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  • Transfection
  • American Association for the Advancement of Science (AAAS)  (14)
  • American Association of Petroleum Geologists (AAPG)
  • Emerald
  • 2010-2014  (14)
  • 1995-1999
  • 2010  (14)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (14)
  • American Association of Petroleum Geologists (AAPG)
  • Emerald
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  • 2010-2014  (14)
  • 1995-1999
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  • 1
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    Btbd7 regulates epithelial cell dynamics and branching morphogenesis (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-31
    Description: During embryonic development, many organs form by extensive branching of epithelia through the formation of clefts and buds. In cleft formation, buds are delineated by the conversion of epithelial cell-cell adhesions to cell-matrix adhesions, but the mechanisms of cleft formation are not clear. We have identified Btbd7 as a dynamic regulator of branching morphogenesis. Btbd7 provides a mechanistic link between the extracellular matrix and cleft propagation through its highly focal expression leading to local regulation of Snail2 (Slug), E-cadherin, and epithelial cell motility. Inhibition experiments show that Btbd7 is required for branching of embryonic mammalian salivary glands and lungs. Hence, Btbd7 is a regulatory gene that promotes epithelial tissue remodeling and formation of branched organs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3412157/" 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/PMC3412157/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Onodera, Tomohiro -- Sakai, Takayoshi -- Hsu, Jeff Chi-feng -- Matsumoto, Kazue -- Chiorini, John A -- Yamada, Kenneth M -- ZIA DE000525-20/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2010 Jul 30;329(5991):562-5. doi: 10.1126/science.1191880.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cell and Developmental Biology, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892-4370, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20671187" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cadherins/metabolism ; Cell Adhesion ; Cell Line ; Cell Movement ; Dogs ; Epithelial Cells/*physiology ; Fibronectins/genetics/metabolism ; Genes, Regulator ; Lung/*embryology/metabolism ; Mice ; Mice, Inbred ICR ; Models, Biological ; Molecular Sequence Data ; *Morphogenesis ; Nuclear Proteins ; Organ Culture Techniques ; Proteins/chemistry/*genetics/*physiology ; RNA, Small Interfering ; Salivary Glands/*embryology/metabolism ; Submandibular Gland/embryology ; Transcription Factors/genetics/metabolism ; Transfection
    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
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    Glutamine deamidation and dysfunction of ubiquitin/NEDD8 induced by a bacterial effector family (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-08-07
    Description: A family of bacterial effectors including Cif homolog from Burkholderia pseudomallei (CHBP) and Cif from Enteropathogenic Escherichia coli (EPEC) adopt a functionally important papain-like hydrolytic fold. We show here that CHBP was a potent inhibitor of the eukaryotic ubiquitination pathway. CHBP acted as a deamidase that specifically and efficiently deamidated Gln40 in ubiquitin and ubiquitin-like protein NEDD8 both in vitro and during Burkholderia infection. Deamidated ubiquitin was impaired in supporting ubiquitin-chain synthesis. Cif selectively deamidated NEDD8, which abolished the activity of neddylated Cullin-RING ubiquitin ligases (CRLs). Ubiquitination and ubiquitin-dependent degradation of multiple CRL substrates were impaired by Cif in EPEC-infected cells. Mutations of substrate-contacting residues in Cif abolished or attenuated EPEC-induced cytopathic phenotypes of cell cycle arrest and actin stress fiber formation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3031172/" 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/PMC3031172/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cui, Jixin -- Yao, Qing -- Li, Shan -- Ding, Xiaojun -- Lu, Qiuhe -- Mao, Haibin -- Liu, Liping -- Zheng, Ning -- Chen, She -- Shao, Feng -- R01 CA107134/CA/NCI NIH HHS/ -- R01 CA107134-08/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Sep 3;329(5996):1215-8. doi: 10.1126/science.1193844. Epub 2010 Aug 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate Program in Chinese Academy of Medical Sciences and Beijing Union Medical College, Beijing 100730, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20688984" target="_blank"〉PubMed〈/a〉
    Keywords: Amidohydrolases/*metabolism ; Bacterial Proteins/*metabolism ; Burkholderia/pathogenicity ; Burkholderia pseudomallei/*metabolism/pathogenicity ; Cell Cycle ; Cell Line ; Cullin Proteins/metabolism ; Enteropathogenic Escherichia coli/*metabolism/pathogenicity ; Escherichia coli Proteins/genetics/*metabolism ; Glutamine/*metabolism ; HeLa Cells ; Humans ; Point Mutation ; Stress Fibers/metabolism ; Transfection ; Ubiquitin/*metabolism ; Ubiquitin C/metabolism ; Ubiquitin-Conjugating Enzymes/metabolism ; Ubiquitin-Protein Ligases/metabolism ; Ubiquitination ; Ubiquitins/*metabolism
    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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  • 3
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    Genetic reactivation of cone photoreceptors restores visual responses in retinitis pigmentosa (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-06-26
    Description: Retinitis pigmentosa refers to a diverse group of hereditary diseases that lead to incurable blindness, affecting two million people worldwide. As a common pathology, rod photoreceptors die early, whereas light-insensitive, morphologically altered cone photoreceptors persist longer. It is unknown if these cones are accessible for therapeutic intervention. Here, we show that expression of archaebacterial halorhodopsin in light-insensitive cones can substitute for the native phototransduction cascade and restore light sensitivity in mouse models of retinitis pigmentosa. Resensitized photoreceptors activate all retinal cone pathways, drive sophisticated retinal circuit functions (including directional selectivity), activate cortical circuits, and mediate visually guided behaviors. Using human ex vivo retinas, we show that halorhodopsin can reactivate light-insensitive human photoreceptors. Finally, we identified blind patients with persisting, light-insensitive cones for potential halorhodopsin-based therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Busskamp, Volker -- Duebel, Jens -- Balya, David -- Fradot, Mathias -- Viney, Tim James -- Siegert, Sandra -- Groner, Anna C -- Cabuy, Erik -- Forster, Valerie -- Seeliger, Mathias -- Biel, Martin -- Humphries, Peter -- Paques, Michel -- Mohand-Said, Saddek -- Trono, Didier -- Deisseroth, Karl -- Sahel, Jose A -- Picaud, Serge -- Roska, Botond -- New York, N.Y. -- Science. 2010 Jul 23;329(5990):413-7. doi: 10.1126/science.1190897. Epub 2010 Jun 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neural Circuit Laboratories, Friedrich Miescher Institute for Biomedical Research, Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20576849" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dependovirus/genetics ; Disease Models, Animal ; Evoked Potentials, Visual ; *Genetic Therapy ; Genetic Vectors ; Halobacteriaceae/genetics ; Halorhodopsins/*genetics/*metabolism ; Humans ; Light ; Mice ; Mice, Knockout ; Promoter Regions, Genetic ; Retina/physiology ; Retinal Cone Photoreceptor Cells/*physiology ; Retinal Ganglion Cells/physiology ; Retinitis Pigmentosa/physiopathology/*therapy ; Tissue Culture Techniques ; Transfection ; Vision, Ocular ; Visual Pathways/physiology
    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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  • 4
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    Partitioning of histone H3-H4 tetramers during DNA replication-dependent chromatin assembly (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-04-03
    Description: Semiconservative DNA replication ensures the faithful duplication of genetic information during cell divisions. However, how epigenetic information carried by histone modifications propagates through mitotic divisions remains elusive. To address this question, the DNA replication-dependent nucleosome partition pattern must be clarified. Here, we report significant amounts of H3.3-H4 tetramers split in vivo, whereas most H3.1-H4 tetramers remained intact. Inhibiting DNA replication-dependent deposition greatly reduced the level of splitting events, which suggests that (i) the replication-independent H3.3 deposition pathway proceeds largely by cooperatively incorporating two new H3.3-H4 dimers and (ii) the majority of splitting events occurred during replication-dependent deposition. Our results support the idea that "silent" histone modifications within large heterochromatic regions are maintained by copying modifications from neighboring preexisting histones without the need for H3-H4 splitting events.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xu, Mo -- Long, Chengzu -- Chen, Xiuzhen -- Huang, Chang -- Chen, She -- Zhu, Bing -- New York, N.Y. -- Science. 2010 Apr 2;328(5974):94-8. doi: 10.1126/science.1178994.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate Program, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing 100730, People's Republic of China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20360108" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Aphidicolin/pharmacology ; Cell Cycle ; Chromatin/metabolism ; *Chromatin Assembly and Disassembly ; *DNA Replication ; Epigenesis, Genetic ; HeLa Cells ; Heterochromatin/metabolism ; Histones/*chemistry/*metabolism ; Humans ; Hydroxyurea/pharmacology ; Mass Spectrometry ; Molecular Sequence Data ; Nucleosomes/*metabolism ; Protein Multimerization ; S Phase ; Transfection
    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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  • 5
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    Siah regulation of Pard3A controls neuronal cell adhesion during germinal zone exit (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-11-27
    Description: The brain's circuitry is established by directed migration and synaptogenesis of neurons during development. Although neurons mature and migrate in specific patterns, little is known about how neurons exit their germinal zone niche. We found that cerebellar granule neuron germinal zone exit is regulated by proteasomal degradation of Pard3A by the Seven in Absentia homolog (Siah) E3 ubiquitin ligase. Pard3A gain of function and Siah loss of function induce precocious radial migration. Time-lapse imaging using a probe to measure neuronal cell contact reveals that Pard3A promotes adhesive interactions needed for germinal zone exit by recruiting the epithelial tight junction adhesion molecule C to the neuronal cell surface. Our findings define a Siah-Pard3A signaling pathway that controls adhesion-dependent exit of neuronal progenitors or immature neurons from a germinal zone niche.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3065828/" 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/PMC3065828/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Famulski, Jakub K -- Trivedi, Niraj -- Howell, Danielle -- Yang, Yuan -- Tong, Yiai -- Gilbertson, Richard -- Solecki, David J -- P01 CA096832/CA/NCI NIH HHS/ -- P01 CA096832-07/CA/NCI NIH HHS/ -- P30 CA021765/CA/NCI NIH HHS/ -- P30 CA021765-33/CA/NCI NIH HHS/ -- R01 CA129541/CA/NCI NIH HHS/ -- R01 CA129541-04/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2010 Dec 24;330(6012):1834-8. doi: 10.1126/science.1198480. Epub 2010 Nov 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Neurobiology, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21109632" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Adhesion ; Cell Adhesion Molecules/chemistry/*metabolism ; Cell Line ; *Cell Movement ; Cell Polarity ; Cerebellum/*cytology/embryology/*metabolism ; Dogs ; Humans ; Immunoglobulins/chemistry/metabolism ; Mice ; Morphogenesis ; Neurons/cytology/*physiology ; Protein Binding ; Protein Interaction Domains and Motifs ; Protein Structure, Tertiary ; RNA Interference ; Signal Transduction ; Stem Cells/physiology ; Transfection ; Ubiquitin-Protein Ligases/genetics/*metabolism ; Ubiquitination
    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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  • 6
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    Piezo1 and Piezo2 are essential components of distinct mechanically activated cation channels (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-09-04
    Description: Mechanical stimuli drive many physiological processes, including touch and pain sensation, hearing, and blood pressure regulation. Mechanically activated (MA) cation channel activities have been recorded in many cells, but the responsible molecules have not been identified. We characterized a rapidly adapting MA current in a mouse neuroblastoma cell line. Expression profiling and RNA interference knockdown of candidate genes identified Piezo1 (Fam38A) to be required for MA currents in these cells. Piezo1 and related Piezo2 (Fam38B) are vertebrate multipass transmembrane proteins with homologs in invertebrates, plants, and protozoa. Overexpression of mouse Piezo1 or Piezo2 induced two kinetically distinct MA currents. Piezos are expressed in several tissues, and knockdown of Piezo2 in dorsal root ganglia neurons specifically reduced rapidly adapting MA currents. We propose that Piezos are components of MA cation channels.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3062430/" 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/PMC3062430/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Coste, Bertrand -- Mathur, Jayanti -- Schmidt, Manuela -- Earley, Taryn J -- Ranade, Sanjeev -- Petrus, Matt J -- Dubin, Adrienne E -- Patapoutian, Ardem -- DE016927/DE/NIDCR NIH HHS/ -- NS046303/NS/NINDS NIH HHS/ -- R01 NS046303/NS/NINDS NIH HHS/ -- R01 NS046303-08/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2010 Oct 1;330(6000):55-60. doi: 10.1126/science.1193270. Epub 2010 Sep 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, The Scripps Research Institute (TSRI), La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20813920" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cations/*metabolism ; Cell Line, Tumor ; Cell Membrane/chemistry ; Cloning, Molecular ; Ganglia, Spinal/cytology ; Ion Channels/analysis/chemistry/genetics/*metabolism ; *Mechanotransduction, Cellular ; Membrane Potentials ; Mice ; Molecular Sequence Data ; Neurons/*metabolism ; Patch-Clamp Techniques ; Pressure ; Protein Structure, Tertiary ; RNA Interference ; RNA, Small Interfering/genetics ; Transfection
    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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  • 7
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    Reprogramming cellular behavior with RNA controllers responsive to endogenous proteins (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-11-27
    Description: Synthetic genetic devices that interface with native cellular pathways can be used to change natural networks to implement new forms of control and behavior. The engineering of gene networks has been limited by an inability to interface with native components. We describe a class of RNA control devices that overcome these limitations by coupling increased abundance of particular proteins to targeted gene expression events through the regulation of alternative RNA splicing. We engineered RNA devices that detect signaling through the nuclear factor kappaB and Wnt signaling pathways in human cells and rewire these pathways to produce new behaviors, thereby linking disease markers to noninvasive sensing and reprogrammed cellular fates. Our work provides a genetic platform that can build programmable sensing-actuation devices enabling autonomous control over cellular behavior.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3171693/" 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/PMC3171693/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Culler, Stephanie J -- Hoff, Kevin G -- Smolke, Christina D -- RC1 GM091298/GM/NIGMS NIH HHS/ -- RC1 GM091298-01/GM/NIGMS NIH HHS/ -- RC1 GM091298-02/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Nov 26;330(6008):1251-5. doi: 10.1126/science.1192128.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Chemistry and Chemical Engineering, 1200 East California Boulevard, MC 210-41, California Institute of Technology, Pasadena, CA 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21109673" target="_blank"〉PubMed〈/a〉
    Keywords: *Alternative Splicing ; Apoptosis ; Aptamers, Nucleotide/chemistry/genetics/*metabolism ; Capsid Proteins/metabolism ; Cell Line ; Cell Nucleus/metabolism ; Exons ; Ganciclovir/pharmacology ; *Gene Expression Regulation ; Gene Regulatory Networks ; *Genetic Engineering ; Green Fluorescent Proteins/genetics ; Humans ; Introns ; Ligands ; Mutation ; NF-kappa B p50 Subunit/genetics/metabolism ; Protein Binding ; Signal Transduction ; Survival of Motor Neuron 1 Protein/genetics ; Transcription Factor RelA/genetics/metabolism ; Transfection ; Wnt Proteins/metabolism ; beta Catenin/genetics/metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Local and long-range reciprocal regulation of cAMP and cGMP in axon/dendrite formation (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-01-30
    Description: Cytosolic cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) often mediate antagonistic cellular actions of extracellular factors, from the regulation of ion channels to cell volume control and axon guidance. We found that localized cAMP and cGMP activities in undifferentiated neurites of cultured hippocampal neurons promote and suppress axon formation, respectively, and exert opposite effects on dendrite formation. Fluorescence resonance energy transfer imaging showed that alterations of the amount of cAMP resulted in opposite changes in the amount of cGMP, and vice versa, through the activation of specific phosphodiesterases and protein kinases. Local elevation of cAMP in one neurite resulted in cAMP reduction in all other neurites of the same neuron. Thus, local and long-range reciprocal regulation of cAMP and cGMP together ensures coordinated development of one axon and multiple dendrites.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shelly, Maya -- Lim, Byung Kook -- Cancedda, Laura -- Heilshorn, Sarah C -- Gao, Hongfeng -- Poo, Mu-ming -- NS-22764/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2010 Jan 29;327(5965):547-52. doi: 10.1126/science.1179735.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neurobiology, Department of Molecular and Cell Biology, Helen Wills Neuroscience Institute, University of California, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20110498" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclase Inhibitors ; Adenylyl Cyclases/metabolism ; Animals ; Axons/metabolism/*physiology ; Cell Differentiation ; Cell Line ; Cell Polarity ; Cells, Cultured ; Cyclic AMP/*metabolism ; Cyclic AMP-Dependent Protein Kinases/antagonists & inhibitors/metabolism ; Cyclic GMP/*metabolism ; Dendrites/metabolism/*physiology ; Enzyme Inhibitors/pharmacology ; Fluorescence Resonance Energy Transfer ; Guanylate Cyclase/antagonists & inhibitors/metabolism ; Hippocampus/*cytology ; Humans ; Neurites/metabolism/physiology ; Neurons/cytology/*physiology ; Phosphodiesterase Inhibitors/pharmacology ; Phosphoric Diester Hydrolases/metabolism ; Phosphorylation ; Rats ; Signal Transduction ; Transfection
    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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  • 9
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    A Vibrio effector protein is an inositol phosphatase and disrupts host cell membrane integrity (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-08-21
    Description: The marine bacterium Vibrio parahaemolyticus causes gastroenteritis in humans and encodes the type III effector protein VPA0450, which contributes to host cell death caused by autophagy, cell rounding, and cell lysis. We found that VPA0450 is an inositol polyphosphate 5-phosphatase that hydrolyzed the D5 phosphate from the plasma membrane phospholipid phosphatidylinositol 4,5-bisphosphate. VPA0450 disrupted cytoskeletal binding sites on the inner surface of membranes of human cells and caused plasma membrane blebbing, which compromised membrane integrity and probably contributed to cell death by facilitating lysis. Thus, bacterial pathogens can disrupt adaptor protein-binding sites required for proper membrane and cytoskeleton dynamics by altering the homeostasis of membrane-bound inositol-signaling molecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Broberg, Christopher A -- Zhang, Lingling -- Gonzalez, Herman -- Laskowski-Arce, Michelle A -- Orth, Kim -- 5T32GM008203/GM/NIGMS NIH HHS/ -- R01-AI056404/AI/NIAID NIH HHS/ -- R01-AI087808/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2010 Sep 24;329(5999):1660-2. doi: 10.1126/science.1192850. Epub 2010 Aug 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20724587" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Amino Acid Sequence ; Autophagy ; Bacterial Proteins/chemistry/genetics/*metabolism ; Binding Sites ; Cell Membrane/*physiology/ultrastructure ; Cell Shape ; Computational Biology ; Cytoskeleton/physiology/ultrastructure ; HeLa Cells ; Homeostasis ; Humans ; Molecular Sequence Data ; Phosphatidylinositol 4,5-Diphosphate/metabolism ; Phosphatidylinositols/*metabolism ; Phosphoric Monoester Hydrolases/chemistry/genetics/*metabolism ; Protein Interaction Domains and Motifs ; Signal Transduction ; Transfection ; Vibrio parahaemolyticus/*enzymology/*pathogenicity
    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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  • 10
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    The calcium store sensor, STIM1, reciprocally controls Orai and CaV1.2 channels (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-12
    Description: Calcium signals, pivotal in controlling cell function, can be generated by calcium entry channels activated by plasma membrane depolarization or depletion of internal calcium stores. We reveal a regulatory link between these two channel subtypes mediated by the ubiquitous calcium-sensing STIM proteins. STIM1 activation by store depletion or mutational modification strongly suppresses voltage-operated calcium (Ca(V)1.2) channels while activating store-operated Orai channels. Both actions are mediated by the short STIM-Orai activating region (SOAR) of STIM1. STIM1 interacts with Ca(V)1.2 channels and localizes within discrete endoplasmic reticulum/plasma membrane junctions containing both Ca(V)1.2 and Orai1 channels. Hence, STIM1 interacts with and reciprocally controls two major calcium channels hitherto thought to operate independently. Such coordinated control of the widely expressed Ca(V)1.2 and Orai channels has major implications for Ca(2+) signal generation in excitable and nonexcitable cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3601900/" 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/PMC3601900/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Youjun -- Deng, Xiaoxiang -- Mancarella, Salvatore -- Hendron, Eunan -- Eguchi, Satoru -- Soboloff, Jonathan -- Tang, Xiang D -- Gill, Donald L -- AI058173/AI/NIAID NIH HHS/ -- HL55426/HL/NHLBI NIH HHS/ -- R01 AI058173/AI/NIAID NIH HHS/ -- R01 HL055426/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2010 Oct 1;330(6000):105-9. doi: 10.1126/science.1191086.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Cardiovascular Research Center, Temple University School of Medicine, 3400 North Broad Street, Philadelphia, PA 19140, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20929813" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Calcium Channels/genetics/*metabolism ; Calcium Channels, L-Type/*metabolism ; Calcium Signaling ; Cell Line ; Cell Membrane/metabolism ; Endoplasmic Reticulum/metabolism ; Humans ; Membrane Glycoproteins/chemistry/genetics/*metabolism ; Muscle, Smooth, Vascular/cytology ; Mutant Proteins/metabolism ; Myocytes, Smooth Muscle/*metabolism ; Patch-Clamp Techniques ; RNA Interference ; Rats ; Transfection
    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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  • 11
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    A septin diffusion barrier at the base of the primary cilium maintains ciliary membrane protein distribution (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-06-19
    Description: In animal cells, the primary cilium transduces extracellular signals through signaling receptors localized in the ciliary membrane, but how these ciliary membrane proteins are retained in the cilium is unknown. We found that ciliary membrane proteins were highly mobile, but their diffusion was impeded at the base of the cilium by a diffusion barrier. Septin 2 (SEPT2), a member of the septin family of guanosine triphosphatases that form a diffusion barrier in budding yeast, localized at the base of the ciliary membrane. SEPT2 depletion resulted in loss of ciliary membrane protein localization and Sonic hedgehog signal transduction, and inhibited ciliogenesis. Thus, SEPT2 is part of a diffusion barrier at the base of the ciliary membrane and is essential for retaining receptor-signaling pathways in the primary cilium.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3092790/" 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/PMC3092790/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hu, Qicong -- Milenkovic, Ljiljana -- Jin, Hua -- Scott, Matthew P -- Nachury, Maxence V -- Spiliotis, Elias T -- Nelson, W James -- GM089933/GM/NIGMS NIH HHS/ -- GM35527/GM/NIGMS NIH HHS/ -- R01 GM089933/GM/NIGMS NIH HHS/ -- R37 GM035527/GM/NIGMS NIH HHS/ -- R37 GM035527-27/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Jul 23;329(5990):436-9. doi: 10.1126/science.1191054. Epub 2010 Jun 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20558667" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axoneme/metabolism ; Cell Line ; Cells, Cultured ; Cilia/*metabolism/ultrastructure ; Cytoskeletal Proteins/*metabolism ; Diffusion ; Fluorescence Recovery After Photobleaching ; GTP-Binding Proteins/*metabolism ; Hedgehog Proteins/metabolism ; Membrane Proteins/*metabolism ; Mice ; RNA, Small Interfering ; Receptors, Cell Surface/metabolism ; Receptors, G-Protein-Coupled/metabolism ; Receptors, Serotonin/metabolism ; Receptors, Somatostatin/metabolism ; Septins ; *Signal Transduction ; Transfection
    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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  • 12
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    MiR-33 contributes to the regulation of cholesterol homeostasis (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-05-15
    Description: Cholesterol metabolism is tightly regulated at the cellular level. Here we show that miR-33, an intronic microRNA (miRNA) located within the gene encoding sterol-regulatory element-binding factor-2 (SREBF-2), a transcriptional regulator of cholesterol synthesis, modulates the expression of genes involved in cellular cholesterol transport. In mouse and human cells, miR-33 inhibits the expression of the adenosine triphosphate-binding cassette (ABC) transporter, ABCA1, thereby attenuating cholesterol efflux to apolipoprotein A1. In mouse macrophages, miR-33 also targets ABCG1, reducing cholesterol efflux to nascent high-density lipoprotein (HDL). Lentiviral delivery of miR-33 to mice represses ABCA1 expression in the liver, reducing circulating HDL levels. Conversely, silencing of miR-33 in vivo increases hepatic expression of ABCA1 and plasma HDL levels. Thus, miR-33 appears to regulate both HDL biogenesis in the liver and cellular cholesterol efflux.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3114628/" 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/PMC3114628/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rayner, Katey J -- Suarez, Yajaira -- Davalos, Alberto -- Parathath, Saj -- Fitzgerald, Michael L -- Tamehiro, Norimasa -- Fisher, Edward A -- Moore, Kathryn J -- Fernandez-Hernando, Carlos -- 1P30HL101270-01/HL/NHLBI NIH HHS/ -- P30 HL101270/HL/NHLBI NIH HHS/ -- R01 AG020255/AG/NIA NIH HHS/ -- R01 AG020255-09/AG/NIA NIH HHS/ -- R01AG02055/AG/NIA NIH HHS/ -- R01HL074136/HL/NHLBI NIH HHS/ -- R01HL084312/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2010 Jun 18;328(5985):1570-3. doi: 10.1126/science.1189862. Epub 2010 May 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Leon H. Charney Division of Cardiology and the Marc and Ruti Bell Vascular Biology and Disease Program, New York University School of Medicine, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20466885" target="_blank"〉PubMed〈/a〉
    Keywords: ATP Binding Cassette Transporter 1 ; ATP-Binding Cassette Transporters/genetics/metabolism ; Animals ; Apolipoprotein A-I/metabolism ; Carrier Proteins/genetics/metabolism ; Cell Line ; Cholesterol/*metabolism ; Cholesterol, Dietary/administration & dosage ; Dietary Fats/administration & dosage ; Gene Expression Regulation ; Homeostasis ; Humans ; Hypercholesterolemia/genetics/metabolism ; Introns ; Lipoproteins/genetics/metabolism ; Lipoproteins, HDL/blood/*metabolism ; Liver/*metabolism ; Macrophages/metabolism ; Macrophages, Peritoneal/metabolism ; Membrane Glycoproteins/genetics/metabolism ; Mice ; Mice, Inbred C57BL ; MicroRNAs/genetics/*metabolism ; Proteins/genetics/metabolism ; Sterol Regulatory Element Binding Protein 2/genetics/metabolism ; Transfection
    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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  • 13
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    A unifying genetic model for facioscapulohumeral muscular dystrophy (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-08-21
    Description: Facioscapulohumeral muscular dystrophy (FSHD) is a common form of muscular dystrophy in adults that is foremost characterized by progressive wasting of muscles in the upper body. FSHD is associated with contraction of D4Z4 macrosatellite repeats on chromosome 4q35, but this contraction is pathogenic only in certain "permissive" chromosomal backgrounds. Here, we show that FSHD patients carry specific single-nucleotide polymorphisms in the chromosomal region distal to the last D4Z4 repeat. This FSHD-predisposing configuration creates a canonical polyadenylation signal for transcripts derived from DUX4, a double homeobox gene of unknown function that straddles the last repeat unit and the adjacent sequence. Transfection studies revealed that DUX4 transcripts are efficiently polyadenylated and are more stable when expressed from permissive chromosomes. These findings suggest that FSHD arises through a toxic gain of function attributable to the stabilized distal DUX4 transcript.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4677822/" 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/PMC4677822/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lemmers, Richard J L F -- van der Vliet, Patrick J -- Klooster, Rinse -- Sacconi, Sabrina -- Camano, Pilar -- Dauwerse, Johannes G -- Snider, Lauren -- Straasheijm, Kirsten R -- van Ommen, Gert Jan -- Padberg, George W -- Miller, Daniel G -- Tapscott, Stephen J -- Tawil, Rabi -- Frants, Rune R -- van der Maarel, Silvere M -- P01 NS069539/NS/NINDS NIH HHS/ -- P01NS069539/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2010 Sep 24;329(5999):1650-3. doi: 10.1126/science.1189044. Epub 2010 Aug 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Genetics, Leiden University Medical Center, 2333 ZA Leiden, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20724583" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; Base Sequence ; Child, Preschool ; Chromosomes, Human, Pair 10/genetics ; Chromosomes, Human, Pair 4/*genetics ; Female ; Genetic Predisposition to Disease ; Haplotypes ; Homeodomain Proteins/*genetics/physiology ; Humans ; Male ; Middle Aged ; Models, Genetic ; Molecular Sequence Data ; Muscular Dystrophy, Facioscapulohumeral/*genetics ; Polyadenylation ; Polymorphism, Single Nucleotide ; RNA Stability ; RNA, Messenger/genetics/metabolism ; *Repetitive Sequences, Nucleic Acid ; Transcription, Genetic ; Transfection ; Young Adult
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 14
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    Human-restricted bacterial pathogens block shedding of epithelial cells by stimulating integrin activation (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-09-04
    Description: Colonization of mucosal surfaces is the key initial step in most bacterial infections. One mechanism protecting the mucosa is the rapid shedding of epithelial cells, also termed exfoliation, but it is unclear how pathogens counteract this process. We found that carcinoembryonic antigen (CEA)-binding bacteria colonized the urogenital tract of CEA transgenic mice, but not of wild-type mice, by suppressing exfoliation of mucosal cells. CEA binding triggered de novo expression of the transforming growth factor receptor CD105, changing focal adhesion composition and activating beta1 integrins. This manipulation of integrin inside-out signaling promotes efficient mucosal colonization and represents a potential target to prevent or cure bacterial infections.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Muenzner, Petra -- Bachmann, Verena -- Zimmermann, Wolfgang -- Hentschel, Jochen -- Hauck, Christof R -- New York, N.Y. -- Science. 2010 Sep 3;329(5996):1197-201. doi: 10.1126/science.1190892.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lehrstuhl Zellbiologie, Fachbereich Biologie, Universitat Konstanz, 78457 Konstanz, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20813953" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Bacterial/metabolism ; Antigens, CD/metabolism ; Carcinoembryonic Antigen/genetics/*metabolism ; Cytoskeletal Proteins/metabolism ; Epithelial Cells/microbiology/*pathology ; Female ; Focal Adhesions ; GPI-Linked Proteins ; Glycoproteins/metabolism ; Gonorrhea/*microbiology ; Humans ; Integrin beta Chains/*metabolism ; Intracellular Signaling Peptides and Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mucous Membrane/microbiology ; Neisseria gonorrhoeae/isolation & purification/*metabolism/*pathogenicity ; Receptors, Cell Surface/metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Transfection ; Vagina/cytology/*microbiology/pathology ; Zyxin
    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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