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  • 1
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    Nek1 primes ATR for activation [Cell Biology] (2013)
    National Academy of Sciences
    Details
    Publication Date: 2013-02-06
    Description: The master checkpoint kinase ATR (ATM and Rad3-related) and its partner ATRIP (ATR-interacting protein) exist as a complex and function together in the DNA damage response. Unexpectedly, we found that the stability of the ATR–ATRIP complex is regulated by an unknown kinase independently of DNA damage. In search for this...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 2
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    A myocardial lineage derives from Tbx18 epicardial cells (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-05-16
    Description: Understanding the origins and roles of cardiac progenitor cells is important for elucidating the pathogenesis of congenital and acquired heart diseases. Moreover, manipulation of cardiac myocyte progenitors has potential for cell-based repair strategies for various myocardial disorders. Here we report the identification in mouse of a previously unknown cardiac myocyte lineage that derives from the proepicardial organ. These progenitor cells, which express the T-box transcription factor Tbx18, migrate onto the outer cardiac surface to form the epicardium, and then make a substantial contribution to myocytes in the ventricular septum and the atrial and ventricular walls. Tbx18-expressing cardiac progenitors also give rise to cardiac fibroblasts and coronary smooth muscle cells. The pluripotency of Tbx18 proepicardial cells provides a theoretical framework for applying these progenitors to effect cardiac repair and regeneration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cai, Chen-Leng -- Martin, Jody C -- Sun, Yunfu -- Cui, Li -- Wang, Lianchun -- Ouyang, Kunfu -- Yang, Lei -- Bu, Lei -- Liang, Xingqun -- Zhang, Xiaoxue -- Stallcup, William B -- Denton, Christopher P -- McCulloch, Andrew -- Chen, Ju -- Evans, Sylvia M -- P41 RR005351/RR/NCRR NIH HHS/ -- T32 HL007444/HL/NHLBI NIH HHS/ -- England -- Nature. 2008 Jul 3;454(7200):104-8. doi: 10.1038/nature06969. Epub 2008 May 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Skaggs School of Pharmacy, University of California, San Diego, La Jolla, California 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18480752" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; *Cell Lineage ; Gene Expression Regulation, Developmental ; Heart/growth & development ; Lac Operon/genetics ; Mice ; Myocardium/*cytology/metabolism ; Myocytes, Cardiac/*cytology/metabolism ; Myocytes, Smooth Muscle/metabolism ; Pericardium/*cytology/*metabolism ; Stem Cells/*cytology/metabolism ; T-Box Domain Proteins/genetics/*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)
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  • 3
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    Calcium flickers steer cell migration (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-01-02
    Description: Directional movement is a property common to all cell types during development and is critical to tissue remodelling and regeneration after damage. In migrating cells, calcium has a multifunctional role in directional sensing, cytoskeleton redistribution, traction force generation, and relocation of focal adhesions. Here we visualize high-calcium microdomains ('calcium flickers') and their patterned activation in migrating human embryonic lung fibroblasts. Calcium flicker activity is dually coupled to membrane tension (by means of TRPM7, a stretch-activated Ca(2+)-permeant channel of the transient receptor potential superfamily) and chemoattractant signal transduction (by means of type 2 inositol-1,4,5-trisphosphate receptors). Interestingly, calcium flickers are most active at the leading lamella of migrating cells, displaying a 4:1 front-to-rear polarization opposite to the global calcium gradient. When exposed to a platelet-derived growth factor gradient perpendicular to cell movement, asymmetric calcium flicker activity develops across the lamella and promotes the turning of migrating fibroblasts. These findings show how the exquisite spatiotemporal organization of calcium microdomains can orchestrate complex cellular processes such as cell migration.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3505761/" 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/PMC3505761/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wei, Chaoliang -- Wang, Xianhua -- Chen, Min -- Ouyang, Kunfu -- Song, Long-Sheng -- Cheng, Heping -- HL090905/HL/NHLBI NIH HHS/ -- R01 HL090905/HL/NHLBI NIH HHS/ -- England -- Nature. 2009 Feb 12;457(7231):901-5. doi: 10.1038/nature07577. Epub 2008 Dec 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular Medicine, State Key Laboratory of Biomembrane and Membrane Biotechnology, Peking University, Beijing 100871, China. chaoliang.wei@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19118385" target="_blank"〉PubMed〈/a〉
    Keywords: Calcium/*metabolism ; Calcium-Transporting ATPases/antagonists & inhibitors ; Cell Line ; Cell Polarity/physiology ; Chemotaxis/drug effects/*physiology ; Endoplasmic Reticulum/drug effects/metabolism ; Enzyme Inhibitors/pharmacology ; Fibroblasts/cytology/physiology ; Gene Expression Regulation, Developmental ; Humans ; Inositol 1,4,5-Trisphosphate Receptors/metabolism ; Protein-Serine-Threonine Kinases ; TRPM Cation Channels/metabolism ; Thapsigargin/pharmacology
    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)
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  • 4
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    In vivo cardiac reprogramming contributes to zebrafish heart regeneration (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-06-21
    Description: Despite current treatment regimens, heart failure remains the leading cause of morbidity and mortality in the developed world due to the limited capacity of adult mammalian ventricular cardiomyocytes to divide and replace ventricular myocardium lost from ischaemia-induced infarct. Hence there is great interest to identify potential cellular sources and strategies to generate new ventricular myocardium. Past studies have shown that fish and amphibians and early postnatal mammalian ventricular cardiomyocytes can proliferate to help regenerate injured ventricles; however, recent studies have suggested that additional endogenous cellular sources may contribute to this overall ventricular regeneration. Here we have developed, in the zebrafish (Danio rerio), a combination of fluorescent reporter transgenes, genetic fate-mapping strategies and a ventricle-specific genetic ablation system to discover that differentiated atrial cardiomyocytes can transdifferentiate into ventricular cardiomyocytes to contribute to zebrafish cardiac ventricular regeneration. Using in vivo time-lapse and confocal imaging, we monitored the dynamic cellular events during atrial-to-ventricular cardiomyocyte transdifferentiation to define intermediate cardiac reprogramming stages. We observed that Notch signalling becomes activated in the atrial endocardium following ventricular ablation, and discovered that inhibiting Notch signalling blocked the atrial-to-ventricular transdifferentiation and cardiac regeneration. Overall, these studies not only provide evidence for the plasticity of cardiac lineages during myocardial injury, but more importantly reveal an abundant new potential cardiac resident cellular source for cardiac ventricular regeneration.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4090927/" 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/PMC4090927/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Ruilin -- Han, Peidong -- Yang, Hongbo -- Ouyang, Kunfu -- Lee, Derek -- Lin, Yi-Fan -- Ocorr, Karen -- Kang, Guson -- Chen, Ju -- Stainier, Didier Y R -- Yelon, Deborah -- Chi, Neil C -- DP2 OD007464/OD/NIH HHS/ -- HL104239/HL/NHLBI NIH HHS/ -- HL54737/HL/NHLBI NIH HHS/ -- OD007464/OD/NIH HHS/ -- R01 HD069305/HD/NICHD NIH HHS/ -- R01 HL054737/HL/NHLBI NIH HHS/ -- R01 HL069594/HL/NHLBI NIH HHS/ -- R01 HL104239/HL/NHLBI NIH HHS/ -- R01 HL108599/HL/NHLBI NIH HHS/ -- England -- Nature. 2013 Jun 27;498(7455):497-501. doi: 10.1038/nature12322. Epub 2013 Jun 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Division of Cardiology, University of California, San Diego, La Jolla, California 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23783515" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Death ; *Cell Transdifferentiation ; *Cellular Reprogramming ; Heart/embryology/*physiology ; Heart Atria/cytology/embryology ; Heart Ventricles/cytology ; Myocardium/*cytology/metabolism ; Myocytes, Cardiac/cytology/metabolism ; Receptor, Notch1/metabolism ; Regeneration/*physiology ; Signal Transduction ; Zebrafish/embryology/*physiology
    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)
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  • 5
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    Inositol-1,4,5-trisphosphate receptor regulates hepatic gluconeogenesis in fasting and diabetes (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-04-13
    Description: In the fasted state, increases in circulating glucagon promote hepatic glucose production through induction of the gluconeogenic program. Triggering of the cyclic AMP pathway increases gluconeogenic gene expression via the de-phosphorylation of the CREB co-activator CRTC2 (ref. 1). Glucagon promotes CRTC2 dephosphorylation in part through the protein kinase A (PKA)-mediated inhibition of the CRTC2 kinase SIK2. A number of Ser/Thr phosphatases seem to be capable of dephosphorylating CRTC2 (refs 2, 3), but the mechanisms by which hormonal cues regulate these enzymes remain unclear. Here we show in mice that glucagon stimulates CRTC2 dephosphorylation in hepatocytes by mobilizing intracellular calcium stores and activating the calcium/calmodulin-dependent Ser/Thr-phosphatase calcineurin (also known as PP3CA). Glucagon increased cytosolic calcium concentration through the PKA-mediated phosphorylation of inositol-1,4,5-trisphosphate receptors (InsP(3)Rs), which associate with CRTC2. After their activation, InsP(3)Rs enhanced gluconeogenic gene expression by promoting the calcineurin-mediated dephosphorylation of CRTC2. During feeding, increases in insulin signalling reduced CRTC2 activity via the AKT-mediated inactivation of InsP(3)Rs. InsP(3)R activity was increased in diabetes, leading to upregulation of the gluconeogenic program. As hepatic downregulation of InsP(3)Rs and calcineurin improved circulating glucose levels in insulin resistance, these results demonstrate how interactions between cAMP and calcium pathways at the level of the InsP(3)R modulate hepatic glucose production under fasting conditions and in diabetes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3343222/" 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/PMC3343222/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Yiguo -- Li, Gang -- Goode, Jason -- Paz, Jose C -- Ouyang, Kunfu -- Screaton, Robert -- Fischer, Wolfgang H -- Chen, Ju -- Tabas, Ira -- Montminy, Marc -- HL087123/HL/NHLBI NIH HHS/ -- P01 HL087123/HL/NHLBI NIH HHS/ -- P01 HL087123-05/HL/NHLBI NIH HHS/ -- R01 DK049777/DK/NIDDK NIH HHS/ -- R01 DK049777-19/DK/NIDDK NIH HHS/ -- R01 DK091618/DK/NIDDK NIH HHS/ -- R01 DK091618-02/DK/NIDDK NIH HHS/ -- R01-DK049777/DK/NIDDK NIH HHS/ -- R01-DK083834/DK/NIDDK NIH HHS/ -- R01-DK091618/DK/NIDDK NIH HHS/ -- R37 DK083834/DK/NIDDK NIH HHS/ -- R37 DK083834-29/DK/NIDDK NIH HHS/ -- T32 GM008666/GM/NIGMS NIH HHS/ -- England -- Nature. 2012 Apr 8;485(7396):128-32. doi: 10.1038/nature10988.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Clayton Foundation Laboratories for Peptide Biology, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22495310" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Glucose/*metabolism ; Calcineurin/metabolism ; Calcium/metabolism ; Calcium Signaling ; Cells, Cultured ; Cyclic AMP/metabolism ; Diabetes Mellitus/blood/genetics/*metabolism ; Fasting/blood/*metabolism ; Gene Expression Regulation/drug effects ; Glucagon/pharmacology ; *Gluconeogenesis/genetics ; HEK293 Cells ; Hepatocytes/metabolism ; Humans ; Inositol 1,4,5-Trisphosphate Receptors/*metabolism ; Insulin Resistance ; Liver/cytology/*metabolism ; Mice ; Phosphorylation/drug effects ; Trans-Activators/metabolism ; Transcription Factors
    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)
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  • 6
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    Pollution evaluation of heavy metals in soil near smelting area by index of geoaccumulation (Igeo) (2017)
    Institute of Physics (IOP)
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    Publication Date: 2017-02-14
    Description: In order to investigate the heavy metal pollution conditions of soil of smelting area in Zijiang of Chenzhou, Hunan province, 42 samples were studied. The concentrations of heavy metals As, Pb, Cd, Zn and Cu in the soil were determined by using atomic absorption spectrometry(AAS) and atomic fluorescence spectrometry(AFS). Then the potential pollution risks of heavy metal in the soil were evaluated by method of geological acumination index (I geo ). The results indicated that the average concentrations of As, Pb, Cd, Zn and Cu were 187.79, 2074.52, 15.72, 2178.89, 39.69 mg/kg respectively. The geological evaluation of the cumulative index results showed that the contamination degree of 5 heavy metals follow the sequence of Cd〉 Zn 〉Pb 〉 As 〉Cu. The results show that Cd reached extremely pollution degree, Zn reached strong pollution-extremely pollution levels, the pollution of Pb in the soil is classified as strong pollution degree, Cu and As of no pollution ac...
    Print ISSN: 1755-1307
    Electronic ISSN: 1755-1315
    Topics: Geography , Geosciences , Physics
    Published by Institute of Physics (IOP)
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  • 7
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    Ca2+ sparks and secretion in dorsal root ganglion neurons (2005)
    National Academy of Sciences
    Details
    Publication Date: 2005-08-15
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 8
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    Epitaxial growth of nitride semiconductor films by laser ablation (1999)
    Elsevier
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    Publication Date: 1999-04-01
    Print ISSN: 0040-6090
    Electronic ISSN: 1879-2731
    Topics: Physics
    Published by Elsevier
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  • 9
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    Disruption of both nesprin 1 and desmin results in nuclear anchorage defects and fibrosis in skeletal muscle (2014)
    Oxford University Press
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    Publication Date: 2014-10-22
    Description: Proper localization and anchorage of nuclei within skeletal muscle is critical for cellular function. Alterations in nuclear anchoring proteins modify a number of cellular functions including mechanotransduction, nuclear localization, chromatin positioning/compaction and overall organ function. In skeletal muscle, nesprin 1 and desmin are thought to link the nucleus to the cytoskeletal network. Thus, we hypothesize that both of these factors play a key role in skeletal muscle function. To examine this question, we utilized global ablation murine models of nesprin 1, desmin or both nesprin 1 and desmin. Herein, we have created the nesprin-desmin double-knockout (DKO) mouse, eliminating a major fraction of nuclear-cytoskeletal connections and enabling understanding of the importance of nuclear anchorage in skeletal muscle. Globally, DKO mice are marked by decreased lifespan, body weight and muscle strength. With regard to skeletal muscle, DKO myonuclear anchorage was dramatically decreased compared with wild-type, nesprin 1 –/– and desmin –/– mice. Additionally, nuclear-cytoskeletal strain transmission was decreased in DKO skeletal muscle. Finally, loss of nuclear anchorage in DKO mice coincided with a fibrotic response as indicated by increased collagen and extracellular matrix deposition and increased passive mechanical properties of muscle bundles. Overall, our data demonstrate that nesprin 1 and desmin serve redundant roles in nuclear anchorage and that the loss of nuclear anchorage in skeletal muscle results in a pathological response characterized by increased tissue fibrosis and mechanical stiffness.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
    Published by Oxford University Press
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  • 10
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    Connexin defects underlie arrhythmogenic right ventricular cardiomyopathy in a novel mouse model (2014)
    Oxford University Press
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    Publication Date: 2014-02-08
    Description: Arrhythmogenic right ventricular cardiomyopathy (ARVC) termed a ‘disease of the desmosome’ is an inherited cardiomyopathy that recently underwent reclassification owing to the identification of left-dominant and biventricular disease forms. Homozygous loss-of-function mutations in the desmosomal component, desmoplakin, are found in patients exhibiting a biventricular form of ARVC; however, no models recapitulate the postnatal hallmarks of the disease as seen in these patients. To gain insights into the homozygous loss-of-function effects of desmoplakin in the heart, we generated cardiomyocyte-specific desmoplakin-deficient mice (DSP-cKO) using ventricular myosin light chain-2-Cre mice. Homozygous DSP-cKO mice are viable but display early ultrastructural defects in desmosomal integrity leading to a cardiomyopathy reminiscent of a biventricular form of ARVC, which includes cell death and fibro-fatty replacement within the ventricle leading to biventricular dysfunction, failure and premature death. DSP-cKO mice also exhibited ventricular arrhythmias that are exacerbated with exercise and catecholamine stimulation. Furthermore, DSP-cKO hearts exhibited right ventricular conduction defects associated with loss of connexin 40 expression and electrical wavefront propagation defects associated with loss of connexin 43 expression. Dose-dependent assessment of the effects of loss of desmoplakin in neonatal ventricular cardiomyocytes revealed primary loss of connexin 43 levels, phosphorylation and function independent of the molecular dissociation of the mechanical junction complex and fibro-fatty manifestation associated with ARVC, suggesting a role for desmoplakin as a primary stabilizer of connexin integrity. In summary, we provide evidence for a novel mouse model, which is reminiscent of the postnatal onset of ARVC while highlighting mechanisms underlying a biventricular form of human ARVC.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
    Published by Oxford University Press
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