8,328 research outputs found
sj-pdf-1-cep-10.1177_03331024221079296 - Supplemental material for Headache characteristics and postoperative course in Chiari I malformation
No full textSupplemental material, sj-pdf-1-cep-10.1177_03331024221079296 for Headache characteristics and postoperative course in Chiari I malformation by Dennis C Thunstedt, Michael Schmutzer, Matthias P Fabritius, Jun Thorsteinsdottir, Mathias Kunz, Ruth Ruscheweyh and Andreas Straube in Cephalalgia</p
Proline-rich tyrosine kinase 2 mediates gonadotropin-releasing hormone signaling to a specific extracellularly regulated kinase-sensitive transcriptional locus in the luteinizing hormone beta-subunit gene
Get PDFG protein-coupled receptor regulation of gene transcription primarily occurs through the phosphorylation of transcription factors by MAPKs. This requires transduction of an activating signal via scaffold proteins that can ultimately determine the outcome by binding signaling kinases and adapter proteins with effects on the target transcription factor and locus of activation. By investigating these mechanisms, we have elucidated how pituitary gonadotrope cells decode an input GnRH signal into coherent transcriptional output from the LH beta-subunit gene promoter. We show that GnRH activates c-Src and multiple members of the MAPK family, c-Jun NH2-terminal kinase 1/2, p38MAPK, and ERK1/2. Using dominant-negative point mutations and chemical inhibitors, we identified that calcium-dependent proline-rich tyrosine kinase 2 specifically acts as a scaffold for a focal adhesion/cytoskeleton-dependent complex comprised of c-Src, Grb2, and mSos that translocates an ERK-activating signal to the nucleus. The locus of action of ERK was specifically mapped to early growth response-1 (Egr-1) DNA binding sites within the LH beta-subunit gene proximal promoter, which was also activated by p38MAPK, but not c-Jun NH2-terminal kinase 1/2. Egr-1 was confirmed as the transcription factor target of ERK and p38MAPK by blockade of protein expression, transcriptional activity, and DNA binding. We have identified a novel GnRH-activated proline-rich tyrosine kinase 2-dependent ERK-mediated signal transduction pathway that specifically regulates Egr-1 activation of the LH beta-subunit proximal gene promoter, and thus provide insight into the molecular mechanisms required for differential regulation of gonadotropin gene expression
author
No full textauthorIn other places [Old Joe, the trapper] pointed out otter (or, as he pronounced it, "author") slidesPRINTED ITEM G.M.Story April 1959Not UsedNot UsedWithdrawn[see 'otter']Checked by Jordyn Hughes on Thu 09 Jun 201
Jia ru ju he wu dui jun yun tuan liu ji jun yun tuan liu dui liu de ying xiang
No full textWong, Chai Kwok = 加入聚合物對均勻湍流及均勻湍流對流的影響 / 黃濟國.Thesis M.Phil. Chinese University of Hong Kong 2013.Includes bibliographical references (leaves 89-91).Abstracts also in Chinese.Title from PDF title page (viewed on 01, November, 2016).Wong, Chai Kwok = Jia ru ju he wu dui jun yun tuan liu ji jun yun tuan liu dui liu de ying xiang / Huang Jiguo
Author Correction: Manipulating anion intercalation enables a high-voltage aqueous dual ion battery
No full textThe original version of this Article did not acknowledge Prof. Jun Fan as a corresponding author. This has now been corrected in both the PDF and HTML versions of the Article.link_to_subscribed_fulltex
Author Correction: A proteomic landscape of diffuse-type gastric cancer
Get PDFThe original version of this Article contained an error in the email address of the corresponding author Jun Qin. The correct email is [email protected]. The error has been corrected in the HTML and PDF versions of the Article.</jats:p
Corrigendum: The taeniaticornis-group of genus Apanteles Foerster (Hymenoptera, Braconidae, Microgastrinae) from China with one new species. Journal of Hymenoptera Research 96: 21–31. doi: 10.3897/jhr.96.99649
Get PDFIn a paper about a new species of Apanteles (Microgastrinae)(Liu & Chen, 2023), we regret the omission of one author Jun-hua Chen in the second place of the author list who did great job in construction of the ZJUH collection for this study and the mistake in institution order and corresponding author. We provide the correct information below.Zhen Liu1, 2, Jun-hua He1, Xue-xin Chen11 Institute of Insect Sciences, Zhejiang University, Hangzhou 310058, China. 2 Zoology Key Laboratory of Hunan Higher Education, College of Life and Environmental Sciences, Hunan University of Arts and Science, Changde 415000, China
The granulocytic inducer C/EBPalpha inactivates the myeloid master regulator PU.1
Get PDFVerschiedene Transkriptionsfaktoren spielen eine Rolle in der Entwicklung myeloischer Zellen. PU.1, ein Transkriptionsfaktor aus der ETS-Familie, ist sowohl für die Entwicklung lymphatischer als auch für die Entwicklung myeloischer Zellen von Bedeutung. Der Transkriptions
faktor C/EBPalpha, ein an den CCAAT-Enhancer bindendes Protein, ist hingegen wesentlich verantwortlich für die Entwicklung von Granulozyten. Wir stellen hier den ersten Nachweis dafür vor, dass C/EBPalpha die Funktion von PU.1 blockiert. PU.1 und C/EBPalpha können einander binden und sind in myeloischen Zellen kolokalisiert. Wenn C/EBPalpha PU.1 bindet, kann PU.1 einen minimalen Promotor mit Bindungsstelle für PU.1 nicht mehr aktivieren. Wir zeigen, dass der Leuzin-Zipper in der DNA-bindenden Domäne von C/EBPalpha mit der beta3/beta4-Region in der DNA-bindenden Domäne von PU.1 interagieren kann. Dadurch wird der Koaktivator von PU.1, c-jun, aus seiner Bindung mit PU.1 verdrängt. C/EBPalpha hemmt PU.1 nicht, indem es Korepressoren rekrutiert. Vielmehr vermindert C/EBPalpha die Expression von PU.1 in U-937-Zellen mit induzierbarem C/EBPalpha, indem es den autoregulatorischen Effekt PU.1 auf den PU.1-Promotor hemmt.
Ausserdem blockiert C/EBPalpha die durch PU.1 bedingte Entwicklung dendritischer Zellen aus CD34+ menschlichen Nabel blutzellen. Diese funktionelle Blockade von PU.1 durch C/EBPalpha könnte einer der Mechanismen sein, mit denen C/EBPalpha den durch PU.1 determinierten Weg der Zelldifferenzierung hemmt und sich Zellen unter dem Einfluss von C/EBPalpha zu Granulozyten entwickeln.Several transcription factors have been shown to play a role in myelopoiesis. PU.1, an ets-family transcription factor, is required for the development of both myeloid and lymphoid lineages while the transcription factor CCAAT/enhancer binding protein family member C/EBPalpha is essential for granulocytic development. We present here the first evidence that C/EBPalpha blocks the function of PU.1. PU.1 and C/EBPalpha interact physically and co-localize in myeloid cells. As a consequence of this interaction C/EBPalpha can inhibit the function of PU.1 to activate a minimal promoter containing only PU.1 DNA binding sites. We further demonstrate that the leucine zipper in the DNA binding domain of C/EBPalpha interacts with the beta3/beta4 region in the DNA binding domain of PU.1, and as a result displaces the PU.1 co-activator c-Jun. Finally, C/EBPalpha blocks PU.1 induced dendritic cell development from CD34+ human cord blood cells. The functional blocking of PU.1 by C/EBPalpha could be the mechanism by which C/EBPalpha inhibits the cell fates specified by PU.1, and directs cell development to the granulocytic lineage
Effekte einer anti-VEGF-A-Therapie (Bevacizumab) auf humane cerebrale Endothelzellen sowie Tumor- und Endothelzellen in humanen Gliomen
Get PDFYong yu you hua zhi bei chao leng yuan zi hun he wu de guang xue ou ji jing
No full textChen, Jun = 用於優化製備超冷原子混合物的光學偶極阱 / 陳軍.Thesis M.Phil. Chinese University of Hong Kong 2014.Includes bibliographical references (leaves 109-117).Abstracts also in Chinese.Title from PDF title page (viewed on 29, November, 2016).Chen, Jun = Yong yu you hua zhi bei chao leng yuan zi hun he wu de guang xue ou ji jing / Chen Jun
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