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Science

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Institución detectada Período Navegá Descargá Solicitá
No detectada desde mar. 1997 / hasta dic. 2023 Science Journals

Información

Tipo de recurso:

revistas

ISSN impreso

0036-8075

ISSN electrónico

1095-9203

Editor responsable

American Association for the Advancement of Science (AAAS)

País de edición

Estados Unidos

Fecha de publicación

Cobertura temática

Tabla de contenidos

Chinese COVID-19 vaccine maintains protection in variant-plagued Brazil

Sofia Moutinho

Palabras clave: Multidisciplinary.

Pp. No disponible

Honey bees rally to their queen via ‘game of telephone’

Nikk Ogasa

Palabras clave: Multidisciplinary.

Pp. No disponible

Biden wants $6.5 billion for new health agency to speed treatments

Jocelyn Kaiser

Palabras clave: Multidisciplinary.

Pp. No disponible

A pigment from red cabbage could help turn your favorite foods blue

Kai Kupferschmidt

Palabras clave: Multidisciplinary.

Pp. No disponible

Biden’s first budget request goes big on science

Jeffrey Mervis

Palabras clave: Multidisciplinary.

Pp. No disponible

Epigenetics, fragmentomics, and topology of cell-free DNA in liquid biopsies

Y. M. Dennis LoORCID; Diana S. C. HanORCID; Peiyong JiangORCID; Rossa W. K. ChiuORCID

<jats:title>Enhancing liquid biopsies</jats:title> <jats:p> Liquid biopsies, analyses of cell-free DNA that circulates in the blood, can be used in prenatal testing, oncology, and to monitor organ transplant recipients. Lo <jats:italic>et al.</jats:italic> review the nongenetic information that can be gleaned from analyses of cell-free DNA, which offers additional promise for the applications of this procedure. These analyses include DNA methylation patterns, fragmentation profiles, and topology, which can be informative about the health and origin of the tissue from which they are derived. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" related-article-type="in-this-issue" xlink:href="10.1126/science.aaw3616">eaaw3616</jats:related-article> </jats:p>

Palabras clave: Multidisciplinary.

Pp. No disponible

Response to Comment on “Tumor-initiating cells establish an IL-33–TGF-β niche signaling loop to promote cancer progression”

Sachiko TaniguchiORCID; Ajit Elhance; Avery Van DuzerORCID; Sushil KumarORCID; Justin LeitenbergerORCID; Naoki OshimoriORCID

<jats:p> Kamphuis <jats:italic>et al</jats:italic> . argue that macrophages accumulated in the proximity of tumor-initiating cells do not express the high-affinity immunoglobulin E receptor FcεRIα. Although we cannot exclude the possibility of nonspecific binding of anti-FcεRIα antibody (clone MAR-1), we provide evidence that macrophages in squamous cell carcinomas express FcεRIα and that IL-33 induces FcεRIα expression in bone marrow cell–derived macrophages. </jats:p>

Palabras clave: Multidisciplinary.

Pp. No disponible

Imaging cell lineage with a synthetic digital recording system

Ke-Huan K. ChowORCID; Mark W. BuddeORCID; Alejandro A. GranadosORCID; Maria CabreraORCID; Shinae Yoon; Soomin ChoORCID; Ting-hao HuangORCID; Noushin KoulenaORCID; Kirsten L. Frieda; Long CaiORCID; Carlos LoisORCID; Michael B. ElowitzORCID

<jats:title>intMEMOIR traces cell lineages</jats:title> <jats:p> Cell lineage plays a pivotal role in cell fate determination. Chow <jats:italic>et al.</jats:italic> demonstrate the use of an integrase-based synthetic barcode system called intMEMOIR, which uses the serine integrase Bxb1 to perform irreversible nucleotide edits. Inducible editing either deletes or inverts its target region, thus encoding information in three-state memory elements, or trits, and avoiding undesired recombination events. Using intMEMOIR combined with single-molecule fluorescence in situ hybridization, the authors were able to identify clonal structures as well as gene expression patterns in the fly brain, enabling both clonal analysis and expression profiling with intact spatial information. The ability to visualize cell lineage relationships directly within their native tissue context provides insights into development and disease. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" related-article-type="in-this-issue" xlink:href="10.1126/science.abb3099">eabb3099</jats:related-article> </jats:p>

Palabras clave: Multidisciplinary.

Pp. No disponible

QSER1 protects DNA methylation valleys from de novo methylation

Gary DixonORCID; Heng PanORCID; Dapeng Yang; Bess P. RosenORCID; Therande JashariORCID; Nipun Verma; Julian PulecioORCID; Inbal CaspiORCID; Kihyun LeeORCID; Stephanie StranskyORCID; Abigail GlezerORCID; Chang LiuORCID; Marco RivasORCID; Ritu KumarORCID; Yahui Lan; Ingrid TorregrozaORCID; Chuan HeORCID; Simone SidoliORCID; Todd Evans; Olivier ElementoORCID; Danwei HuangfuORCID

<jats:title>Screen identifies demethylation regulator</jats:title> <jats:p> DNA methylation was one of the first epigenetic mechanisms discovered, but there is a limited understanding of its regulation and dysregulation in the context of development and disease. Dixon <jats:italic>et al.</jats:italic> performed a genome-wide CRISPR-Cas9 screen in human embryonic stem cells to identify DNA methylation regulators (see the Perspective by Gu and Goodell). A top screen hit, QSER1, proved to be essential for maintaining low methylation at DNA methylation valleys, which overlap with developmental genes and broad H3K27me3 and EZH2 peaks. Mechanistic examination revealed that QSER1 and the demethylating enzyme TET1 cooperate to safeguard developmental programs from de novo methylation by the enzyme DNMT3. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" related-article-type="in-this-issue" xlink:href="10.1126/science.abd0875">eabd0875</jats:related-article> ; see also p. <jats:related-article issue="6538" page="128" related-article-type="in-this-issue" vol="372">128</jats:related-article> </jats:p>

Palabras clave: Multidisciplinary.

Pp. No disponible

Estimated transmissibility and impact of SARS-CoV-2 lineage B.1.1.7 in England

Nicholas G. DaviesORCID; Sam AbbottORCID; Rosanna C. BarnardORCID; Christopher I. JarvisORCID; Adam J. Kucharski; James D. MundayORCID; Carl A. B. PearsonORCID; Timothy W. RussellORCID; Damien C. TullyORCID; Alex D. WashburneORCID; Tom WenseleersORCID; Amy Gimma; William WaitesORCID; Kerry L. M. WongORCID; Kevin van ZandvoortORCID; Justin D. SilvermanORCID; Karla Diaz-OrdazORCID; Ruth KeoghORCID; Rosalind M. EggoORCID; Sebastian FunkORCID; Mark JitORCID; Katherine E. AtkinsORCID; W. John EdmundsORCID; ;

<jats:title>UK variant transmission</jats:title> <jats:p> Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has the capacity to generate variants with major genomic changes. The UK variant B.1.1.7 (also known as VOC 202012/01) has many mutations that alter virus attachment and entry into human cells. Using a variety of statistical and dynamic modeling approaches, Davies <jats:italic>et al.</jats:italic> characterized the spread of the B.1.1.7 variant in the United Kingdom. The authors found that the variant is 43 to 90% more transmissible than the predecessor lineage but saw no clear evidence for a change in disease severity, although enhanced transmission will lead to higher incidence and more hospital admissions. Large resurgences of the virus are likely to occur after the easing of control measures, and it may be necessary to greatly accelerate vaccine roll-out to control the epidemic. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" related-article-type="in-this-issue" xlink:href="10.1126/science.abg3055">eabg3055</jats:related-article> </jats:p>

Palabras clave: Multidisciplinary.

Pp. No disponible