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Nature

Resumen/Descripción – provisto por la editorial en inglés
Nature is a weekly international journal publishing the finest peer-reviewed research in all fields of science and technology on the basis of its originality, importance, interdisciplinary interest, timeliness, accessibility, elegance and surprising conclusions. Nature also provides rapid, authoritative, insightful and arresting news and interpretation of topical and coming trends affecting science, scientists and the wider public.
Palabras clave – provistas por la editorial

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Institución detectada Período Navegá Descargá Solicitá
No detectada desde jul. 2012 / hasta dic. 2023 Nature.com
No detectada desde jul. 2006 / hasta ago. 2012 Ovid

Información

Tipo de recurso:

revistas

ISSN impreso

0028-0836

ISSN electrónico

1476-4687

Editor responsable

Springer Nature

País de edición

Reino Unido

Fecha de publicación

Tabla de contenidos

Human neural tube morphogenesis in vitro by geometric constraints

Eyal KarzbrunORCID; Aimal H. Khankhel; Heitor C. Megale; Stella M. K. GlasauerORCID; Yofiel Wyle; George Britton; Aryeh WarmflashORCID; Kenneth S. KosikORCID; Eric D. Siggia; Boris I. Shraiman; Sebastian J. StreichanORCID

Palabras clave: Multidisciplinary.

Pp. 268-272

Cell surface and intracellular auxin signalling for H+ fluxes in root growth

Lanxin Li; Inge VerstraetenORCID; Mark Roosjen; Koji TakahashiORCID; Lesia Rodriguez; Jack Merrin; Jian Chen; Lana Shabala; Wouter Smet; Hong Ren; Steffen VannesteORCID; Sergey Shabala; Bert De Rybel; Dolf WeijersORCID; Toshinori KinoshitaORCID; William M. GrayORCID; Jiří FrimlORCID

Palabras clave: Multidisciplinary.

Pp. 273-277

TMK-based cell-surface auxin signalling activates cell-wall acidification

Wenwei Lin; Xiang ZhouORCID; Wenxin Tang; Koji TakahashiORCID; Xue PanORCID; Jiawei Dai; Hong Ren; Xiaoyue Zhu; Songqin Pan; Haiyan ZhengORCID; William M. GrayORCID; Tongda XuORCID; Toshinori KinoshitaORCID; Zhenbiao YangORCID

<jats:title>Abstract</jats:title><jats:p>The phytohormone auxin controls many processes in plants, at least in part through its regulation of cell expansion<jats:sup>1</jats:sup>. The acid growth hypothesis has been proposed to explain auxin-stimulated cell expansion for five decades, but the mechanism that underlies auxin-induced cell-wall acidification is poorly characterized. Auxin induces the phosphorylation and activation of the plasma membrane H<jats:sup>+</jats:sup>-ATPase that pumps protons into the apoplast<jats:sup>2</jats:sup>, yet how auxin activates its phosphorylation remains unclear. Here we show that the transmembrane kinase (TMK) auxin-signalling proteins interact with plasma membrane H<jats:sup>+</jats:sup>-ATPases, inducing their phosphorylation, and thereby promoting cell-wall acidification and hypocotyl cell elongation in <jats:italic>Arabidopsis</jats:italic>. Auxin induced interactions between TMKs and H<jats:sup>+</jats:sup>-ATPases in the plasma membrane within seconds, as well as TMK-dependent phosphorylation of the penultimate threonine residue on the H+-ATPases. Our genetic, biochemical and molecular evidence demonstrates that TMKs directly phosphorylate plasma membrane H<jats:sup>+</jats:sup>-ATPase and are required for auxin-induced H<jats:sup>+</jats:sup>-ATPase activation, apoplastic acidification and cell expansion. Thus, our findings reveal a crucial connection between auxin and plasma membrane H<jats:sup>+</jats:sup>-ATPase activation in regulating apoplastic pH changes and cell expansion through TMK-based cell surface auxin signalling.</jats:p>

Palabras clave: Multidisciplinary.

Pp. 278-282

Virus-induced senescence is a driver and therapeutic target in COVID-19

Soyoung LeeORCID; Yong Yu; Jakob TrimpertORCID; Fahad BenthaniORCID; Mario Mairhofer; Paulina Richter-Pechanska; Emanuel WylerORCID; Dimitri BelenkiORCID; Sabine Kaltenbrunner; Maria Pammer; Lea Kausche; Theresa C. FirschingORCID; Kristina Dietert; Michael SchotsaertORCID; Carles Martínez-RomeroORCID; Gagandeep SinghORCID; Séverine KunzORCID; Daniela NiemeyerORCID; Riad Ghanem; Helmut J. F. Salzer; Christian Paar; Michael Mülleder; Melissa Uccellini; Edward G. Michaelis; Amjad Khan; Andrea Lau; Martin Schönlein; Anna Habringer; Josef Tomasits; Julia M. Adler; Susanne KimeswengerORCID; Achim D. GruberORCID; Wolfram Hoetzenecker; Herta Steinkellner; Bettina Purfürst; Reinhard Motz; Francesco Di Pierro; Bernd LamprechtORCID; Nikolaus Osterrieder; Markus LandthalerORCID; Christian DrostenORCID; Adolfo García-SastreORCID; Rupert Langer; Markus Ralser; Roland EilsORCID; Maurice Reimann; Dorothy N. Y. Fan; Clemens A. SchmittORCID

Palabras clave: Multidisciplinary.

Pp. 283-289

Shigella evades pyroptosis by arginine ADP-riboxanation of caspase-11

Zilin LiORCID; Wang Liu; Jiaqi Fu; Sen Cheng; Yue Xu; Zhiqiang Wang; Xiaofan Liu; Xuyan Shi; Yaxin Liu; Xiangbing QiORCID; Xiaoyun LiuORCID; Jingjin Ding; Feng ShaoORCID

Palabras clave: Multidisciplinary.

Pp. 290-295

Glycogen metabolism links glucose homeostasis to thermogenesis in adipocytes

Omer Keinan; Joseph M. Valentine; Haopeng XiaoORCID; Sushil K. Mahata; Shannon M. ReillyORCID; Mohammad Abu-Odeh; Julia H. Deluca; Benyamin DadpeyORCID; Leslie Cho; Austin Pan; Ruth T. YuORCID; Yang Dai; Christopher LiddleORCID; Michael Downes; Ronald M. EvansORCID; Aldons J. LusisORCID; Markku LaaksoORCID; Edward T. ChouchaniORCID; Mikael RydénORCID; Alan R. SaltielORCID

Palabras clave: Multidisciplinary.

Pp. 296-301

Low glycaemic diets alter lipid metabolism to influence tumour growth

Evan C. Lien; Anna M. Westermark; Yin ZhangORCID; Chen Yuan; Zhaoqi Li; Allison N. Lau; Kiera M. SappORCID; Brian M. Wolpin; Matthew G. Vander HeidenORCID

Palabras clave: Multidisciplinary.

Pp. 302-307

eccDNAs are apoptotic products with high innate immunostimulatory activity

Yuangao Wang; Meng WangORCID; Mohamed Nadhir DjekidelORCID; Huan Chen; Di Liu; Frederick W. AltORCID; Yi ZhangORCID

Palabras clave: Multidisciplinary.

Pp. 308-314

The structure of neurofibromin isoform 2 reveals different functional states

Andreas Naschberger; Rozbeh BaradaranORCID; Bernhard RuppORCID; Marta CarroniORCID

<jats:title>Abstract</jats:title><jats:p>The autosomal dominant monogenetic disease neurofibromatosis type 1 (NF1) affects approximately one in 3,000 individuals and is caused by mutations in the <jats:italic>NF1</jats:italic> tumour suppressor gene, leading to dysfunction in the protein neurofibromin (Nf1)<jats:sup>1,2</jats:sup>. As a GTPase-activating protein, a key function of Nf1 is repression of the Ras oncogene signalling cascade. We determined the human Nf1 dimer structure at an overall resolution of 3.3 Å. The cryo-electron microscopy structure reveals domain organization and structural details of the Nf1 exon 23a splicing<jats:sup>3</jats:sup> isoform 2 in a closed, self-inhibited, Zn-stabilized state and an open state. In the closed conformation, HEAT/ARM core domains shield the GTPase-activating protein-related domain (GRD) so that Ras binding is sterically inhibited. In a distinctly different, open conformation of one protomer, a large-scale movement of the GRD occurs, which is necessary to access Ras, whereas Sec14-PH reorients to allow interaction with the cellular membrane<jats:sup>4</jats:sup>. Zn incubation of Nf1 leads to reduced Ras-GAP activity with both protomers in the self-inhibited, closed conformation stabilized by a Zn binding site between the N-HEAT/ARM domain and the GRD–Sec14-PH linker. The transition between closed, self-inhibited states of Nf1 and open states provides guidance for targeted studies deciphering the complex molecular mechanism behind the widespread neurofibromatosis syndrome and Nf1 dysfunction in carcinogenesis.</jats:p>

Palabras clave: Multidisciplinary.

Pp. 315-319

Dispatched uses Na+ flux to power release of lipid-modified Hedgehog

Qianqian WangORCID; Daniel E. AsarnowORCID; Ke Ding; Randall K. MannORCID; Jason HatakeyamaORCID; Yunxiao ZhangORCID; Yong Ma; Yifan ChengORCID; Philip A. BeachyORCID

Palabras clave: Multidisciplinary.

Pp. 320-324