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  • Cell Line  (12)
  • 2000-2004  (12)
  • 1960-1964
  • 2002  (12)
  • 1
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    Inhibition of excess nodal signaling during mouse gastrulation by the transcriptional corepressor DRAP1 (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-12-10
    Description: The formation and patterning of mesoderm during mammalian gastrulation require the activity of Nodal, a secreted mesoderm-inducing factor of the transforming growth factor-beta (TGF-beta) family. Here we show that the transcriptional corepressor DRAP1 has a very specific role in regulation of Nodal activity during mouse embryogenesis. We find that loss of Drap1 leads to severe gastrulation defects that are consistent with increased expression of Nodal and can be partially suppressed by Nodal heterozygosity. Biochemical studies indicate that DRAP1 interacts with and inhibits DNA binding by the winged-helix transcription factor FoxH1 (FAST), a critical component of a positive feedback loop for Nodal activity. We propose that DRAP1 limits the spread of a morphogenetic signal by down-modulating the response to the Nodal autoregulatory loop.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Iratni, Rabah -- Yan, Yu-Ting -- Chen, Canhe -- Ding, Jixiang -- Zhang, Yi -- Price, Sandy M -- Reinberg, Danny -- Shen, Michael M -- New York, N.Y. -- Science. 2002 Dec 6;298(5600):1996-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Biochemistry, Division of Nucleic Acids Enzymology, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, Piscataway, NJ 08854, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12471260" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Cell Line ; Crosses, Genetic ; DNA/metabolism ; DNA-Binding Proteins/metabolism ; *Embryonic and Fetal Development ; Female ; Forkhead Transcription Factors ; Gastrula/*physiology ; Gene Expression Regulation, Developmental ; Gene Targeting ; Heterozygote ; In Situ Hybridization ; Left-Right Determination Factors ; Male ; Mesoderm/cytology/physiology ; Mice ; Morphogenesis ; Mutation ; Nodal Protein ; Phenotype ; Protein Binding ; RNA Interference ; Recombinant Fusion Proteins/metabolism ; Repressor Proteins/genetics/*metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; *Signal Transduction ; Transcription Factors/metabolism ; Transforming Growth Factor beta/genetics/*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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  • 2
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    An essential role of N-terminal arginylation in cardiovascular development (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-07-06
    Description: The enzymatic conjugation of arginine to the N-termini of proteins is a part of the ubiquitin-dependent N-end rule pathway of protein degradation. In mammals, three N-terminal residues-aspartate, glutamate, and cysteine-are substrates for arginylation. The mouse ATE1 gene encodes a family of Arg-tRNA-protein transferases (R-transferases) that mediate N-terminal arginylation. We constructed ATE1-lacking mouse strains and found that ATE1-/- embryos die with defects in heart development and in angiogenic remodeling of the early vascular plexus. Through biochemical analyses, we show that N-terminal cysteine, in contrast to N-terminal aspartate and glutamate, is oxidized before its arginylation by R-transferase, suggesting that the arginylation branch of the N-end rule pathway functions as an oxygen sensor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kwon, Yong Tae -- Kashina, Anna S -- Davydov, Ilia V -- Hu, Rong-Gui -- An, Jee Young -- Seo, Jai Wha -- Du, Fangyong -- Varshavsky, Alexander -- GM31530/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2002 Jul 5;297(5578):96-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, 147-75, California Institute of Technology, 1200 East California Boulevard, Pasadena, CA 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12098698" target="_blank"〉PubMed〈/a〉
    Keywords: Alkylation ; Aminoacyltransferases/*genetics/*metabolism ; Animals ; Aorta/embryology ; Arginine/*metabolism ; Aspartic Acid/metabolism ; Blood Vessels/*embryology ; Cell Line ; Cysteic Acid/metabolism ; Cysteine/metabolism ; Female ; Glutamic Acid/metabolism ; Heart/*embryology ; Heart Defects, Congenital/embryology ; Heart Septal Defects/embryology ; Hypoxia-Inducible Factor 1, alpha Subunit ; Male ; Mice ; Mice, Inbred C57BL ; Neovascularization, Physiologic ; Oxidation-Reduction ; Proteins/*metabolism ; Pulmonary Artery/embryology ; RGS Proteins/metabolism ; Recombinant Proteins/metabolism ; Sulfinic Acids/metabolism ; Transcription Factors/metabolism ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 3
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    An LRR receptor kinase involved in perception of a peptide plant hormone, phytosulfokine (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-05-25
    Description: The sulfated peptide phytosulfokine (PSK) is an intercellular signal that plays a key role in cellular dedifferentiation and proliferation in plants. Using ligand-based affinity chromatography, we purified a 120-kilodalton membrane protein, specifically interacting with PSK, from carrot microsomal fractions. The corresponding complementary DNA encodes a 1021-amino acid receptor kinase that contains extracellular leucine-rich repeats, a single transmembrane domain, and a cytoplasmic kinase domain. Overexpression of this receptor kinase in carrot cells caused enhanced callus growth in response to PSK and a substantial increase in the number of tritium-labeled PSK binding sites, suggesting that PSK and this receptor kinase act as a ligand-receptor pair.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Matsubayashi, Yoshikatsu -- Ogawa, Mari -- Morita, Akiko -- Sakagami, Youji -- New York, N.Y. -- Science. 2002 May 24;296(5572):1470-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate School of Bio-Agricultural Sciences, Nagoya University, Chikusa, Nagoya 464-8601, Japan. matsu@agr.nagoya-u.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12029134" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Binding, Competitive ; Cell Line ; Chromatography, Affinity ; DNA, Complementary ; Daucus carota/cytology/*enzymology/genetics/growth & development ; Genes, Plant ; Glycosylation ; Leucine ; Ligands ; Microsomes/enzymology ; Molecular Sequence Data ; Molecular Weight ; Peptide Hormones ; *Plant Growth Regulators ; Plant Proteins/*chemistry/genetics/isolation & purification/*metabolism ; Plants, Genetically Modified ; Polymerase Chain Reaction ; Protein Structure, Tertiary ; Receptors, Cell Surface/*chemistry/genetics/isolation & purification/*metabolism ; Repetitive Sequences, Amino Acid
    Print ISSN: 0036-8075
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  • 4
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    Spider silk fibers spun from soluble recombinant silk produced in mammalian cells (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-01-19
    Description: Spider silks are protein-based "biopolymer" filaments or threads secreted by specialized epithelial cells as concentrated soluble precursors of highly repetitive primary sequences. Spider dragline silk is a flexible, lightweight fiber of extraordinary strength and toughness comparable to that of synthetic high-performance fibers. We sought to "biomimic" the process of spider silk production by expressing in mammalian cells the dragline silk genes (ADF-3/MaSpII and MaSpI) of two spider species. We produced soluble recombinant (rc)-dragline silk proteins with molecular masses of 60 to 140 kilodaltons. We demonstrated the wet spinning of silk monofilaments spun from a concentrated aqueous solution of soluble rc-spider silk protein (ADF-3; 60 kilodaltons) under modest shear and coagulation conditions. The spun fibers were water insoluble with a fine diameter (10 to 40 micrometers) and exhibited toughness and modulus values comparable to those of native dragline silks but with lower tenacity. Dope solutions with rc-silk protein concentrations 〉20% and postspinning draw were necessary to achieve improved mechanical properties of the spun fibers. Fiber properties correlated with finer fiber diameter and increased birefringence.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lazaris, Anthoula -- Arcidiacono, Steven -- Huang, Yue -- Zhou, Jiang-Feng -- Duguay, Francois -- Chretien, Nathalie -- Welsh, Elizabeth A -- Soares, Jason W -- Karatzas, Costas N -- New York, N.Y. -- Science. 2002 Jan 18;295(5554):472-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Nexia Biotechnologies, Vaudreuil-Dorion, Quebec J7V 8P5, Canada. alazaris@nexiabiotech.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11799236" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Amino Acid Sequence ; Animals ; Biopolymers ; Birefringence ; Cattle ; Cell Line ; Cloning, Molecular ; Cricetinae ; Culture Media, Conditioned ; DNA, Complementary ; Elasticity ; Epithelial Cells/metabolism ; *Fibroins ; Materials Testing ; Mechanics ; Molecular Sequence Data ; Molecular Weight ; *Protein Biosynthesis ; Protein Structure, Secondary ; Proteins/chemistry/*genetics/isolation & purification ; Recombinant Proteins/biosynthesis/chemistry/isolation & purification ; Solubility ; Spiders/*genetics/metabolism ; Stress, Mechanical ; Tensile Strength ; Water
    Print ISSN: 0036-8075
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  • 5
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    MAPKK-independent activation of p38alpha mediated by TAB1-dependent autophosphorylation of p38alpha (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-02-16
    Description: Phosphorylation of mitogen-activated protein kinases (MAPKs) on specific tyrosine and threonine sites by MAP kinase kinases (MAPKKs) is thought to be the sole activation mechanism. Here, we report an unexpected activation mechanism for p38alpha MAPK that does not involve the prototypic kinase cascade. Rather it depends on interaction of p38alpha with TAB1 [transforming growth factor-beta-activated protein kinase 1 (TAK1)-binding protein 1] leading to autophosphorylation and activation of p38alpha. We detected formation of a TRAF6-TAB1-p38alpha complex and showed stimulus-specific TAB1-dependent and TAB1-independent p38alpha activation. These findings suggest that alternative activation pathways contribute to the biological responses of p38alpha to various stimuli.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ge, Baoxue -- Gram, Hermann -- Di Padova, Franco -- Huang, Betty -- New, Liguo -- Ulevitch, Richard J -- Luo, Ying -- Han, Jiahuai -- AI41637/AI/NIAID NIH HHS/ -- HL07195/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2002 Feb 15;295(5558):1291-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11847341" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Binding Sites ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Carrier Proteins/chemistry/genetics/*metabolism ; Cell Line ; *Drosophila Proteins ; Enzyme Activation ; Enzyme Inhibitors/pharmacology ; Humans ; Imidazoles/pharmacology ; *Intracellular Signaling Peptides and Proteins ; MAP Kinase Kinase 6 ; *MAP Kinase Signaling System ; Membrane Glycoproteins/metabolism ; Mitogen-Activated Protein Kinase 14 ; Mitogen-Activated Protein Kinase Kinases/metabolism ; Mitogen-Activated Protein Kinases/antagonists & ; inhibitors/chemistry/genetics/*metabolism ; Mutation ; Peptide Mapping ; Peroxynitrous Acid/pharmacology ; Phosphorylation ; Proteins/metabolism ; Pyridines/pharmacology ; Receptors, Cell Surface/metabolism ; Recombinant Fusion Proteins/metabolism ; TNF Receptor-Associated Factor 6 ; Toll-Like Receptors ; Tumor Necrosis Factor-alpha/pharmacology ; Two-Hybrid System Techniques ; p38 Mitogen-Activated Protein Kinases
    Print ISSN: 0036-8075
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  • 6
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    Signal transduction. Decoding NF-kappaB signaling (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-11-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ting, Alice Y -- Endy, Drew -- New York, N.Y. -- Science. 2002 Nov 8;298(5596):1189-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12424362" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Nucleus/metabolism ; Chemokine CCL5/genetics ; Chemokine CXCL10 ; Chemokines, CXC/genetics ; Computer Simulation ; Cytoplasm/metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Feedback, Physiological ; *Gene Expression Regulation ; Humans ; I-kappa B Proteins/genetics/*metabolism ; Mice ; Mice, Knockout ; Models, Biological ; NF-kappa B/*metabolism ; Proto-Oncogene Proteins/genetics/metabolism ; *Signal Transduction ; Tumor Necrosis Factor-alpha/metabolism/pharmacology
    Print ISSN: 0036-8075
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  • 7
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    SynCAM, a synaptic adhesion molecule that drives synapse assembly (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-08-31
    Description: Synapses, the junctions between nerve cells through which they communicate, are formed by the coordinated assembly and tight attachment of pre- and postsynaptic specializations. We now show that SynCAM is a brain-specific, immunoglobulin domain-containing protein that binds to intracellular PDZ-domain proteins and functions as a homophilic cell adhesion molecule at the synapse. Expression of the isolated cytoplasmic tail of SynCAM in neurons inhibited synapse assembly. Conversely, expression of full-length SynCAM in nonneuronal cells induced synapse formation by cocultured hippocampal neurons with normal release properties. Glutamatergic synaptic transmission was reconstituted in these nonneuronal cells by coexpressing glutamate receptors with SynCAM, which suggests that a single type of adhesion molecule and glutamate receptor are sufficient for a functional postsynaptic response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Biederer, Thomas -- Sara, Yildirim -- Mozhayeva, Marina -- Atasoy, Deniz -- Liu, Xinran -- Kavalali, Ege T -- Sudhof, Thomas C -- New York, N.Y. -- Science. 2002 Aug 30;297(5586):1525-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Basic Neuroscience, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. Thomas.Biederer@UTSouthwestern.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12202822" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Brain/cytology/*physiology ; Brain Chemistry ; Cell Adhesion Molecules/chemistry/isolation & purification/*physiology ; Cell Adhesion Molecules, Neuronal/chemistry/isolation & purification/*physiology ; Cell Line ; Coculture Techniques ; Exocytosis ; Humans ; Immunoglobulins ; Molecular Sequence Data ; Neurons/physiology ; Prosencephalon/chemistry/physiology ; Protein Structure, Tertiary ; Rats ; Receptors, AMPA/physiology ; Recombinant Fusion Proteins/metabolism ; Sequence Homology, Amino Acid ; Synapses/chemistry/*physiology ; Synaptic Transmission/physiology ; Transfection ; Tumor Suppressor Proteins
    Print ISSN: 0036-8075
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  • 8
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    Sp1 and TAFII130 transcriptional activity disrupted in early Huntington's disease (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-05-04
    Description: Huntington's disease (HD) is an inherited neurodegenerative disease caused by expansion of a polyglutamine tract in the huntingtin protein. Transcriptional dysregulation has been implicated in HD pathogenesis. Here, we report that huntingtin interacts with the transcriptional activator Sp1 and coactivator TAFII130. Coexpression of Sp1 and TAFII130 in cultured striatal cells from wild-type and HD transgenic mice reverses the transcriptional inhibition of the dopamine D2 receptor gene caused by mutant huntingtin, as well as protects neurons from huntingtin-induced cellular toxicity. Furthermore, soluble mutant huntingtin inhibits Sp1 binding to DNA in postmortem brain tissues of both presymptomatic and affected HD patients. Understanding these early molecular events in HD may provide an opportunity to interfere with the effects of mutant huntingtin before the development of disease symptoms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dunah, Anthone W -- Jeong, Hyunkyung -- Griffin, April -- Kim, Yong-Man -- Standaert, David G -- Hersch, Steven M -- Mouradian, M Maral -- Young, Anne B -- Tanese, Naoko -- Krainc, Dimitri -- 5R37AG13617/AG/NIA NIH HHS/ -- AT00613/AT/NCCIH NIH HHS/ -- NS02174/NS/NINDS NIH HHS/ -- NS34361/NS/NINDS NIH HHS/ -- NS35255/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2002 Jun 21;296(5576):2238-43. Epub 2002 May 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Center for Aging, Genetics and Neurodegeneration, Charlestown, MA 02129, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11988536" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/metabolism ; Caudate Nucleus/metabolism ; Cell Death ; Cell Line ; Cell Nucleus/metabolism ; Cells, Cultured ; Corpus Striatum/cytology/embryology/metabolism ; DNA/*metabolism ; DNA-Binding Proteins/chemistry/*metabolism ; Down-Regulation ; Gene Expression Regulation ; Humans ; Huntington Disease/*genetics/metabolism ; Mice ; Mice, Transgenic ; Mutation ; Nerve Tissue Proteins/chemistry/genetics/*metabolism ; Neurons/physiology ; Nuclear Proteins/chemistry/genetics/*metabolism ; Peptides ; Promoter Regions, Genetic ; Rats ; Receptors, Dopamine D2/genetics ; Solubility ; Sp1 Transcription Factor/chemistry/*metabolism ; *TATA-Binding Protein Associated Factors ; *Transcription Factor TFIID ; Transcription Factors/chemistry/*metabolism ; *Transcription, Genetic ; Transfection ; Trinucleotide Repeat Expansion ; Two-Hybrid System Techniques
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  • 9
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    Partitioning of lipid-modified monomeric GFPs into membrane microdomains of live cells (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-05-04
    Description: Many proteins associated with the plasma membrane are known to partition into submicroscopic sphingolipid- and cholesterol-rich domains called lipid rafts, but the determinants dictating this segregation of proteins in the membrane are poorly understood. We suppressed the tendency of Aequorea fluorescent proteins to dimerize and targeted these variants to the plasma membrane using several different types of lipid anchors. Fluorescence resonance energy transfer measurements in living cells revealed that acyl but not prenyl modifications promote clustering in lipid rafts. Thus the nature of the lipid anchor on a protein is sufficient to determine submicroscopic localization within the plasma membrane.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zacharias, David A -- Violin, Jonathan D -- Newton, Alexandra C -- Tsien, Roger Y -- 2T32 GM07752/GM/NIGMS NIH HHS/ -- DK54441/DK/NIDDK NIH HHS/ -- NS27177/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2002 May 3;296(5569):913-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Biomedical Sciences Graduate Program, and, Howard Hughes Medical Institute, University of California, San Diego, La Jolla, CA 92093-0647, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11988576" target="_blank"〉PubMed〈/a〉
    Keywords: Acylation ; Animals ; Bacterial Proteins/chemistry/*metabolism ; Caveolin 1 ; Caveolins/metabolism ; Cell Line ; Detergents ; Dimerization ; Dogs ; Energy Transfer ; Fluorescence ; Green Fluorescent Proteins ; Luminescent Proteins/chemistry/*metabolism ; Membrane Microdomains/*metabolism ; Myristic Acid/metabolism ; Oligopeptides/chemistry/*metabolism ; Palmitic Acid/metabolism ; Protein Prenylation ; Recombinant Fusion Proteins/metabolism ; Solubility ; Spectrometry, Fluorescence ; Transfection
    Print ISSN: 0036-8075
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  • 10
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    Oscillatory expression of the bHLH factor Hes1 regulated by a negative feedback loop (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-10-26
    Description: Transcription of messenger RNAs (mRNAs) for Notch signaling molecules oscillates with 2-hour cycles, and this oscillation is important for coordinated somite segmentation. However, the molecular mechanism of such oscillation remains to be determined. Here, we show that serum treatment of cultured cells induces cyclic expression of both mRNA and protein of the Notch effector Hes1, a basic helix-loop-helix (bHLH) factor, with 2-hour periodicity. Cycling is cell-autonomous and depends on negative autoregulation of hes1 transcription and ubiquitin-proteasome-mediated degradation of Hes1 protein. Because Hes1 oscillation can be seen in many cell types, this clock may regulate timing in many biological systems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hirata, Hiromi -- Yoshiura, Shigeki -- Ohtsuka, Toshiyuki -- Bessho, Yasumasa -- Harada, Takahiro -- Yoshikawa, Kenichi -- Kageyama, Ryoichiro -- New York, N.Y. -- Science. 2002 Oct 25;298(5594):840-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Virus Research, Kyoto University, Kyoto 606-8507, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12399594" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcysteine/*analogs & derivatives/pharmacology ; Animals ; Basic Helix-Loop-Helix Transcription Factors ; Biological Clocks ; Blood ; Cell Line ; Cycloheximide/pharmacology ; Cysteine Endopeptidases/metabolism ; Feedback, Physiological ; Gene Expression Regulation ; Glycosyltransferases/genetics/metabolism ; Half-Life ; Homeodomain Proteins/biosynthesis/*genetics/*metabolism ; Leupeptins/pharmacology ; Mesoderm/metabolism ; Mice ; Multienzyme Complexes/metabolism ; PC12 Cells ; *Periodicity ; Protease Inhibitors/pharmacology ; Proteasome Endopeptidase Complex ; Protein Biosynthesis ; Protein Synthesis Inhibitors/pharmacology ; RNA, Messenger/biosynthesis/genetics/metabolism ; Rats ; Transcription, Genetic ; Transfection ; Ubiquitin/metabolism
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