ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Your email was sent successfully. Check your inbox.

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

Proceed reservation?

Export
  • 1
    facet.materialart.
    Unknown
    Genes, Vol. 9, Pages 643: Exploring the Variable Phenotypes of RPGR Carrier Females in Assessing Their Potential for Retinal Gene Therapy (2018)
    MDPI
    In: Genes
    Details
    Publication Date: 2018
    Description: Inherited retinal degenerations are the leading cause of blindness in the working population. X-linked retinitis pigmentosa (XLRP), caused by mutations in the Retinitis pigmentosa GTPase regulator (RPGR) gene is one of the more severe forms, and female carriers of RPGR mutations have a variable presentation. A retrospective review of twenty-three female RPGR carriers aged between 8 and 76 years old was carried out using fundoscopy, autofluorescence imaging (AF), blue reflectance (BR) imaging and optical coherence tomography (OCT). Confirmation of the genetic mutation was obtained from male relatives or Sanger genetic sequencing. Fundus examination and AF demonstrate phenotypic variability in RPGR carriers. The genetic mutation appears indeterminate of the degree of change. We found four distinct classifications based on AF images to describe RPGR carriers; normal (N) representing normal or near-normal AF appearance (n = 1, 4%); radial (R) pattern reflex without pigmentary retinopathy (n = 14, 61%); focal (F) pigmentary retinopathy (n = 5, 22%) and; male (M) phenotype (n = 3, 13%). The phenotypes were precisely correlated in both eyes (rs = 1.0, p 〈 0.0001). Skewed X-inactivation can result in severely affected carrier females—in some cases indistinguishable from the male pattern and these patients should be considered for RPGR gene therapy. In the cases of the male (M) phenotype where the X-inactivation was skewed, the pattern was similar in both eyes, suggesting that the mechanism is not truly random but may have an underlying genetic basis.
    Electronic ISSN: 2073-4425
    Topics: Biology
    Published by MDPI
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 2
    facet.materialart.
    Unknown
    Controls on circulation, cross-shelf exchange and dense water formation in an Antarctic polynya (2016)
    Wiley
    Details
    Publication Date: 2016-06-17
    Description: Circulation on the Antarctic continental shelf influence cross-shelf exchange, Antarctic Bottom Water formation, and ocean heat flux to floating ice shelves. The physical processes driving the shelf circulation and its seasonal and interannual variability remain poorly understood. We use a unique time series of repeat hydrographic observations from the Adélie Land continental shelf and a box inverse model to explore the relationship between surface forcing, shelf circulation, cross-shelf exchange, and dense water formation. A wind-driven northwestward coastal current, set up by onshore Ekman transport, dominates the summer circulation. During winter, strong buoyancy loss creates dense shelf water. This dense water flows off the shelf, with a compensating on-shelf flow that is an order of magnitude larger in winter than in summer. The results demonstrate the importance of winter buoyancy loss in driving the shelf circulation and cross-shelf exchange, as well as dense water mass formation.
    Print ISSN: 0094-8276
    Electronic ISSN: 1944-8007
    Topics: Geosciences , Physics
    Published by Wiley on behalf of American Geophysical Union (AGU).
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 3
    facet.materialart.
    Unknown
    Impacts of wind stress on the Antarctic Circumpolar Current fronts and associated subduction (2011)
    Wiley
    Details
    Publication Date: 2011-06-14
    Description: Recent studies suggest that the overturning circulation in the Antarctic Circumpolar Current (ACC) region shows a weak sensitivity to overlying wind stress changes, due to balancing of changes in the eddy-induced and Eulerian mean transports. Using an eddy-permitting coupled climate model, we analyze the response of the ACC transport, and associated water mass subduction rates, in response to an idealized poleward shift and intensification of the westerlies. As in previous studies, we find a small increase in the net ACC transport, and a poleward shift in the mean position of the ACC flow. However, the ACC is restructured, with the Subantarctic Front (SAF) and Polar Front (PF) branches shifting poleward by between 0.9° and 2.5° of latitude, resulting in a weaker ACC flow in both the SAF and PF zones. The wind stress anomaly drives a stronger northward Ekman transport of cool surface waters, deepening the winter mixed layer and causing a 12.7 Sv increase in the subduction of Subantarctic Mode Water (SAMW) north of the SAF zone and a 6.5 Sv increase in the subduction of Antarctic Intermediate Water (AAIW) within the SAF and PF zones. Our results suggest that changes in the wind stress restructure the Southern Ocean large-scale circulation, including the flow of the ACC in its primary jets, and that this affects the formation rates of SAMW and AAIW in this complex region.
    Print ISSN: 0094-8276
    Electronic ISSN: 1944-8007
    Topics: Geosciences , Physics
    Published by Wiley on behalf of American Geophysical Union (AGU).
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 4
    facet.materialart.
    Unknown
    Radial variation in Kraft pulp yield and cellulose content in Eucalyptus globulus wood across three contrasting sites predicted by near infrared spectroscopy (2012)
    National Research Council Canada (NRC)
    Details
    Publication Date: 2012-07-29
    Description: Canadian Journal of Forest Research, Volume 0, Issue 0, Page 1577-1586, e-First articles.
    Print ISSN: 0045-5067
    Electronic ISSN: 1208-6037
    Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition
    Published by National Research Council Canada (NRC)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 5
    facet.materialart.
    Unknown
    Hydrothermal Heat Enhances Abyssal Mixing in the Antarctic Circumpolar Current (2019)
    Wiley
    Details
    Publication Date: 2019
    Description: Abstract Upwelling in the world's strongest current, the Antarctic Circumpolar Current, is thought to be driven by wind stress, surface buoyancy flux, and mixing generated from the interaction between bottom currents and rough topography. However, the impact of localized injection of heat by hydrothermal vents where the Antarctic Circumpolar Current interacts with mid‐ocean ridges remains poorly understood. Here a circumpolar compilation of helium and physical measurements are used to show that while geothermal heat is transferred to the ocean over a broad area by conduction, heat transfer by convection dominates near hydrothermal vents. Buoyant hydrothermal plumes decrease stratification above the vent source and increase stratification to the south, altering the local vertical diffusivity and diapycnal upwelling within 500 m of the sea floor by an order of magnitude. Both the helium tracer and stratification signals induced by hydrothermal input are advected by the flow and influence properties downstream.
    Print ISSN: 0094-8276
    Electronic ISSN: 1944-8007
    Topics: Geosciences , Physics
    Published by Wiley on behalf of American Geophysical Union (AGU).
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 6
    facet.materialart.
    Unknown
    Cryptochromes mediate rhythmic repression of the glucocorticoid receptor (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-12-16
    Description: Mammalian metabolism is highly circadian and major hormonal circuits involving nuclear hormone receptors display interlinked diurnal cycling. However, mechanisms that logically explain the coordination of nuclear hormone receptors and the clock are poorly understood. Here we show that two circadian co-regulators, cryptochromes 1 and 2, interact with the glucocorticoid receptor in a ligand-dependent fashion and globally alter the transcriptional response to glucocorticoids in mouse embryonic fibroblasts: cryptochrome deficiency vastly decreases gene repression and approximately doubles the number of dexamethasone-induced genes, suggesting that cryptochromes broadly oppose glucocorticoid receptor activation and promote repression. In mice, genetic loss of cryptochrome 1 and/or 2 results in glucose intolerance and constitutively high levels of circulating corticosterone, suggesting reduced suppression of the hypothalamic-pituitary-adrenal axis coupled with increased glucocorticoid transactivation in the liver. Genomically, cryptochromes 1 and 2 associate with a glucocorticoid response element in the phosphoenolpyruvate carboxykinase 1 promoter in a hormone-dependent manner, and dexamethasone-induced transcription of the phosphoenolpyruvate carboxykinase 1 gene was strikingly increased in cryptochrome-deficient livers. These results reveal a specific mechanism through which cryptochromes couple the activity of clock and receptor target genes to complex genomic circuits underpinning normal metabolic homeostasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3245818/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3245818/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lamia, Katja A -- Papp, Stephanie J -- Yu, Ruth T -- Barish, Grant D -- Uhlenhaut, N Henriette -- Jonker, Johan W -- Downes, Michael -- Evans, Ronald M -- DK057978/DK/NIDDK NIH HHS/ -- DK062434/DK/NIDDK NIH HHS/ -- DK090188/DK/NIDDK NIH HHS/ -- K01 DK090188/DK/NIDDK NIH HHS/ -- K01 DK090188-01/DK/NIDDK NIH HHS/ -- K01 DK090188-02/DK/NIDDK NIH HHS/ -- P30 CA014195/CA/NCI NIH HHS/ -- R37 DK057978/DK/NIDDK NIH HHS/ -- R37 DK057978-22/DK/NIDDK NIH HHS/ -- U19 DK062434/DK/NIDDK NIH HHS/ -- U19 DK062434-01/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Dec 14;480(7378):552-6. doi: 10.1038/nature10700.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gene Expression Laboratory, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA. klamia@scripps.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22170608" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Circadian Rhythm ; Corticosterone/blood ; Cryptochromes/genetics/*metabolism ; Dexamethasone/pharmacology ; Female ; *Gene Expression Regulation/drug effects ; Glucocorticoids/pharmacology ; Glucose Intolerance/genetics ; HEK293 Cells ; Humans ; Liver/enzymology/metabolism ; Mice ; Phosphoenolpyruvate Carboxykinase (GTP)/blood/metabolism ; Receptors, Glucocorticoid/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 7
    facet.materialart.
    Unknown
    Corrigendum: Endocrinization of FGF1 produces a neomorphic and potent insulin sensitizer (2015)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2015-03-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suh, Jae Myoung -- Jonker, Johan W -- Ahmadian, Maryam -- Goetz, Regina -- Lackey, Denise -- Osborn, Olivia -- Huang, Zhifeng -- Liu, Weilin -- Yoshihara, Eiji -- van Dijk, Theo H -- Havinga, Rick -- Fan, Weiwei -- Yin, Yun-Qiang -- Yu, Ruth T -- Liddle, Christopher -- Atkins, Annette R -- Olefsky, Jerrold M -- Mohammadi, Moosa -- Downes, Michael -- Evans, Ronald M -- P01 HL088093/HL/NHLBI NIH HHS/ -- P42 ES010337/ES/NIEHS NIH HHS/ -- R01 DE013686/DE/NIDCR NIH HHS/ -- R01 HL105278/HL/NHLBI NIH HHS/ -- R24 DK090962/DK/NIDDK NIH HHS/ -- R37 DK057978/DK/NIDDK NIH HHS/ -- England -- Nature. 2015 Apr 16;520(7547):388. doi: 10.1038/nature14304. Epub 2015 Mar 4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25739500" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 8
    facet.materialart.
    Unknown
    Endocrinization of FGF1 produces a neomorphic and potent insulin sensitizer (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-07-22
    Description: Fibroblast growth factor 1 (FGF1) is an autocrine/paracrine regulator whose binding to heparan sulphate proteoglycans effectively precludes its circulation. Although FGF1 is known as a mitogenic factor, FGF1 knockout mice develop insulin resistance when stressed by a high-fat diet, suggesting a potential role in nutrient homeostasis. Here we show that parenteral delivery of a single dose of recombinant FGF1 (rFGF1) results in potent, insulin-dependent lowering of glucose levels in diabetic mice that is dose-dependent but does not lead to hypoglycaemia. Chronic pharmacological treatment with rFGF1 increases insulin-dependent glucose uptake in skeletal muscle and suppresses the hepatic production of glucose to achieve whole-body insulin sensitization. The sustained glucose lowering and insulin sensitization attributed to rFGF1 are not accompanied by the side effects of weight gain, liver steatosis and bone loss associated with current insulin-sensitizing therapies. We also show that the glucose-lowering activity of FGF1 can be dissociated from its mitogenic activity and is mediated predominantly via FGF receptor 1 signalling. Thus we have uncovered an unexpected, neomorphic insulin-sensitizing action for exogenous non-mitogenic human FGF1 with therapeutic potential for the treatment of insulin resistance and type 2 diabetes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4184286/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4184286/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suh, Jae Myoung -- Jonker, Johan W -- Ahmadian, Maryam -- Goetz, Regina -- Lackey, Denise -- Osborn, Olivia -- Huang, Zhifeng -- Liu, Weilin -- Yoshihara, Eiji -- van Dijk, Theo H -- Havinga, Rick -- Fan, Weiwei -- Yin, Yun-Qiang -- Yu, Ruth T -- Liddle, Christopher -- Atkins, Annette R -- Olefsky, Jerrold M -- Mohammadi, Moosa -- Downes, Michael -- Evans, Ronald M -- DE13686/DE/NIDCR NIH HHS/ -- DK-033651/DK/NIDDK NIH HHS/ -- DK-063491/DK/NIDDK NIH HHS/ -- DK-074868/DK/NIDDK NIH HHS/ -- DK057978/DK/NIDDK NIH HHS/ -- DK090962/DK/NIDDK NIH HHS/ -- ES010337/ES/NIEHS NIH HHS/ -- HL088093/HL/NHLBI NIH HHS/ -- HL105278/HL/NHLBI NIH HHS/ -- P01 DK054441/DK/NIDDK NIH HHS/ -- P01 DK074868/DK/NIDDK NIH HHS/ -- P01 HL088093/HL/NHLBI NIH HHS/ -- P01-DK054441-14A1/DK/NIDDK NIH HHS/ -- P30 DK063491/DK/NIDDK NIH HHS/ -- P42 ES010337/ES/NIEHS NIH HHS/ -- R01 HL105278/HL/NHLBI NIH HHS/ -- R24 DK090962/DK/NIDDK NIH HHS/ -- R37 DK033651/DK/NIDDK NIH HHS/ -- R37 DK057978/DK/NIDDK NIH HHS/ -- T32 DK007494/DK/NIDDK NIH HHS/ -- T32-DK-007494/DK/NIDDK NIH HHS/ -- U54 HD012303/HD/NICHD NIH HHS/ -- U54-HD-012303-25/HD/NICHD NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 Sep 18;513(7518):436-9. doi: 10.1038/nature13540. Epub 2014 Jul 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Gene Expression Laboratory, Salk Institute for Biological Studies, La Jolla, California 92037, USA [2]. ; 1] Center for Liver, Digestive and Metabolic Diseases, Departments of Pediatrics and Laboratory Medicine, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9713 GZ Groningen, The Netherlands [2]. ; Gene Expression Laboratory, Salk Institute for Biological Studies, La Jolla, California 92037, USA. ; Department of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, New York 10016, USA. ; Department of Medicine, Division of Endocrinology and Metabolism, University of California at San Diego, La Jolla, California 92093, USA. ; 1] Department of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, New York 10016, USA [2] School of Pharmacy, Wenzhou Medical University, Wenzhou, Zhejiang 325035, China. ; Center for Liver, Digestive and Metabolic Diseases, Departments of Pediatrics and Laboratory Medicine, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9713 GZ Groningen, The Netherlands. ; The Storr Liver Unit, Westmead Millennium Institute and University of Sydney, Westmead Hospital, Westmead, New South Wales 2145, Australia. ; 1] Gene Expression Laboratory, Salk Institute for Biological Studies, La Jolla, California 92037, USA [2] Howard Hughes Medical Institute, Salk Institute for Biological Studies, La Jolla, California 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25043058" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Glucose/metabolism ; Body Weight/drug effects ; Diabetes Mellitus, Experimental/drug therapy/metabolism ; Diabetes Mellitus, Type 2/metabolism ; Diet, High-Fat ; Dose-Response Relationship, Drug ; Fibroblast Growth Factor 1/administration & dosage/adverse effects/*pharmacology ; Glucose/*metabolism ; Glucose Tolerance Test ; Humans ; Insulin/*metabolism ; Insulin Resistance ; Liver/drug effects/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; Mitogens/pharmacology ; Muscle, Skeletal/drug effects/metabolism ; Receptor, Fibroblast Growth Factor, Type 1/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 9
    facet.materialart.
    Unknown
    Hotspots of aberrant epigenomic reprogramming in human induced pluripotent stem cells (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-02-04
    Description: Induced pluripotent stem cells (iPSCs) offer immense potential for regenerative medicine and studies of disease and development. Somatic cell reprogramming involves epigenomic reconfiguration, conferring iPSCs with characteristics similar to embryonic stem (ES) cells. However, it remains unknown how complete the reestablishment of ES-cell-like DNA methylation patterns is throughout the genome. Here we report the first whole-genome profiles of DNA methylation at single-base resolution in five human iPSC lines, along with methylomes of ES cells, somatic cells, and differentiated iPSCs and ES cells. iPSCs show significant reprogramming variability, including somatic memory and aberrant reprogramming of DNA methylation. iPSCs share megabase-scale differentially methylated regions proximal to centromeres and telomeres that display incomplete reprogramming of non-CG methylation, and differences in CG methylation and histone modifications. Lastly, differentiation of iPSCs into trophoblast cells revealed that errors in reprogramming CG methylation are transmitted at a high frequency, providing an iPSC reprogramming signature that is maintained after differentiation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3100360/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3100360/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lister, Ryan -- Pelizzola, Mattia -- Kida, Yasuyuki S -- Hawkins, R David -- Nery, Joseph R -- Hon, Gary -- Antosiewicz-Bourget, Jessica -- O'Malley, Ronan -- Castanon, Rosa -- Klugman, Sarit -- Downes, Michael -- Yu, Ruth -- Stewart, Ron -- Ren, Bing -- Thomson, James A -- Evans, Ronald M -- Ecker, Joseph R -- 1U01ES017166-01/ES/NIEHS NIH HHS/ -- DK062434/DK/NIDDK NIH HHS/ -- P30 CA014195/CA/NCI NIH HHS/ -- U01 ES017166/ES/NIEHS NIH HHS/ -- U01 ES017166-01/ES/NIEHS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Mar 3;471(7336):68-73. doi: 10.1038/nature09798. Epub 2011 Feb 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genomic Analysis Laboratory, The Salk Institute for Biological Studies, La Jolla, California 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21289626" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Differentiation/genetics ; Cell Line ; Cellular Reprogramming/*genetics ; CpG Islands/genetics ; DNA Methylation/*genetics ; Embryonic Stem Cells/cytology/metabolism ; Epigenomics ; Epistasis, Genetic/*genetics ; Fibroblasts/cytology/metabolism ; Genome, Human/*genetics ; Histones/metabolism ; Humans ; Induced Pluripotent Stem Cells/cytology/*metabolism ; Trophoblasts/cytology/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 10
    facet.materialart.
    Unknown
    Regulation of circadian behaviour and metabolism by REV-ERB-alpha and REV-ERB-beta (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-03-31
    Description: The circadian clock acts at the genomic level to coordinate internal behavioural and physiological rhythms via the CLOCK-BMAL1 transcriptional heterodimer. Although the nuclear receptors REV-ERB-alpha and REV-ERB-beta have been proposed to form an accessory feedback loop that contributes to clock function, their precise roles and importance remain unresolved. To establish their regulatory potential, we determined the genome-wide cis-acting targets (cistromes) of both REV-ERB isoforms in murine liver, which revealed shared recognition at over 50% of their total DNA binding sites and extensive overlap with the master circadian regulator BMAL1. Although REV-ERB-alpha has been shown to regulate Bmal1 expression directly, our cistromic analysis reveals a more profound connection between BMAL1 and the REV-ERB-alpha and REV-ERB-beta genomic regulatory circuits than was previously suspected. Genes within the intersection of the BMAL1, REV-ERB-alpha and REV-ERB-beta cistromes are highly enriched for both clock and metabolic functions. As predicted by the cistromic analysis, dual depletion of Rev-erb-alpha and Rev-erb-beta function by creating double-knockout mice profoundly disrupted circadian expression of core circadian clock and lipid homeostatic gene networks. As a result, double-knockout mice show markedly altered circadian wheel-running behaviour and deregulated lipid metabolism. These data now unite REV-ERB-alpha and REV-ERB-beta with PER, CRY and other components of the principal feedback loop that drives circadian expression and indicate a more integral mechanism for the coordination of circadian rhythm and metabolism.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3367514/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3367514/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cho, Han -- Zhao, Xuan -- Hatori, Megumi -- Yu, Ruth T -- Barish, Grant D -- Lam, Michael T -- Chong, Ling-Wa -- DiTacchio, Luciano -- Atkins, Annette R -- Glass, Christopher K -- Liddle, Christopher -- Auwerx, Johan -- Downes, Michael -- Panda, Satchidananda -- Evans, Ronald M -- DK057978/DK/NIDDK NIH HHS/ -- DK062434/DK/NIDDK NIH HHS/ -- DK090962/DK/NIDDK NIH HHS/ -- DK091618/DK/NIDDK NIH HHS/ -- HL105278/HL/NHLBI NIH HHS/ -- P30 CA014195/CA/NCI NIH HHS/ -- R01 DK091618/DK/NIDDK NIH HHS/ -- R01 HL105278/HL/NHLBI NIH HHS/ -- R01 HL105278-21/HL/NHLBI NIH HHS/ -- R24 DK090962/DK/NIDDK NIH HHS/ -- R24 DK090962-02/DK/NIDDK NIH HHS/ -- R37 DK057978/DK/NIDDK NIH HHS/ -- R37 DK057978-34/DK/NIDDK NIH HHS/ -- T32 HL007770/HL/NHLBI NIH HHS/ -- T32 HL007770-15/HL/NHLBI NIH HHS/ -- T32-HL007770/HL/NHLBI NIH HHS/ -- U19 DK062434/DK/NIDDK NIH HHS/ -- U19 DK062434-10/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Mar 29;485(7396):123-7. doi: 10.1038/nature11048.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gene Expression Laboratory, Salk Institute for Biological Studies, La Jolla, California 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22460952" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Clocks/drug effects/genetics ; Circadian Rhythm/genetics/*physiology ; Cryptochromes/deficiency/genetics/metabolism ; *Energy Metabolism/genetics ; Feedback, Physiological ; Gene Expression Regulation ; Gene Regulatory Networks/genetics ; Homeostasis/genetics ; *Lipid Metabolism/genetics ; Liver/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Molecular Sequence Data ; Motor Activity/genetics/physiology ; Nuclear Receptor Subfamily 1, Group D, Member 1/deficiency/genetics/*metabolism ; Period Circadian Proteins/deficiency/genetics/metabolism ; Receptors, Cytoplasmic and Nuclear/deficiency/genetics/*metabolism ; Repressor Proteins/deficiency/genetics/*metabolism ; Transcriptome/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...