe, Kimal -- Naff, Katherine -- Parker-Thornburg, Jan -- Bankson, James A -- Tsai, Kenneth Y -- Gunaratne, Preethi H -- Flores, Elsa R -- CA-16672/CA/NCI NIH HHS/ -- P30 CA016672/CA/NCI NIH HHS/ -- P50CA136411/CA/NCI NIH HHS/ -- R01 CA134796/CA/NCI NIH HHS/ -- R01 CA160394/CA/NCI NIH HHS/ -- R01CA134796/CA/NCI NIH HHS/ -- R01CA160394/CA/NCI NIH HHS/ -- England -- Nature. 2015 Jan 29;517(7536):626-30. doi: 10.1038/nature13910. Epub 2014 Nov 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Molecular and Cellular Oncology, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA [2] Department of Translational Molecular Pathology, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA [3] Graduate School of Biomedical Sciences, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA [4] Metastasis Research Center, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA. ; 1] Department of Molecular and Cellular Oncology, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA [2] Department of Translational Molecular Pathology, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA. ; Department of Veterinary Medicine and Surgery, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA. ; Department of Molecular and Cellular Biology, Baylor College of Medicine, 1 Baylor Plaza, Houston, Texas 77030, USA. ; 1] Department of Molecular and Cellular Oncology, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA [2] Department of Translational Molecular Pathology, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA [3] Metastasis Research Center, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA. ; 1] Department of Molecular and Cellular Oncology, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA [2] Department of Translational Molecular Pathology, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA [3] Metastasis Research Center, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA [4] Radiation Biology &Health Sciences Division, Bhabha Atomic Research Center, Mumbai 400085, India. ; Department of Imaging Physics, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA. ; Department of Genetics, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA. ; 1] Department of Translational Molecular Pathology, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA [2] Department of Dermatology, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA. ; Department of Biology and Biochemistry, University of Houston, Houston, Texas 77204, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25409149" target="_blank"〉PubMed〈/a〉

Description: Cytotoxic chemotherapy is effective in debulking tumour masses initially; however, in some patients tumours become progressively unresponsive after multiple treatment cycles. Previous studies have demonstrated that cancer stem cells (CSCs) are selectively enriched after chemotherapy through enhanced survival. Here we reveal a new mechanism by which bladder CSCs actively contribute to therapeutic resistance via an unexpected proliferative response to repopulate residual tumours between chemotherapy cycles, using human bladder cancer xenografts. Further analyses demonstrate the recruitment of a quiescent label-retaining pool of CSCs into cell division in response to chemotherapy-induced damages, similar to mobilization of normal stem cells during wound repair. While chemotherapy effectively induces apoptosis, associated prostaglandin E2 (PGE2) release paradoxically promotes neighbouring CSC repopulation. This repopulation can be abrogated by a PGE2-neutralizing antibody and celecoxib drug-mediated blockade of PGE2 signalling. In vivo administration of the cyclooxygenase-2 (COX2) inhibitor celecoxib effectively abolishes a PGE2- and COX2-mediated wound response gene signature, and attenuates progressive manifestation of chemoresistance in xenograft tumours, including primary xenografts derived from a patient who was resistant to chemotherapy. Collectively, these findings uncover a new underlying mechanism that models the progressive development of clinical chemoresistance, and implicate an adjunctive therapy to enhance chemotherapeutic response of bladder urothelial carcinomas by abrogating early tumour repopulation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4465385/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4465385/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kurtova, Antonina V -- Xiao, Jing -- Mo, Qianxing -- Pazhanisamy, Senthil -- Krasnow, Ross -- Lerner, Seth P -- Chen, Fengju -- Roh, Terrence T -- Lay, Erica -- Ho, Philip Levy -- Chan, Keith Syson -- AI036211/AI/NIAID NIH HHS/ -- CA125123/CA/NCI NIH HHS/ -- CA129640/CA/NCI NIH HHS/ -- CA175397/CA/NCI NIH HHS/ -- R00 CA129640/CA/NCI NIH HHS/ -- R01 CA175397/CA/NCI NIH HHS/ -- RR024574/RR/NCRR NIH HHS/ -- England -- Nature. 2015 Jan 8;517(7533):209-13. doi: 10.1038/nature14034. Epub 2014 Dec 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Molecular &Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA [2] Program in Translational Biology and Molecular Medicine, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA. ; Department of Molecular &Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA. ; Dan L Duncan Cancer Center and Center for Cell Gene &Therapy, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA. ; Scott Department of Urology, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA. ; 1] Department of Molecular &Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA [2] Summer Medical and Research Training (SMART) Program, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA. ; 1] Department of Molecular &Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA [2] Program in Translational Biology and Molecular Medicine, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA [3] Dan L Duncan Cancer Center and Center for Cell Gene &Therapy, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA [4] Scott Department of Urology, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25470039" target="_blank"〉PubMed〈/a〉

Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tannock, Ian F -- England -- Nature. 2015 Jan 8;517(7533):152-3. doi: 10.1038/nature14075. Epub 2014 Dec 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Oncology, Princess Margaret Cancer Centre, Toronto, Ontario M5G 2M9, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25470047" target="_blank"〉PubMed〈/a〉

Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gregersen, Peter K -- New York, N.Y. -- Science. 2014 Mar 7;343(6175):1087-8. doi: 10.1126/science.1251426.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Robert S. Boas Center for Genomics and Human Genetics, The Feinstein Institute for Medical Research, North Shore LIJ Health System, 350 Community Drive, Manhasset, NY 110430, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24604188" target="_blank"〉PubMed〈/a〉

Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbons, Ann -- New York, N.Y. -- Science. 2014 Oct 24;346(6208):405-6. doi: 10.1126/science.346.6208.405.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25342776" target="_blank"〉PubMed〈/a〉

Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4340075/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4340075/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Churcher, Thomas S -- Cohen, Justin M -- Novotny, Joseph -- Ntshalintshali, Nyasatu -- Kunene, Simon -- Cauchemez, Simon -- MR/K010174/1/Medical Research Council/United Kingdom -- U54 GM088491/GM/NIGMS NIH HHS/ -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2014 Jun 13;344(6189):1230-2. doi: 10.1126/science.1251449.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Infectious Disease Epidemiology, Imperial College London, London, UK. ; Clinton Health Access Initiative, Boston, MA 02127, USA. ; Clinton Health Access Initiative, Boston, MA 02127, USA. Global Health Group, University of California, San Francisco, CA 94143, USA. ; National Malaria Control Program, Manzini, Swaziland. ; Department of Infectious Disease Epidemiology, Imperial College London, London, UK. Mathematical Modelling of Infectious Diseases Unit, Institut Pasteur, Paris, France. simon.cauchemez@pasteur.fr.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24926005" target="_blank"〉PubMed〈/a〉

Description: The neuromuscular junction (NMJ) is the synapse between a motor neuron and skeletal muscle. Defects in NMJ transmission cause muscle weakness, termed myasthenia. The muscle protein Dok-7 is essential for activation of the receptor kinase MuSK, which governs NMJ formation, and DOK7 mutations underlie familial limb-girdle myasthenia (DOK7 myasthenia), a neuromuscular disease characterized by small NMJs. Here, we show in a mouse model of DOK7 myasthenia that therapeutic administration of an adeno-associated virus (AAV) vector encoding the human DOK7 gene resulted in an enlargement of NMJs and substantial increases in muscle strength and life span. When applied to model mice of another neuromuscular disorder, autosomal dominant Emery-Dreifuss muscular dystrophy, DOK7 gene therapy likewise resulted in enlargement of NMJs as well as positive effects on motor activity and life span. These results suggest that therapies aimed at enlarging the NMJ may be useful for a range of neuromuscular disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arimura, Sumimasa -- Okada, Takashi -- Tezuka, Tohru -- Chiyo, Tomoko -- Kasahara, Yuko -- Yoshimura, Toshiro -- Motomura, Masakatsu -- Yoshida, Nobuaki -- Beeson, David -- Takeda, Shin'ichi -- Yamanashi, Yuji -- G0701521/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2014 Sep 19;345(6203):1505-8. doi: 10.1126/science.1250744.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Genetics, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan. ; Department of Molecular Therapy, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan. ; Department of Occupational Therapy, Nagasaki University School of Health Sciences, Nagasaki, Japan. ; Department of Electrical and Electronics Engineering, Faculty of Engineering, Nagasaki Institute of Applied Science, Nagasaki, Japan. ; Laboratory of Developmental Genetics, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan. ; Neurosciences Group, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, UK. ; Division of Genetics, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan. yyamanas@ims.u-tokyo.ac.jp.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25237101" target="_blank"〉PubMed〈/a〉

Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, Jocelyn -- New York, N.Y. -- Science. 2014 Mar 28;343(6178):1460-1. doi: 10.1126/science.343.6178.1460.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24675951" target="_blank"〉PubMed〈/a〉

Description: After an infection, pathogen-specific tissue-resident memory T cells (T(RM) cells) persist in nonlymphoid tissues to provide rapid control upon reinfection, and vaccination strategies that create T(RM) cell pools at sites of pathogen entry are therefore attractive. However, it is not well understood how T(RM) cells provide such pathogen protection. Here, we demonstrate that activated T(RM) cells in mouse skin profoundly alter the local tissue environment by inducing a number of broadly active antiviral and antibacterial genes. This "pathogen alert" allows skin T(RM) cells to protect against an antigenically unrelated virus. These data describe a mechanism by which tissue-resident memory CD8(+) T cells protect previously infected sites that is rapid, amplifies the activation of a small number of cells into an organ-wide response, and has the capacity to control escape variants.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ariotti, Silvia -- Hogenbirk, Marc A -- Dijkgraaf, Feline E -- Visser, Lindy L -- Hoekstra, Mirjam E -- Song, Ji-Ying -- Jacobs, Heinz -- Haanen, John B -- Schumacher, Ton N -- New York, N.Y. -- Science. 2014 Oct 3;346(6205):101-5. doi: 10.1126/science.1254803. Epub 2014 Aug 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Immunology, Netherlands Cancer Institute, 1066 CX Amsterdam, Netherlands. ; Division of Biological Stress Response, Netherlands Cancer Institute, 1066 CX Amsterdam, Netherlands. ; Experimental Animal Pathology, Netherlands Cancer Institute, 1066 CX Amsterdam, Netherlands. ; Division of Immunology, Netherlands Cancer Institute, 1066 CX Amsterdam, Netherlands. t.schumacher@nki.nl.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25278612" target="_blank"〉PubMed〈/a〉

Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4143233/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4143233/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mann, Richard S -- R01 NS070644/NS/NINDS NIH HHS/ -- R01NS070644/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2014 Apr 4;344(6179):48-9. doi: 10.1126/science.1252431.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biophysics, Columbia University, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24700848" target="_blank"〉PubMed〈/a〉

Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbons, Ann -- New York, N.Y. -- Science. 2014 Jun 13;344(6189):1213-4. doi: 10.1126/science.344.6189.1213.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24925995" target="_blank"〉PubMed〈/a〉

Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couzin-Frankel, Jennifer -- New York, N.Y. -- Science. 2014 May 16;344(6185):679. doi: 10.1126/science.344.6185.679.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24833367" target="_blank"〉PubMed〈/a〉

Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbons, Ann -- New York, N.Y. -- Science. 2014 Jan 31;343(6170):471-2. doi: 10.1126/science.343.6170.471.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24482455" target="_blank"〉PubMed〈/a〉

Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Silvente-Poirot, Sandrine -- Poirot, Marc -- New York, N.Y. -- Science. 2014 Mar 28;343(6178):1445-6. doi: 10.1126/science.1252787.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉UMR 1037 INSERM-University Toulouse III, Cancer Research Center of Toulouse, and Institut Claudius Regaud, 31052 Toulouse, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24675946" target="_blank"〉PubMed〈/a〉

Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- New York, N.Y. -- Science. 2014 Oct 17;346(6207):292-5. doi: 10.1126/science.346.6207.292.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25324367" target="_blank"〉PubMed〈/a〉

Description: Birds are the most species-rich class of tetrapod vertebrates and have wide relevance across many research fields. We explored bird macroevolution using full genomes from 48 avian species representing all major extant clades. The avian genome is principally characterized by its constrained size, which predominantly arose because of lineage-specific erosion of repetitive elements, large segmental deletions, and gene loss. Avian genomes furthermore show a remarkably high degree of evolutionary stasis at the levels of nucleotide sequence, gene synteny, and chromosomal structure. Despite this pattern of conservation, we detected many non-neutral evolutionary changes in protein-coding genes and noncoding regions. These analyses reveal that pan-avian genomic diversity covaries with adaptations to different lifestyles and convergent evolution of traits.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4390078/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4390078/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Guojie -- Li, Cai -- Li, Qiye -- Li, Bo -- Larkin, Denis M -- Lee, Chul -- Storz, Jay F -- Antunes, Agostinho -- Greenwold, Matthew J -- Meredith, Robert W -- Odeen, Anders -- Cui, Jie -- Zhou, Qi -- Xu, Luohao -- Pan, Hailin -- Wang, Zongji -- Jin, Lijun -- Zhang, Pei -- Hu, Haofu -- Yang, Wei -- Hu, Jiang -- Xiao, Jin -- Yang, Zhikai -- Liu, Yang -- Xie, Qiaolin -- Yu, Hao -- Lian, Jinmin -- Wen, Ping -- Zhang, Fang -- Li, Hui -- Zeng, Yongli -- Xiong, Zijun -- Liu, Shiping -- Zhou, Long -- Huang, Zhiyong -- An, Na -- Wang, Jie -- Zheng, Qiumei -- Xiong, Yingqi -- Wang, Guangbiao -- Wang, Bo -- Wang, Jingjing -- Fan, Yu -- da Fonseca, Rute R -- Alfaro-Nunez, Alonzo -- Schubert, Mikkel -- Orlando, Ludovic -- Mourier, Tobias -- Howard, Jason T -- Ganapathy, Ganeshkumar -- Pfenning, Andreas -- Whitney, Osceola -- Rivas, Miriam V -- Hara, Erina -- Smith, Julia -- Farre, Marta -- Narayan, Jitendra -- Slavov, Gancho -- Romanov, Michael N -- Borges, Rui -- Machado, Joao Paulo -- Khan, Imran -- Springer, Mark S -- Gatesy, John -- Hoffmann, Federico G -- Opazo, Juan C -- Hastad, Olle -- Sawyer, Roger H -- Kim, Heebal -- Kim, Kyu-Won -- Kim, Hyeon Jeong -- Cho, Seoae -- Li, Ning -- Huang, Yinhua -- Bruford, Michael W -- Zhan, Xiangjiang -- Dixon, Andrew -- Bertelsen, Mads F -- Derryberry, Elizabeth -- Warren, Wesley -- Wilson, Richard K -- Li, Shengbin -- Ray, David A -- Green, Richard E -- O'Brien, Stephen J -- Griffin, Darren -- Johnson, Warren E -- Haussler, David -- Ryder, Oliver A -- Willerslev, Eske -- Graves, Gary R -- Alstrom, Per -- Fjeldsa, Jon -- Mindell, David P -- Edwards, Scott V -- Braun, Edward L -- Rahbek, Carsten -- Burt, David W -- Houde, Peter -- Zhang, Yong -- Yang, Huanming -- Wang, Jian -- Avian Genome Consortium -- Jarvis, Erich D -- Gilbert, M Thomas P -- Wang, Jun -- DP1 OD000448/OD/NIH HHS/ -- DP1OD000448/OD/NIH HHS/ -- R01 HL087216/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Dec 12;346(6215):1311-20. doi: 10.1126/science.1251385. Epub 2014 Dec 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉China National GeneBank, Beijing Genomics Institute (BGI)-Shenzhen, Shenzhen, 518083, China. Centre for Social Evolution, Department of Biology, Universitetsparken 15, University of Copenhagen, DK-2100 Copenhagen, Denmark. zhanggj@genomics.cn jarvis@neuro.duke.edu mtpgilbert@gmail.com wangj@genomics.cn. ; China National GeneBank, Beijing Genomics Institute (BGI)-Shenzhen, Shenzhen, 518083, China. Centre for GeoGenetics, Natural History Museum of Denmark, University of Copenhagen, Oster Voldgade 5-7, 1350 Copenhagen, Denmark. ; China National GeneBank, Beijing Genomics Institute (BGI)-Shenzhen, Shenzhen, 518083, China. ; Royal Veterinary College, University of London, London, UK. ; Interdisciplinary Program in Bioinformatics, Seoul National University, Seoul 151-742, Republic of Korea. Cho and Kim Genomics, Seoul National University Research Park, Seoul 151-919, Republic of Korea. ; School of Biological Sciences, University of Nebraska, Lincoln, NE 68588, USA. ; Centro de Investigacion en Ciencias del Mar y Limnologia (CIMAR)/Centro Interdisciplinar de Investigacao Marinha e Ambiental (CIIMAR), Universidade do Porto, Rua dos Bragas, 177, 4050-123 Porto, Portugal. Departamento de Biologia, Faculdade de Ciencias, Universidade do Porto, Rua do Campo Alegre, 4169-007 Porto, Portugal. ; Department of Biological Sciences, University of South Carolina, Columbia, SC, USA. ; Department of Biology and Molecular Biology, Montclair State University, Montclair, NJ 07043, USA. ; Department of Animal Ecology, Uppsala University, Norbyvagen 18D, S-752 36 Uppsala, Sweden. ; Marie Bashir Institute for Infectious Diseases and Biosecurity, Charles Perkins Centre, School of Biological Sciences and Sydney Medical School, The University of Sydney, Sydney, NSW 2006, Australia. Program in Emerging Infectious Diseases, Duke-NUS Graduate Medical School, Singapore 169857, Singapore. ; Department of Integrative Biology University of California, Berkeley, CA 94720, USA. ; China National GeneBank, Beijing Genomics Institute (BGI)-Shenzhen, Shenzhen, 518083, China. College of Life Sciences, Wuhan University, Wuhan 430072, China. ; China National GeneBank, Beijing Genomics Institute (BGI)-Shenzhen, Shenzhen, 518083, China. School of Bioscience and Bioengineering, South China University of Technology, Guangzhou 510006, China. ; China National GeneBank, Beijing Genomics Institute (BGI)-Shenzhen, Shenzhen, 518083, China. BGI Education Center,University of Chinese Academy of Sciences,Shenzhen, 518083, China. ; Key Laboratory of Animal Models and Human Disease Mechanisms of Chinese Academy of Sciences and Yunnan Province, Kunming Institute of Zoology, Kunming, Yunnan 650223, China. ; Centre for GeoGenetics, Natural History Museum of Denmark, University of Copenhagen, Oster Voldgade 5-7, 1350 Copenhagen, Denmark. ; Department of Neurobiology, Howard Hughes Medical Institute, Duke University Medical Center, Durham, NC 27710, USA. ; Institute of Biological, Environmental and Rural Sciences, Aberystwyth University, Aberystwyth, UK. ; School of Biosciences, University of Kent, Canterbury CT2 7NJ, UK. ; Centro de Investigacion en Ciencias del Mar y Limnologia (CIMAR)/Centro Interdisciplinar de Investigacao Marinha e Ambiental (CIIMAR), Universidade do Porto, Rua dos Bragas, 177, 4050-123 Porto, Portugal. Instituto de Ciencias Biomedicas Abel Salazar (ICBAS), Universidade do Porto, Portugal. ; Department of Biology, University of California Riverside, Riverside, CA 92521, USA. ; Department of Biochemistry, Molecular Biology, Entomology and Plant Pathology, Mississippi State University, Mississippi State, MS 39762, USA. Institute for Genomics, Biocomputing and Biotechnology, Mississippi State University, Mississippi State, MS 39762, USA. ; Instituto de Ciencias Ambientales y Evolutivas, Facultad de Ciencias, Universidad Austral de Chile, Valdivia, Chile. ; Department of Anatomy, Physiology and Biochemistry, Swedish University of Agricultural Sciences, Post Office Box 7011, S-750 07, Uppsala, Sweden. ; Interdisciplinary Program in Bioinformatics, Seoul National University, Seoul 151-742, Republic of Korea. Cho and Kim Genomics, Seoul National University Research Park, Seoul 151-919, Republic of Korea. Department of Agricultural Biotechnology and Research Institute for Agriculture and Life Sciences, Seoul National University, Seoul 151-742, Republic of Korea. ; Interdisciplinary Program in Bioinformatics, Seoul National University, Seoul 151-742, Republic of Korea. ; Cho and Kim Genomics, Seoul National University Research Park, Seoul 151-919, Republic of Korea. ; State Key Laboratory for Agrobiotechnology, China Agricultural University, Beijing 100094, China. ; State Key Laboratory for Agrobiotechnology, China Agricultural University, Beijing 100094, China. College of Animal Science and Technology, China Agricultural University, Beijing 100094, China. ; Organisms and Environment Division, Cardiff School of Biosciences, Cardiff University, Cardiff CF10 3AX, Wales, UK. ; Organisms and Environment Division, Cardiff School of Biosciences, Cardiff University, Cardiff CF10 3AX, Wales, UK. Key Lab of Animal Ecology and Conservation Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101 China. ; International Wildlife Consultants, Carmarthen SA33 5YL, Wales, UK. ; Centre for Zoo and Wild Animal Health, Copenhagen Zoo, Roskildevej 38, DK-2000 Frederiksberg, Denmark. ; Department of Ecology and Evolutionary Biology, Tulane University, New Orleans, LA, USA. Museum of Natural Science, Louisiana State University, Baton Rouge, LA 70803, USA. ; The Genome Institute at Washington University, St. Louis, MO 63108, USA. ; College of Medicine and Forensics, Xi'an Jiaotong University, Xi'an, 710061, China. ; Institute for Genomics, Biocomputing and Biotechnology, Mississippi State University, Mississippi State, MS 39762, USA. ; Department of Biomolecular Engineering, University of California, Santa Cruz, CA 95064, USA. ; Theodosius Dobzhansky Center for Genome Bioinformatics, St. Petersburg State University, St. Petersburg, Russia. Nova Southeastern University Oceanographic Center 8000 N Ocean Drive, Dania, FL 33004, USA. ; Smithsonian Conservation Biology Institute, National Zoological Park, 1500 Remount Road, Front Royal, VA 22630, USA. ; Genetics Division, San Diego Zoo Institute for Conservation Research, 15600 San Pasqual Valley Road, Escondido, CA 92027, USA. ; Department of Vertebrate Zoology, MRC-116, National Museum of Natural History, Smithsonian Institution, Post Office Box 37012, Washington, DC 20013-7012, USA. Center for Macroecology, Evolution and Climate, the Natural History Museum of Denmark, University of Copenhagen, Universitetsparken 15, DK-2100 Copenhagen O, Denmark. ; Key Laboratory of Zoological Systematics and Evolution, Institute of Zoology, Chinese Academy of Sciences, 1 Beichen West Road, Chaoyang District, Beijing 100101, China. Swedish Species Information Centre, Swedish University of Agricultural Sciences, Box 7007, SE-750 07 Uppsala, Sweden. ; Center for Macroecology, Evolution and Climate, the Natural History Museum of Denmark, University of Copenhagen, Universitetsparken 15, DK-2100 Copenhagen O, Denmark. ; Department of Biochemistry & Biophysics, University of California, San Francisco, CA 94158, USA. ; Department of Organismic and Evolutionary Biology and Museum of Comparative Zoology, Harvard University, 26 Oxford Street, Cambridge, MA 02138, USA. ; Department of Biology and Genetics Institute, University of Florida, Gainesville, FL 32611, USA. ; Center for Macroecology, Evolution and Climate, the Natural History Museum of Denmark, University of Copenhagen, Universitetsparken 15, DK-2100 Copenhagen O, Denmark. Imperial College London, Grand Challenges in Ecosystems and the Environment Initiative, Silwood Park Campus, Ascot, Berkshire SL5 7PY, UK. ; Division of Genetics and Genomics, The Roslin Institute and Royal (Dick) School of Veterinary Studies, The Roslin Institute Building, University of Edinburgh, Easter Bush Campus, Midlothian EH25 9RG, UK. ; Department of Biology, New Mexico State University, Box 30001 MSC 3AF, Las Cruces, NM 88003, USA. ; China National GeneBank, Beijing Genomics Institute (BGI)-Shenzhen, Shenzhen, 518083, China. Macau University of Science and Technology, Avenida Wai long, Taipa, Macau 999078, China. ; Department of Neurobiology, Howard Hughes Medical Institute, Duke University Medical Center, Durham, NC 27710, USA. zhanggj@genomics.cn jarvis@neuro.duke.edu mtpgilbert@gmail.com wangj@genomics.cn. ; Centre for GeoGenetics, Natural History Museum of Denmark, University of Copenhagen, Oster Voldgade 5-7, 1350 Copenhagen, Denmark. Trace and Environmental DNA Laboratory, Department of Environment and Agriculture, Curtin University, Perth, Western Australia, 6102, Australia. zhanggj@genomics.cn jarvis@neuro.duke.edu mtpgilbert@gmail.com wangj@genomics.cn. ; China National GeneBank, Beijing Genomics Institute (BGI)-Shenzhen, Shenzhen, 518083, China. Macau University of Science and Technology, Avenida Wai long, Taipa, Macau 999078, China. Department of Biology, University of Copenhagen, Ole Maaloes Vej 5, 2200 Copenhagen, Denmark. Princess Al Jawhara Center of Excellence in the Research of Hereditary Disorders, King Abdulaziz University, Jeddah 21589, Saudi Arabia. Department of Medicine, University of Hong Kong, Hong Kong. zhanggj@genomics.cn jarvis@neuro.duke.edu mtpgilbert@gmail.com wangj@genomics.cn.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25504712" target="_blank"〉PubMed〈/a〉

Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stone, Richard -- New York, N.Y. -- Science. 2014 Jul 11;345(6193):130-1, 133. doi: 10.1126/science.345.6193.130.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25013042" target="_blank"〉PubMed〈/a〉

Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Benderly, Beryl Lieff -- New York, N.Y. -- Science. 2014 Mar 14;343(6176):1200. doi: 10.1126/science.343.6176.1200-b.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Science Careers Columnist.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24626915" target="_blank"〉PubMed〈/a〉

Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kean, Sam -- New York, N.Y. -- Science. 2014 Mar 28;343(6178):1457-9. doi: 10.1126/science.343.6178.1457.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24675950" target="_blank"〉PubMed〈/a〉

Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Promislow, Daniel E L -- Kaeberlein, Matt -- R01 AG031108/AG/NIA NIH HHS/ -- R01 AG033598/AG/NIA NIH HHS/ -- R01 GM102279/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2014 Jan 31;343(6170):491-2. doi: 10.1126/science.1250174.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Washington, Seattle, WA 98195 USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24482469" target="_blank"〉PubMed〈/a〉

Description: Comparative genomic analyses have revealed that genes may arise from ancestrally nongenic sequence. However, the origin and spread of these de novo genes within populations remain obscure. We identified 142 segregating and 106 fixed testis-expressed de novo genes in a population sample of Drosophila melanogaster. These genes appear to derive primarily from ancestral intergenic, unexpressed open reading frames, with natural selection playing a significant role in their spread. These results reveal a heretofore unappreciated dynamism of gene content.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4391638/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4391638/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhao, Li -- Saelao, Perot -- Jones, Corbin D -- Begun, David J -- GM084056/GM/NIGMS NIH HHS/ -- R01 GM084056/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2014 Feb 14;343(6172):769-72. doi: 10.1126/science.1248286. Epub 2014 Jan 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Evolution and Ecology, University of California, Davis, CA 95616, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24457212" target="_blank"〉PubMed〈/a〉

Description: Most land animals normally walk forward but switch to backward walking upon sensing an obstacle or danger in the path ahead. A change in walking direction is likely to be triggered by descending "command" neurons from the brain that act upon local motor circuits to alter the timing of leg muscle activation. Here we identify descending neurons for backward walking in Drosophila--the MDN neurons. MDN activity is required for flies to walk backward when they encounter an impassable barrier and is sufficient to trigger backward walking under conditions in which flies would otherwise walk forward. We also identify ascending neurons, MAN, that promote persistent backward walking, possibly by inhibiting forward walking. These findings provide an initial glimpse into the circuits and logic that control walking direction in Drosophila.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bidaye, Salil S -- Machacek, Christian -- Wu, Yang -- Dickson, Barry J -- New York, N.Y. -- Science. 2014 Apr 4;344(6179):97-101. doi: 10.1126/science.1249964.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Research Institute of Molecular Pathology (IMP), Dr. Bohrgasse 7, A-1030 Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24700860" target="_blank"〉PubMed〈/a〉

Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- New York, N.Y. -- Science. 2014 Jan 17;343(6168):239. doi: 10.1126/science.343.6168.239.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24436399" target="_blank"〉PubMed〈/a〉

Description: How we attend to objects and their features that cannot be separated by location is not understood. We presented two temporally and spatially overlapping streams of objects, faces versus houses, and used magnetoencephalography and functional magnetic resonance imaging to separate neuronal responses to attended and unattended objects. Attention to faces versus houses enhanced the sensory responses in the fusiform face area (FFA) and parahippocampal place area (PPA), respectively. The increases in sensory responses were accompanied by induced gamma synchrony between the inferior frontal junction, IFJ, and either FFA or PPA, depending on which object was attended. The IFJ appeared to be the driver of the synchrony, as gamma phases were advanced by 20 ms in IFJ compared to FFA or PPA. Thus, the IFJ may direct the flow of visual processing during object-based attention, at least in part through coupled oscillations with specialized areas such as FFA and PPA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baldauf, Daniel -- Desimone, Robert -- P30EY2621/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 2014 Apr 25;344(6182):424-7. doi: 10.1126/science.1247003. Epub 2014 Apr 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉McGovern Institute for Brain Research, Massachusetts Institute of Technology, Cambridge, 02139 MA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24763592" target="_blank"〉PubMed〈/a〉

Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Blair, H T -- New York, N.Y. -- Science. 2014 Feb 21;343(6173):846-7. doi: 10.1126/science.1251252.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Psychology Department and Brain Research Institute, University of California, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24558150" target="_blank"〉PubMed〈/a〉

Description: Sex-specific chromosomes, like the W of most female birds and the Y of male mammals, usually have lost most genes owing to a lack of recombination. We analyze newly available genomes of 17 bird species representing the avian phylogenetic range, and find that more than half of them do not have as fully degenerated W chromosomes as that of chicken. We show that avian sex chromosomes harbor tremendous diversity among species in their composition of pseudoautosomal regions and degree of Z/W differentiation. Punctuated events of shared or lineage-specific recombination suppression have produced a gradient of "evolutionary strata" along the Z chromosome, which initiates from the putative avian sex-determining gene DMRT1 and ends at the pseudoautosomal region. W-linked genes are subject to ongoing functional decay after recombination was suppressed, and the tempo of degeneration slows down in older strata. Overall, we unveil a complex history of avian sex chromosome evolution.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, Qi -- Zhang, Jilin -- Bachtrog, Doris -- An, Na -- Huang, Quanfei -- Jarvis, Erich D -- Gilbert, M Thomas P -- Zhang, Guojie -- GM076007/GM/NIGMS NIH HHS/ -- GM093182/GM/NIGMS NIH HHS/ -- R01 GM076007/GM/NIGMS NIH HHS/ -- R01 GM093182/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Dec 12;346(6215):1246338. doi: 10.1126/science.1246338. Epub 2014 Dec 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Integrative Biology, University of California, Berkeley, CA94720, USA. zhouqi@berkeley.edu zhanggj@genomics.org.cn. ; China National Genebank, BGI-Shenzhen, Shenzhen, 518083. China. ; Department of Integrative Biology, University of California, Berkeley, CA94720, USA. ; Department of Neurobiology, Howard Hughes Medical Institute, Duke University Medical Center, Durham, NC 27710, USA. ; Centre for GeoGenetics, Natural History Museum of Denmark, University of Copenhagen, Oster Voldgade 5-7, 1350 Copenhagen, Denmark. Trace and Environmental DNA laboratory, Department of Environment and Agriculture, Curtin University, Perth, Western Australia 6102, Australia. ; China National Genebank, BGI-Shenzhen, Shenzhen, 518083. China. Centre for Social Evolution, Department of Biology, Universitetsparken 15, University of Copenhagen, DK-2100 Copenhagen, Denmark. zhouqi@berkeley.edu zhanggj@genomics.org.cn.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25504727" target="_blank"〉PubMed〈/a〉

Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Blanton, Richard E -- New York, N.Y. -- Science. 2014 Jan 31;343(6170):485-6. doi: 10.1126/science.343.6170.485-b.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anthropology, Purdue University, West Lafayette, IN 47907, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24482466" target="_blank"〉PubMed〈/a〉

Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zimmerman, Andrew W -- Connors, Susan L -- New York, N.Y. -- Science. 2014 Feb 7;343(6171):620-1. doi: 10.1126/science.1250214.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics (Neurology), Center for Autism and Neurodevelopmental Disorders, University of Massachusetts Medical School, Worcester, MA 01655, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24503843" target="_blank"〉PubMed〈/a〉

Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Susiarjo, Martha -- Bartolomei, Marisa S -- P30 ES013508/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 2014 Aug 15;345(6198):733-4. doi: 10.1126/science.1258654.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. ; Department of Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. bartolom@mail.med.upenn.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25124413" target="_blank"〉PubMed〈/a〉

Description: How sleep helps learning and memory remains unknown. We report in mouse motor cortex that sleep after motor learning promotes the formation of postsynaptic dendritic spines on a subset of branches of individual layer V pyramidal neurons. New spines are formed on different sets of dendritic branches in response to different learning tasks and are protected from being eliminated when multiple tasks are learned. Neurons activated during learning of a motor task are reactivated during subsequent non-rapid eye movement sleep, and disrupting this neuronal reactivation prevents branch-specific spine formation. These findings indicate that sleep has a key role in promoting learning-dependent synapse formation and maintenance on selected dendritic branches, which contribute to memory storage.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4447313/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4447313/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, Guang -- Lai, Cora Sau Wan -- Cichon, Joseph -- Ma, Lei -- Li, Wei -- Gan, Wen-Biao -- P01 NS074972/NS/NINDS NIH HHS/ -- R01 NS047325/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2014 Jun 6;344(6188):1173-8. doi: 10.1126/science.1249098.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Skirball Institute, Department of Neuroscience and Physiology, New York University School of Medicine, New York, NY 10016, USA. Department of Anesthesiology, New York University School of Medicine, New York, NY 10016, USA. ; Skirball Institute, Department of Neuroscience and Physiology, New York University School of Medicine, New York, NY 10016, USA. ; Skirball Institute, Department of Neuroscience and Physiology, New York University School of Medicine, New York, NY 10016, USA. Drug Discovery Center, Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen, 518055, China. ; Drug Discovery Center, Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen, 518055, China. ; Skirball Institute, Department of Neuroscience and Physiology, New York University School of Medicine, New York, NY 10016, USA. gan@saturn.med.nyu.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24904169" target="_blank"〉PubMed〈/a〉

Description: Environmental exposures affect gamete function and fertility, but the mechanisms are poorly understood. Here, we show that pheromones sensed by ciliated neurons in the Caenorhabditis elegans nose alter the lipid microenvironment within the oviduct, thereby affecting sperm motility. In favorable environments, pheromone-responsive sensory neurons secrete a transforming growth factor-beta ligand called DAF-7, which acts as a neuroendocrine factor that stimulates prostaglandin-endoperoxide synthase [cyclooxygenase (Cox)]-independent prostaglandin synthesis in the ovary. Oocytes secrete F-class prostaglandins that guide sperm toward them. These prostaglandins are also synthesized in Cox knockout mice, raising the possibility that similar mechanisms exist in other animals. Our data indicate that environmental cues perceived by the female nervous system affect sperm function.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4094289/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4094289/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McKnight, Katherine -- Hoang, Hieu D -- Prasain, Jeevan K -- Brown, Naoko -- Vibbert, Jack -- Hollister, Kyle A -- Moore, Ray -- Ragains, Justin R -- Reese, Jeff -- Miller, Michael A -- GM085105/GM/NIGMS NIH HHS/ -- HL096967/HL/NHLBI NIH HHS/ -- HL109199/HL/NHLBI NIH HHS/ -- HL110950/HL/NHLBI NIH HHS/ -- HL114439/HL/NHLBI NIH HHS/ -- P30 AR050948/AR/NIAMS NIH HHS/ -- P30 DK079337/DK/NIDDK NIH HHS/ -- P40 OD010440/OD/NIH HHS/ -- R01 GM085105/GM/NIGMS NIH HHS/ -- R01 HL096967/HL/NHLBI NIH HHS/ -- R01 HL109199/HL/NHLBI NIH HHS/ -- S10 RR19261/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2014 May 16;344(6185):754-7. doi: 10.1126/science.1250598.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, University of Alabama at Birmingham, Birmingham, AL 35294, USA. ; Department of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL 35294, USA. ; Department of Pharmacology and Toxicology, University of Alabama at Birmingham, Birmingham, AL 35294, USA. ; Department of Pediatrics, Vanderbilt University, Nashville, TN 37232, USA. ; Department of Chemistry, Louisiana State University, Baton Rouge, LA 70803, USA. ; Department of Pediatrics, Vanderbilt University, Nashville, TN 37232, USA. Department of Cell and Developmental Biology, Vanderbilt University, Nashville, TN 37232, USA. ; Department of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL 35294, USA. mamiller@uab.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24833393" target="_blank"〉PubMed〈/a〉

Description: Tyzio et al. (Reports, 7 February 2014, p. 675) reported that bumetanide restored the impaired oxytocin-mediated gamma-aminobutyric acid (GABA) excitatory-inhibitory shift during delivery in animal models of autism, ameliorating some autistic-like characteristics in the offspring. However, standard practices in the study of these models, such as the use of sex-dimorphic or males-only analyses and implementation of tests measuring social behavior, are lacking to definitely associate their findings to autism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bambini-Junior, Victorio -- Nunes, Gustavo Della Flora -- Schneider, Tomasz -- Gottfried, Carmem -- New York, N.Y. -- Science. 2014 Oct 10;346(6206):176. doi: 10.1126/science.1255679.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Federal University of Rio Grande do Sul, Research Group in Neuroglial Plasticity at the Department of Biochemistry, Institute of Health's Basic Science, Porto Alegre, Rio Grande do Sul, Brazil. Federal University of Rio Grande do Sul, Translational Research Group in Autism Spectrum Disorders (GETTEA), Porto Alegre, RS, Brazil. victoriobambini@gmail.com. ; Federal University of Rio Grande do Sul, Research Group in Neuroglial Plasticity at the Department of Biochemistry, Institute of Health's Basic Science, Porto Alegre, Rio Grande do Sul, Brazil. Federal University of Rio Grande do Sul, Translational Research Group in Autism Spectrum Disorders (GETTEA), Porto Alegre, RS, Brazil. ; School of Medicine, Pharmacy and Health, TS17 6BH, Durham University, Durham, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25301610" target="_blank"〉PubMed〈/a〉

Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Vrieze, Jop -- New York, N.Y. -- Science. 2014 Jan 17;343(6168):241-3. doi: 10.1126/science.343.6168.241.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24436401" target="_blank"〉PubMed〈/a〉

Description: Cross-cultural psychologists have mostly contrasted East Asia with the West. However, this study shows that there are major psychological differences within China. We propose that a history of farming rice makes cultures more interdependent, whereas farming wheat makes cultures more independent, and these agricultural legacies continue to affect people in the modern world. We tested 1162 Han Chinese participants in six sites and found that rice-growing southern China is more interdependent and holistic-thinking than the wheat-growing north. To control for confounds like climate, we tested people from neighboring counties along the rice-wheat border and found differences that were just as large. We also find that modernization and pathogen prevalence theories do not fit the data.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Talhelm, T -- Zhang, X -- Oishi, S -- Shimin, C -- Duan, D -- Lan, X -- Kitayama, S -- New York, N.Y. -- Science. 2014 May 9;344(6184):603-8. doi: 10.1126/science.1246850.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, University of Virginia, Charlottesville, VA 22904, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24812395" target="_blank"〉PubMed〈/a〉

Description: During limb development, digits emerge from the undifferentiated mesenchymal tissue that constitutes the limb bud. It has been proposed that this process is controlled by a self-organizing Turing mechanism, whereby diffusible molecules interact to produce a periodic pattern of digital and interdigital fates. However, the identities of the molecules remain unknown. By combining experiments and modeling, we reveal evidence that a Turing network implemented by Bmp, Sox9, and Wnt drives digit specification. We develop a realistic two-dimensional simulation of digit patterning and show that this network, when modulated by morphogen gradients, recapitulates the expression patterns of Sox9 in the wild type and in perturbation experiments. Our systems biology approach reveals how a combination of growth, morphogen gradients, and a self-organizing Turing network can achieve robust and reproducible pattern formation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Raspopovic, J -- Marcon, L -- Russo, L -- Sharpe, J -- New York, N.Y. -- Science. 2014 Aug 1;345(6196):566-70. doi: 10.1126/science.1252960.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Systems Biology Program, Centre for Genomic Regulation (CRG), and Universitat Pompeu Fabra (UPF), Dr. Aiguader 88, 08003 Barcelona, Spain. ; Systems Biology Program, Centre for Genomic Regulation (CRG), and Universitat Pompeu Fabra (UPF), Dr. Aiguader 88, 08003 Barcelona, Spain. Institucio Catalana de Recerca i Estudis Avancats (ICREA), Passeig Lluis Companys 23, 08010 Barcelona, Spain. james.sharpe@crg.eu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25082703" target="_blank"〉PubMed〈/a〉

Description: Genetic errors in meiosis can lead to birth defects and spontaneous abortions. Checkpoint mechanisms of hitherto unknown nature eliminate oocytes with unrepaired DNA damage, causing recombination-defective mutant mice to be sterile. Here, we report that checkpoint kinase 2 (Chk2 or Chek2), is essential for culling mouse oocytes bearing unrepaired meiotic or induced DNA double-strand breaks (DSBs). Female infertility caused by a meiotic recombination mutation or irradiation was reversed by mutation of Chk2. Both meiotically programmed and induced DSBs trigger CHK2-dependent activation of TRP53 (p53) and TRP63 (p63), effecting oocyte elimination. These data establish CHK2 as essential for DNA damage surveillance in female meiosis and indicate that the oocyte DSB damage response primarily involves a pathway hierarchy in which ataxia telangiectasia and Rad3-related (ATR) signals to CHK2, which then activates p53 and p63.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4048839/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4048839/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bolcun-Filas, Ewelina -- Rinaldi, Vera D -- White, Michelle E -- Schimenti, John C -- GM45415/GM/NIGMS NIH HHS/ -- R01 GM045415/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2014 Jan 31;343(6170):533-6. doi: 10.1126/science.1247671.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biomedical Sciences, Cornell University, Ithaca, NY 14850, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24482479" target="_blank"〉PubMed〈/a〉

Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McNutt, Marcia -- New York, N.Y. -- Science. 2014 Aug 15;345(6198):739. doi: 10.1126/science.345.6198.739-b. Epub 2014 Aug 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Editor-in-Chief.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25124417" target="_blank"〉PubMed〈/a〉

Description: The existence of BRCA1 was proven in 1990 by mapping predisposition to young-onset breast cancer in families to chromosome 17q21. Knowing that such a gene existed and approximately where it lay triggered efforts by public and private groups to clone and sequence it. The press baptized the competition "the race" and reported on it in detail for the next 4 years. BRCA1 was positionally cloned in September 1994. Twenty years later, I reflect on "the race" and its consequences for breast cancer prevention and treatment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉King, Mary-Claire -- R01 CA157744/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2014 Mar 28;343(6178):1462-5. doi: 10.1126/science.1251900.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine and Department of Genome Sciences, University of Washington, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24675952" target="_blank"〉PubMed〈/a〉

Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉You, Jia -- New York, N.Y. -- Science. 2014 Sep 19;345(6203):1440-1. doi: 10.1126/science.345.6203.1440.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25237081" target="_blank"〉PubMed〈/a〉

Description: Germline mutations in BRCA1 and BRCA2 predispose to common human malignancies, most notably tumors of the breast and ovaries. The proteins encoded by these genes have been implicated in a plethora of biochemical interactions and biological functions, confounding attempts to coherently explain how their inactivation promotes carcinogenesis. Here, I argue that tumor suppression by BRCA1 and BRCA2 originates from their fundamental role in controlling the assembly and activity of macromolecular complexes that monitor chromosome duplication, maintenance, and segregation across the cell cycle. A tumor-suppressive role for the BRCA proteins as "chromosome custodians" helps to explain the clinical features of cancer susceptibility after their inactivation, provides foundations for the rational therapy of BRCA-deficient cancers, and offers general insights into the mechanisms opposing early steps in human carcinogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Venkitaraman, Ashok R -- G1001521/Medical Research Council/United Kingdom -- G1001522/Medical Research Council/United Kingdom -- MC_U105359877/Medical Research Council/United Kingdom -- MC_UU_12022/1/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2014 Mar 28;343(6178):1470-5. doi: 10.1126/science.1252230.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council Cancer Unit, University of Cambridge, Hills Road, Cambridge CB2 0XZ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24675954" target="_blank"〉PubMed〈/a〉

Description: Parental care, including feeding and protection of young, is essential for the survival as well as mental and physical well-being of the offspring. A large variety of parental behaviors has been described across species and sexes, raising fascinating questions about how animals identify the young and how brain circuits drive and modulate parental displays in males and females. Recent studies have begun to uncover a striking antagonistic interplay between brain systems underlying parental care and infant-directed aggression in both males and females, as well as a large range of intrinsic and environmentally driven neural modulation and plasticity. Improved understanding of the neural control of parental interactions in animals should provide novel insights into the complex issue of human parental care in both health and disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4230532/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4230532/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dulac, Catherine -- O'Connell, Lauren A -- Wu, Zheng -- R01 DC009019/DC/NIDCD NIH HHS/ -- R01 DC013087/DC/NIDCD NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Aug 15;345(6198):765-70. doi: 10.1126/science.1253291. Epub 2014 Aug 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Molecular and Cellular Biology, Center for Brain Science, Harvard University, Cambridge, MA 02138, USA. dulac@fas.harvard.edu. ; FAS Center for System Biology, Harvard University, Cambridge, MA 02138, USA. ; Howard Hughes Medical Institute, Department of Molecular and Cellular Biology, Center for Brain Science, Harvard University, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25124430" target="_blank"〉PubMed〈/a〉