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  • 1
    Publication Date: 1996-05-03
    Description: Signal transducers and activators of transcription (STAT) proteins can be conditionally activated in response to epidermal growth factor (EGF) and interferon (IFN)-gamma. STAT activation was correlated with cell growth inhibition in response to EGF and IFN-gamma. Activated STAT proteins specifically recognized the conserved STAT-responsive elements in the promoter of the gene encoding the cyclin-dependent kinase (CDK) inhibitor p21 WAF1/CIP1 and regulated the induction of p21 messenger RNA. IFN-gamma did not inhibit the growth of U3A cells, which are deficient in STAT1, but did inhibit the growth of U3A cells into which STAT1 alpha was reintroduced. Thus, STAT1 protein is essential for cell growth suppression in response to IFN-gamma. The STAT signaling pathway appears to negatively regulate the cell cycle by inducing CDK inhibitors in response to cytokines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chin, Y E -- Kitagawa, M -- Su, W C -- You, Z H -- Iwamoto, Y -- Fu, X Y -- R01 AI34522/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1996 May 3;272(5262):719-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Yale University School of Medicine, New Haven, CT 06520-8023, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8614832" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Binding Sites ; *Cell Division/drug effects ; Cell Line ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclins/biosynthesis/*genetics ; DNA/biosynthesis ; DNA-Binding Proteins/metabolism/*physiology ; Epidermal Growth Factor/pharmacology ; *Gene Expression Regulation ; Humans ; Interferon-gamma/pharmacology ; Molecular Sequence Data ; Promoter Regions, Genetic ; RNA, Messenger/genetics/metabolism ; STAT1 Transcription Factor ; STAT3 Transcription Factor ; *Signal Transduction ; Trans-Activators/metabolism/*physiology ; Transfection ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2019
    Description: Abstract Based on broadband seismic data from 102 stations in the eastern Himalayan collision zone, the crustal thickness and Poisson's ratio were determined by using the H‐κ stacking analysis of teleseismic P‐wave receiver functions. The Moho topography rapidly deepens northwards in the northern Lhasa terrane, inferring the northern limit of the Indian plate underthrusting beneath Tibetan Plateau. Our seismic images show that steep subduction of the Indian plate occurs to the west of the Eastern Himalayan Syntaxis while gentle subduction to the east. The variation of subduction geometry of the Indian plate may be one of the causes for the formation of the eastern Himalayan Syntaxis. 2‐D crustal density modeling of the gravity measurements shows that the average crustal density in the eastern Himalayan collision zone is less dense than the global average continental crust, and our preferred model has 5‐to‐10‐km‐thick, high density layer (2970‐3000 kg/m3) in the lower crust beneath the eastern Lhasa terrane, consistent with mafic underplating. The attributes of a thickened crust with northward deepening Moho and low‐to‐normal Poisson's ratio might be the geophysical signature of delamination beneath the Lhasa terrane and underthrusting of Indian plate. We hypothesize the orogenic root of the Lhasa terrane was removed by convective‐driven delamination, followed by northward subduction of the Indian plate. Thus, delamination and continental subduction are the dominant deep processes in the post‐collisional stage in the eastern Himalayan collision zone.
    Print ISSN: 0278-7407
    Electronic ISSN: 1944-9194
    Topics: Geosciences
    Published by Wiley on behalf of American Geophysical Union (AGU).
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  • 3
    Publication Date: 2010-09-03
    Print ISSN: 1367-4803
    Electronic ISSN: 1460-2059
    Topics: Biology , Computer Science , Medicine
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