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Article ; Online: Hyperphosphorylation amplifies UPF1 activity to resolve stalls in nonsense-mediated mRNA decay.

Durand, Sébastien / Franks, Tobias M / Lykke-Andersen, Jens

Nature communications

2016 Volume 7, Page(s) 12434

Abstract: Many gene expression factors contain repetitive phosphorylation sites for single kinases, but the functional significance is poorly understood. Here we present evidence for hyperphosphorylation as a mechanism allowing UPF1, the central factor in nonsense- ...

Abstract	Many gene expression factors contain repetitive phosphorylation sites for single kinases, but the functional significance is poorly understood. Here we present evidence for hyperphosphorylation as a mechanism allowing UPF1, the central factor in nonsense-mediated decay (NMD), to increasingly attract downstream machinery with time of residence on target mRNAs. Indeed, slowing NMD by inhibiting late-acting factors triggers UPF1 hyperphosphorylation, which in turn enhances affinity for factors linking UPF1 to decay machinery. Mutational analyses reveal multiple phosphorylation sites contributing to different extents to UPF1 activity with no single site being essential. Moreover, the ability of UPF1 to undergo hyperphosphorylation becomes increasingly important for NMD when downstream factors are depleted. This hyperphosphorylation-dependent feedback mechanism may serve as a molecular clock ensuring timely degradation of target mRNAs while preventing degradation of non-targets, which, given the prevalence of repetitive phosphorylation among central gene regulatory factors, may represent an important general principle in gene expression.
MeSH term(s)	Adenosine Triphosphate/chemistry ; Animals ; Binding Sites ; DNA Mutational Analysis ; Electrophoresis, Gel, Two-Dimensional ; HeLa Cells ; Humans ; Mice ; NIH 3T3 Cells ; Nonsense Mediated mRNA Decay ; Phosphorylation ; RAW 264.7 Cells ; RNA Helicases/genetics ; RNA Helicases/metabolism ; RNA, Messenger/metabolism ; Trans-Activators/genetics ; Trans-Activators/metabolism
Chemical Substances	RNA, Messenger ; Rent1 protein, mouse ; Trans-Activators ; Adenosine Triphosphate (8L70Q75FXE) ; RNA Helicases (EC 3.6.4.13) ; UPF1 protein, human (EC 3.6.4.13)
Language	English
Publishing date	2016-08-11
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2041-1723
ISSN (online)	2041-1723
DOI	10.1038/ncomms12434
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Hyperphosphorylation amplifies UPF1 activity to resolve stalls in nonsense-mediated mRNA decay

Sébastien Durand / Tobias M. Franks / Jens Lykke-Andersen

Nature Communications, Vol 7, Iss 1, Pp 1-

2016 Volume 12

Abstract: Gene expression is regulated by a range of mechanisms, including post-translational modifications such as phosphorylation. Here the authors present evidence for a feedback mechanism whereby hyperphosphorylation of UPF1 in response to delays in nonsense- ... ...

Abstract	Gene expression is regulated by a range of mechanisms, including post-translational modifications such as phosphorylation. Here the authors present evidence for a feedback mechanism whereby hyperphosphorylation of UPF1 in response to delays in nonsense-mediated decay enhances recruitment of mRNA decay machinery.
Keywords	Science ; Q
Language	English
Publishing date	2016-08-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: DNA methylation patterns reflect individual's lifestyle independent of obesity.

Klemp, Ireen / Hoffmann, Anne / Müller, Luise / Hagemann, Tobias / Horn, Kathrin / Rohde-Zimmermann, Kerstin / Tönjes, Anke / Thiery, Joachim / Löffler, Markus / Burkhardt, Ralph / Böttcher, Yvonne / Stumvoll, Michael / Blüher, Matthias / Krohn, Knut / Scholz, Markus / Baber, Ronny / Franks, Paul W / Kovacs, Peter / Keller, Maria

Clinical and translational medicine

2022 Volume 12, Issue 6, Page(s) e851

Abstract: ... Results: Differences in DNA methylation patterns between body mass index groups (<25 vs. >30 kg/m ...

Abstract	Objective: Obesity is driven by modifiable lifestyle factors whose effects may be mediated by epigenetics. Therefore, we investigated lifestyle effects on blood DNA methylation in participants of the LIFE-Adult study, a well-characterised population-based cohort from Germany. Research design and methods: Lifestyle scores (LS) based on diet, physical activity, smoking and alcohol intake were calculated in 4107 participants of the LIFE-Adult study. Fifty subjects with an extremely healthy lifestyle and 50 with an extremely unhealthy lifestyle (5th and 95th percentiles LS) were selected for genome-wide DNA methylation analysis in blood samples employing Illumina Infinium® Methylation EPIC BeadChip system technology. Results: Differences in DNA methylation patterns between body mass index groups (<25 vs. >30 kg/m Conclusions: DNA methylation patterns help discriminate individuals with a healthy versus unhealthy lifestyle, which may mask subtle methylation differences derived from obesity.
MeSH term(s)	Adult ; DNA Methylation/genetics ; Epigenesis, Genetic ; Epigenomics ; Healthy Lifestyle ; Humans ; Obesity/genetics
Language	English
Publishing date	2022-06-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2697013-2
ISSN	2001-1326 ; 2001-1326
ISSN (online)	2001-1326
ISSN	2001-1326
DOI	10.1002/ctm2.851
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Article ; Online: The role of Nup98 in transcription regulation in healthy and diseased cells.

Franks, Tobias M / Hetzer, Martin W

Trends in cell biology

2012 Volume 23, Issue 3, Page(s) 112–117

Abstract: Nuclear pore complex (NPC) proteins are known for their critical roles in regulating nucleocytoplasmic traffic of macromolecules across the nuclear envelope. However, recent findings suggest that some nucleoporins (Nups), including Nup98, have additional ...

Abstract	Nuclear pore complex (NPC) proteins are known for their critical roles in regulating nucleocytoplasmic traffic of macromolecules across the nuclear envelope. However, recent findings suggest that some nucleoporins (Nups), including Nup98, have additional functions in developmental gene regulation. Nup98, which exhibits transcription-dependent mobility at the NPC but can also bind chromatin away from the nuclear envelope, is frequently involved in chromosomal translocations in a subset of patients suffering from acute myeloid leukemia (AML). A common paradigm suggests that Nup98 translocations cause aberrant transcription when they are recuited to aberrant genomic loci. Importantly, this model fails to account for the potential loss of wild type (WT) Nup98 function in the presence of Nup98 translocation mutants. Here we examine how the cell might regulate Nup98 nucleoplasmic protein levels to control transcription in healthy cells. In addition, we discuss the possibility that dominant negative Nup98 fusion proteins disrupt the transcriptional activity of WT Nup98 in the nucleoplasm to drive AML.
MeSH term(s)	Active Transport, Cell Nucleus/genetics ; Animals ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/metabolism ; Cell Transformation, Neoplastic/pathology ; Chromatin/genetics ; Chromatin/metabolism ; Gene Expression Regulation, Developmental ; Gene Expression Regulation, Neoplastic ; Humans ; Leukemia, Myeloid, Acute/genetics ; Leukemia, Myeloid, Acute/metabolism ; Leukemia, Myeloid, Acute/pathology ; Nuclear Pore/genetics ; Nuclear Pore/metabolism ; Nuclear Pore Complex Proteins/genetics ; Nuclear Pore Complex Proteins/metabolism ; Oncogene Proteins, Fusion/genetics ; Oncogene Proteins, Fusion/metabolism ; Signal Transduction ; Transcription, Genetic ; Translocation, Genetic
Chemical Substances	Chromatin ; Nuclear Pore Complex Proteins ; Nup98 protein, human ; Oncogene Proteins, Fusion ; nuclear pore complex protein 96
Language	English
Publishing date	2012-12-13
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	30122-x
ISSN	1879-3088 ; 0962-8924
ISSN (online)	1879-3088
ISSN	0962-8924
DOI	10.1016/j.tcb.2012.10.013
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Article ; Online: Social considerations are crucial to success in implementing the 30×30 global conservation target.

Sandbrook, Chris / Albury-Smith, Shenique / Allan, James R / Bhola, Nina / Bingham, Heather C / Brockington, Dan / Byaruhanga, Achilles B / Fajardo, Javier / Fitzsimons, James / Franks, Phil / Fleischman, Forrest / Frechette, Alain / Kakuyo, Kagumaho / Kaptoyo, Edna / Kuemmerle, Tobias / Kalunda, Pauline Nantongo / Nuvunga, Milagre / O'Donnell, Brian / Onyai, Fred /

Pfeifer, Marion / Pritchard, Rose / Ramos, Ameyali / Rao, Madhu / Ryan, Casey M / Shyamsundar, Priya / Tauli, Josefa / Tumusiime, David Mwesigye / Vilaça, Mônica / Watmough, Gary R / Worsdell, Thomas / Zaehringer, Julie G

Nature ecology & evolution

2023 Volume 7, Issue 6, Page(s) 784–785

MeSH term(s)	Conservation of Natural Resources
Language	English
Publishing date	2023-04-05
Publishing country	England
Document type	Letter
ISSN	2397-334X
ISSN (online)	2397-334X
DOI	10.1038/s41559-023-02048-2
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Article ; Online: Corrigendum: Evolution of a transcriptional regulator from a transmembrane nucleoporin.

Franks, Tobias M / Benner, Chris / Narvaiza, Iñigo / Marchetto, Maria C N / Young, Janet M / Malik, Harmit S / Gage, Fred H / Hetzer, Martin W

Genes & development

2017 Volume 31, Issue 8, Page(s) 845

Language	English
Publishing date	2017-04-15
Publishing country	United States
Document type	Journal Article ; Published Erratum
ZDB-ID	806684-x
ISSN	1549-5477 ; 0890-9369
ISSN (online)	1549-5477
ISSN	0890-9369
DOI	10.1101/gad.300699.117
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Article: The role of Nup98 in transcription regulation in healthy and diseased cells

Franks, Tobias M / Hetzer, Martin W

Trends in cell biology. 2013 Mar., v. 23, no. 3

2013

Abstract	Nuclear pore complex (NPC) proteins are known for their critical roles in regulating nucleocytoplasmic traffic of macromolecules across the nuclear envelope. However, recent findings suggest that some nucleoporins (Nups), including Nup98, have additional functions in developmental gene regulation. Nup98, which exhibits transcription-dependent mobility at the NPC but can also bind chromatin away from the nuclear envelope, is frequently involved in chromosomal translocations in a subset of patients suffering from acute myeloid leukemia (AML). A common paradigm suggests that Nup98 translocations cause aberrant transcription when they are recuited to aberrant genomic loci. Importantly, this model fails to account for the potential loss of wild type (WT) Nup98 function in the presence of Nup98 translocation mutants. Here we examine how the cell might regulate Nup98 nucleoplasmic protein levels to control transcription in healthy cells. In addition, we discuss the possibility that dominant negative Nup98 fusion proteins disrupt the transcriptional activity of WT Nup98 in the nucleoplasm to drive AML.
Keywords	chromatin ; chromosome translocation ; genes ; loci ; models ; mutants ; myeloid leukemia ; nuclear membrane ; nucleocytoplasmic transport ; nucleoporins ; patients ; transcription (genetics)
Language	English
Dates of publication	2013-03
Size	p. 112-117.
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	30122-x
ISSN	1879-3088 ; 0962-8924
ISSN (online)	1879-3088
ISSN	0962-8924
DOI	10.1016/j.tcb.2012.10.013
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Article: Role of sociodemographic, clinical, behavioral, and molecular factors in precision prevention of type 2 diabetes: a systematic review.

Bodhini, Dhanasekaran / Morton, Robert W / Santhakumar, Vanessa / Nakabuye, Mariam / Pomares-Millan, Hugo / Clemmensen, Christoffer / Fitzpatrick, Stephanie L / Guasch-Ferre, Marta / Pankow, James S / Ried-Larsen, Mathias / Franks, Paul W / Tobias, Deirdre K / Merino, Jordi / Mohan, Viswanathan / Loos, Ruth J F

medRxiv : the preprint server for health sciences

2023

Abstract: The variability in the effectiveness of type 2 diabetes (T2D) preventive interventions highlights the potential to identify the factors that determine treatment responses and those that would benefit the most from a given intervention. We conducted a ... ...

Abstract	The variability in the effectiveness of type 2 diabetes (T2D) preventive interventions highlights the potential to identify the factors that determine treatment responses and those that would benefit the most from a given intervention. We conducted a systematic review to synthesize the evidence to support whether sociodemographic, clinical, behavioral, and molecular characteristics modify the efficacy of dietary or lifestyle interventions to prevent T2D. Among the 80 publications that met our criteria for inclusion, the evidence was low to very low to attribute variability in intervention effectiveness to individual characteristics such as age, sex, BMI, race/ethnicity, socioeconomic status, baseline behavioral factors, or genetic predisposition. We found evidence, albeit low certainty, to support conclusions that those with poorer health status, particularly those with prediabetes at baseline, tend to benefit more from T2D prevention strategies compared to healthier counterparts. Our synthesis highlights the need for purposefully designed clinical trials to inform whether individual factors influence the success of T2D prevention strategies.
Language	English
Publishing date	2023-05-03
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.05.03.23289433
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Article ; Online: Impact of individual and environmental factors on dietary or lifestyle interventions to prevent type 2 diabetes development: a systematic review.

Communications medicine

2023 Volume 3, Issue 1, Page(s) 133

Abstract: Background: The variability in the effectiveness of type 2 diabetes (T2D) preventive interventions highlights the potential to identify the factors that determine treatment responses and those that would benefit the most from a given intervention. We ... ...

Abstract	Background: The variability in the effectiveness of type 2 diabetes (T2D) preventive interventions highlights the potential to identify the factors that determine treatment responses and those that would benefit the most from a given intervention. We conducted a systematic review to synthesize the evidence to support whether sociodemographic, clinical, behavioral, and molecular factors modify the efficacy of dietary or lifestyle interventions to prevent T2D. Methods: We searched MEDLINE, Embase, and Cochrane databases for studies reporting on the effect of a lifestyle, dietary pattern, or dietary supplement interventions on the incidence of T2D and reporting the results stratified by any effect modifier. We extracted relevant statistical findings and qualitatively synthesized the evidence for each modifier based on the direction of findings reported in available studies. We used the Diabetes Canada Clinical Practice Scale to assess the certainty of the evidence for a given effect modifier. Results: The 81 publications that met our criteria for inclusion are from 33 unique trials. The evidence is low to very low to attribute variability in intervention effectiveness to individual characteristics such as age, sex, BMI, race/ethnicity, socioeconomic status, baseline behavioral factors, or genetic predisposition. Conclusions: We report evidence, albeit low certainty, that those with poorer health status, particularly those with prediabetes at baseline, tend to benefit more from T2D prevention strategies compared to healthier counterparts. Our synthesis highlights the need for purposefully designed clinical trials to inform whether individual factors influence the success of T2D prevention strategies.
Language	English
Publishing date	2023-10-05
Publishing country	England
Document type	Journal Article
ISSN	2730-664X
ISSN (online)	2730-664X
DOI	10.1038/s43856-023-00363-0
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Article ; Online: Nup98 recruits the Wdr82-Set1A/COMPASS complex to promoters to regulate H3K4 trimethylation in hematopoietic progenitor cells.

Franks, Tobias M / McCloskey, Asako / Shokirev, Maxim Nikolaievich / Benner, Chris / Rathore, Annie / Hetzer, Martin W

Genes & development

2017 Volume 31, Issue 22, Page(s) 2222–2234

Abstract: Recent studies have shown that a subset of nucleoporins (Nups) can detach from the nuclear pore complex and move into the nuclear interior to regulate transcription. One such dynamic Nup, called Nup98, has been implicated in gene activation in healthy ... ...

Abstract	Recent studies have shown that a subset of nucleoporins (Nups) can detach from the nuclear pore complex and move into the nuclear interior to regulate transcription. One such dynamic Nup, called Nup98, has been implicated in gene activation in healthy cells and has been shown to drive leukemogenesis when mutated in patients with acute myeloid leukemia (AML). Here we show that in hematopoietic cells, Nup98 binds predominantly to transcription start sites to recruit the Wdr82-Set1A/COMPASS (complex of proteins associated with Set1) complex, which is required for deposition of the histone 3 Lys4 trimethyl (H3K4me3)-activating mark. Depletion of Nup98 or Wdr82 abolishes Set1A recruitment to chromatin and subsequently ablates H3K4me3 at adjacent promoters. Furthermore, expression of a Nup98 fusion protein implicated in aggressive AML causes mislocalization of H3K4me3 at abnormal regions and up-regulation of associated genes. Our findings establish a function of Nup98 in hematopoietic gene activation and provide mechanistic insight into which Nup98 leukemic fusion proteins promote AML.
MeSH term(s)	Animals ; Cells, Cultured ; Chromatin/metabolism ; Chromosomal Proteins, Non-Histone/metabolism ; Gene Expression Regulation, Developmental ; Hematopoietic Stem Cells/metabolism ; Histone-Lysine N-Methyltransferase/metabolism ; Histones/metabolism ; Humans ; Methylation ; Mice ; Nuclear Pore Complex Proteins/metabolism ; Promoter Regions, Genetic ; Transcriptional Activation
Chemical Substances	Chromatin ; Chromosomal Proteins, Non-Histone ; Histones ; Nuclear Pore Complex Proteins ; Wdr82 protein, mouse ; nuclear pore complex protein 98 ; Histone-Lysine N-Methyltransferase (EC 2.1.1.43)
Language	English
Publishing date	2017--15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	806684-x
ISSN	1549-5477 ; 0890-9369
ISSN (online)	1549-5477
ISSN	0890-9369
DOI	10.1101/gad.306753.117
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