ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • Articles  (16,702)
  • Latest Papers from Table of Contents or Articles in Press  (16,702)
  • Articles: DFG German National Licenses
  • 2020-2024
  • 2015-2019  (13,527)
  • 1980-1984
  • 1970-1974  (3,175)
  • 1965-1969
  • 1935-1939
  • 2017  (5,430)
  • 2016  (8,097)
  • 1972  (3,175)
  • Nature  (4,319)
  • BioEssays  (459)
  • 2603
  • 328
  • Medicine  (16,702)
  • Sociology
  • Economics
Collection
  • Articles  (16,702)
Source
  • Latest Papers from Table of Contents or Articles in Press  (16,702)
  • Articles: DFG German National Licenses
Publisher
Years
  • 2020-2024
  • 2015-2019  (13,527)
  • 1980-1984
  • 1970-1974  (3,175)
  • 1965-1969
  • +
Year
Topic
  • 1
    Publication Date: 2017-11-02
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Springer Nature
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 2
    Publication Date: 2017-03-30
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Springer Nature
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 3
    Publication Date: 2016-07-16
    Description: The study of cellular senescence and proliferative lifespan is becoming increasingly important because of the promises of autologous cell therapy, the need for model systems for tissue disease and the implication of senescent cell phenotypes in organismal disease states such as sarcopenia, diabetes and various cancers, among others. Here, we explain the concepts of proliferative cellular lifespan and cellular senescence, and we present factors that have been shown to mediate cellular lifespan positively or negatively. We review much recent literature and present potential molecular mechanisms by which lifespan mediation occurs, drawing from the fields of telomere biology, metabolism, NAD + and sirtuin biology, growth factor signaling and oxygen and antioxidants. We conclude that cellular lifespan and senescence are complex concepts that are governed by multiple independent and interdependent pathways, and that greater understanding of these pathways, their interactions and their convergence upon specific cellular phenotypes may lead to viable therapies for tissue regeneration and treatment of age-related pathologies, which are caused by or exacerbated by senescent cells in vivo. Replicative cellular lifespan is regulated by myriad cellular factors and processes, including telomeres, oxygen, DNA damage signaling, growth factors and metabolism. In this review, we will explain some of the molecular means by which these and other factors mediate cellular lifespan.
    Print ISSN: 0265-9247
    Electronic ISSN: 1521-1878
    Topics: Biology , Medicine
    Published by Wiley
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 4
    Publication Date: 2016-07-16
    Description: Uncoupling proteins (UCPs) regulate mitochondrial function, and thus cellular metabolism. Angiotensin-converting enzyme (ACE) is the central component of endocrine and local tissue renin–angiotensin systems (RAS), which also regulate diverse aspects of whole-body metabolism and mitochondrial function (partly through altering mitochondrial UCP expression). We show that ACE expression also appears to be regulated by mitochondrial UCPs. In genetic analysis of two unrelated populations ( healthy young UK men and Scandinavian diabetic patients ) serum ACE (sACE) activity was significantly higher amongst UCP3-55C (rather than T) and UCP2 I (rather than D) allele carriers. RNA interference against UCP2 in human umbilical vein endothelial cells reduced UCP2 mRNA sixfold ( P  〈 0·01) whilst increasing ACE expression within a physiological range (〈1·8-fold at 48 h; P  〈 0·01). Our findings suggest novel hypotheses. Firstly, cellular feedback regulation may occur between UCPs and ACE. Secondly, cellular UCP regulation of sACE suggests a novel means of crosstalk between (and mutual regulation of) cellular and endocrine metabolism. This might partly explain the reduced risk of developing diabetes and metabolic syndrome with RAS antagonists and offer insight into the origins of cardiovascular disease in which UCPs and ACE both play a role. Uncoupling proteins (UCPs) regulate mitochondrial function, and thus cellular metabolism. Angiotensin-converting enzyme (ACE) is the central component of endocrine and local tissue renin–angiotensin systems, which also regulate diverse aspects of whole-body metabolism and mitochondrial function. We demonstrate that ACE expression appears to be regulated by mitochondrial UCPs.
    Print ISSN: 0265-9247
    Electronic ISSN: 1521-1878
    Topics: Biology , Medicine
    Published by Wiley
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 5
    facet.materialart.
    Unknown
    Wiley
    In: BioEssays
    Publication Date: 2016-07-16
    Description: Positive transcription elongation factor (P-TEFb) plays an important role in host cell and viral gene expression. Many viruses, including Herpes Simplex Virus 1, have evolved strategies to hijack this key factor via their own regulatory proteins. The central role of P-TEFb in viral life cycles raises the possibility that Cdk9 inhibitors might be useful antiviral agents. See article “P-TEFb goes viral” by Justyna Zaborowska, Nur F. Isa and Shona Murphy in this issue.
    Print ISSN: 0265-9247
    Electronic ISSN: 1521-1878
    Topics: Biology , Medicine
    Published by Wiley
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 6
    Publication Date: 2016-07-16
    Description: Tumors are often viewed as unique entities with specific behaviors. However, tumors are a mixture of differentially evolved subpopulations of cells in constant Darwinian evolution, selecting the fittest clone and allowing it to outgrow the rest. As in the natural environment, the niche defines the properties the fittest clones must possess. Therefore, there can be multiple fit clones because of the various microenvironments inside a single tumor. Hypoxia is considered to be a major feature of the tumor microenvironment and is a potential contributor to the cancer stem cell (CSC) phenotype and its enhanced tumorigenicity. The acidic microenvironment around hypoxic cells is accompanied by the activation of a subset of proteases that contribute to metastasis. Because of aberrant angiogenesis and the inaccessibility of their locations, hypoxic cells are less likely to accumulate therapeutic concentrations of chemotherapeutics that can lead to therapeutic resistance. Therefore, the targeting of the hypoxic CSC niche in combination with chemotherapy may provide a promising strategy for eradicating CSCs. In this review, we examine the cancer stem cell hypothesis and its relationship to the microenvironment, specifically to hypoxia and the subsequent metabolic switch and how they shape tumor behavior. Tumors are a mixture of differentially evolved subpopulations of cells in constant evolution. As in the natural environment, the niche defines the properties the fittest clones must possess. Therefore, there can be multiple fit clones because of the various microenvironments inside a single tumor. Hypoxia is considered to be a major feature of the tumor microenvironment and is a potential contributor to the cancer stem cell phenotype and its enhanced tumorigenicity.
    Print ISSN: 0265-9247
    Electronic ISSN: 1521-1878
    Topics: Biology , Medicine
    Published by Wiley
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 7
    Publication Date: 2016-07-21
    Description: Eukaryotic gene expression is extensively controlled at the level of mRNA stability and the mechanisms underlying this regulation are markedly different from their archaeal and bacterial counterparts. We propose that two such mechanisms, nonsense-mediated decay (NMD) and motif-specific transcript destabilization by CCCH-type zinc finger RNA-binding proteins, originated as a part of cellular defense against RNA pathogens. These branches of the mRNA turnover pathway might have been used by primeval eukaryotes alongside RNA interference to distinguish their own messages from those of RNA viruses and retrotransposable elements. We further hypothesize that the subsequent advent of “professional” innate and adaptive immunity systems allowed NMD and the motif-triggered mechanisms to be efficiently repurposed for regulation of endogenous cellular transcripts. This scenario explains the rapid emergence of archetypical mRNA destabilization pathways in eukaryotes and argues that other aspects of post-transcriptional gene regulation in this lineage might have been derived through a similar exaptation route. mRNA turnover in eukaryotes is remarkably different from its prokaryotic counterparts and possible reasons underlying this divergence remain unclear. Here we propose that eukaryotic mRNA destabilization pathways evolved as a part of host defense against RNA pathogens and were subsequently repurposed for post-transcriptional regulation of cell-encoded genes.
    Print ISSN: 0265-9247
    Electronic ISSN: 1521-1878
    Topics: Biology , Medicine
    Published by Wiley
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 8
    facet.materialart.
    Unknown
    Springer Nature
    In: Nature
    Publication Date: 2016-07-21
    Description: Science’s status shifts in new Brexit government Nature 535, 7612 (2016). http://www.nature.com/doifinder/10.1038/nature.2016.20264 Author: Davide Castelvecchi Reshuffled UK administration signals change for research and science policy.
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Springer Nature
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 9
    facet.materialart.
    Unknown
    Springer Nature
    In: Nature
    Publication Date: 2016-07-21
    Description: Behavioural ecology: Bees like their pollen sweet Nature 535, 7612 (2016). doi:10.1038/535327d Bees can taste the pollen they collect, and favour the sweet kind.Felicity Muth and her colleagues at the University of Nevada in Reno offered bumblebees (Bombus impatiens) an artificial flower containing one of three types of pollen — sweet, bitter or unflavoured.
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Springer Nature
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 10
    facet.materialart.
    Unknown
    Springer Nature
    In: Nature
    Publication Date: 2016-07-21
    Description: South China Sea ruling sparks conservation fears Nature 535, 7612 (2016). http://www.nature.com/doifinder/10.1038/535334a Author: David Cyranoski Court decision escalates tensions in ecologically sensitive region, but may also push nations to cooperate.
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Springer Nature
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...