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  • 1
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    dbPTM 2016: 10-year anniversary of a resource for post-translational modification of proteins (2016)
    Oxford University Press
    Details
    Publication Date: 2016-01-07
    Description: Owing to the importance of the post-translational modifications (PTMs) of proteins in regulating biological processes, the dbPTM ( http://dbPTM.mbc.nctu.edu.tw/ ) was developed as a comprehensive database of experimentally verified PTMs from several databases with annotations of potential PTMs for all UniProtKB protein entries. For this 10th anniversary of dbPTM, the updated resource provides not only a comprehensive dataset of experimentally verified PTMs, supported by the literature, but also an integrative interface for accessing all available databases and tools that are associated with PTM analysis. As well as collecting experimental PTM data from 14 public databases, this update manually curates over 12 000 modified peptides, including the emerging S -nitrosylation, S -glutathionylation and succinylation, from approximately 500 research articles, which were retrieved by text mining. As the number of available PTM prediction methods increases, this work compiles a non-homologous benchmark dataset to evaluate the predictive power of online PTM prediction tools. An increasing interest in the structural investigation of PTM substrate sites motivated the mapping of all experimental PTM peptides to protein entries of Protein Data Bank (PDB) based on database identifier and sequence identity, which enables users to examine spatially neighboring amino acids, solvent-accessible surface area and side-chain orientations for PTM substrate sites on tertiary structures. Since drug binding in PDB is annotated, this update identified over 1100 PTM sites that are associated with drug binding. The update also integrates metabolic pathways and protein–protein interactions to support the PTM network analysis for a group of proteins. Finally, the web interface is redesigned and enhanced to facilitate access to this resource.
    Print ISSN: 0305-1048
    Electronic ISSN: 1362-4962
    Topics: Biology
    Published by Oxford University Press
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  • 2
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    Activating the translational repressor 4E-BP or reducing S6K-GSK3{beta} activity prevents accelerated axon growth induced by hyperactive mTOR in vivo (2015)
    Oxford University Press
    Details
    Publication Date: 2015-09-25
    Description: Abnormal axonal connectivity and hyperactive mTOR complex 1 (mTORC1) are shared features of several neurological disorders. Hyperactive mTORC1 alters axon length and polarity of hippocampal neurons in vitro , but the impact of hyperactive mTORC1 on axon growth in vivo and the mechanisms underlying those effects remain unclear. Using in utero electroporation during corticogenesis, we show that increasing mTORC1 activity accelerates axon growth without multiple axon formation. This was prevented by counteracting mTORC1 signaling through p70S6Ks (S6K1/2) or eukaryotic initiation factor 4E-binding protein (4E-BP1/2), which both regulate translation. In addition to regulating translational targets, S6K1 indirectly signals through GSK3β, a regulator of axogenesis. Although blocking GSK3β activity did not alter axon growth under physiological conditions in vivo , blocking it using a dominant-negative mutant or lithium chloride prevented mTORC1-induced accelerated axon growth. These data reveal the contribution of translational and non-translational downstream effectors such as GSK3β to abnormal axon growth in neurodevelopmental mTORopathies and open new therapeutic options for restoring long-range connectivity.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
    Published by Oxford University Press
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  • 3
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    Computationally Efficient Composite Likelihood Statistics for Demographic Inference (2016)
    Oxford University Press
    Details
    Publication Date: 2016-01-24
    Description: Many population genetics tools employ composite likelihoods, because fully modeling genomic linkage is challenging. But traditional approaches to estimating parameter uncertainties and performing model selection require full likelihoods, so these tools have relied on computationally expensive maximum-likelihood estimation (MLE) on bootstrapped data. Here, we demonstrate that statistical theory can be applied to adjust composite likelihoods and perform robust computationally efficient statistical inference in two demographic inference tools: a i and TRACTS. On both simulated and real data, the adjustments perform comparably to MLE bootstrapping while using orders of magnitude less computational time.
    Print ISSN: 0737-4038
    Electronic ISSN: 1537-1719
    Topics: Biology
    Published by Oxford University Press
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  • 4
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    Photofrin binds to procaspase-3 and mediates photodynamic treatment-triggered methionine oxidation and inactivation of procaspase-3 (2012)
    Springer Nature
    Details
    Publication Date: 2012-07-13
    Description: Photofrin binds to procaspase-3 and mediates photodynamic treatment-triggered methionine oxidation and inactivation of procaspase-3 Cell Death and Disease 3, e347 (July 2012). doi:10.1038/cddis.2012.85 Authors: Y-J Hsieh, K-Y Chien, S-Y Lin, S Sabu, R-M Hsu, L-M Chi, P-C Lyu & J-S Yu
    Keywords: Photofrinphotodynamic treatmentprocaspase-3cell deathmethionine oxidationmass spectrometry
    Electronic ISSN: 2041-4889
    Topics: Biology , Medicine
    Published by Springer Nature
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  • 5
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    Are exploited fish populations stable? [Letters (Online Only)] (2011)
    National Academy of Sciences
    Details
    Publication Date: 2011-11-30
    Description: Shelton and Mangel (1) examined patterns of variability in fish populations and concluded that the higher stock variability observed in exploited species results from heightened effects of stochastic forcing in the supposed absence of nonlinear dynamics. In contrast, Anderson et al. (2) found that higher variability in these stocks is attributable to amplified nonlinear behavior in noisy ecological systems under exploitation. Here, we reconcile these apparently conflicting views and demonstrate that stochasticity of demographic parameters directly enhances nonlinearity (2–4), thus challenging assessments of stability based on statistical fits to noise-free models.Shelton and Mangel (1) concluded that fish populations are stable...
    Keywords: Letters
    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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  • 6
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    Stellar mass assembly of brightest cluster galaxies at late times (2014)
    Oxford University Press
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    Publication Date: 2014-11-18
    Description: Understanding the formation history of brightest cluster galaxies (BCGs) is an important topic in galaxy formation. Utilizing the Planck Sunyaev–Zel'dovich cluster catalogue, and applying the ansatz that the most massive haloes at one redshift remain among the most massive ones at a slightly later cosmic epoch, we have constructed cluster samples at redshift z ~ 0.4 and z ~ 0.2 that can be statistically regarded as progenitor–descendant pairs. This allows us to study the stellar mass assembly history of BCGs in these massive clusters at late times, finding that the degree of growth between the two epochs is likely at only few per cent level, which is far lower compared to the prediction from a state-of-the-art semi-analytic galaxy formation model.
    Print ISSN: 0035-8711
    Electronic ISSN: 1365-2966
    Topics: Physics
    Published by Oxford University Press
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  • 7
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    Phosphorylation of MLL by ATR is required for execution of mammalian S-phase checkpoint (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-09-08
    Description: Cell cycle checkpoints are implemented to safeguard the genome, avoiding the accumulation of genetic errors. Checkpoint loss results in genomic instability and contributes to the evolution of cancer. Among G1-, S-, G2- and M-phase checkpoints, genetic studies indicate the role of an intact S-phase checkpoint in maintaining genome integrity. Although the basic framework of the S-phase checkpoint in multicellular organisms has been outlined, the mechanistic details remain to be elucidated. Human chromosome-11 band-q23 translocations disrupting the MLL gene lead to poor prognostic leukaemias. Here we assign MLL as a novel effector in the mammalian S-phase checkpoint network and identify checkpoint dysfunction as an underlying mechanism of MLL leukaemias. MLL is phosphorylated at serine 516 by ATR in response to genotoxic stress in the S phase, which disrupts its interaction with, and hence its degradation by, the SCF(Skp2) E3 ligase, leading to its accumulation. Stabilized MLL protein accumulates on chromatin, methylates histone H3 lysine 4 at late replication origins and inhibits the loading of CDC45 to delay DNA replication. Cells deficient in MLL showed radioresistant DNA synthesis and chromatid-type genomic abnormalities, indicative of S-phase checkpoint dysfunction. Reconstitution of Mll(-/-) (Mll also known as Mll1) mouse embryonic fibroblasts with wild-type but not S516A or DeltaSET mutant MLL rescues the S-phase checkpoint defects. Moreover, murine myeloid progenitor cells carrying an Mll-CBP knock-in allele that mimics human t(11;16) leukaemia show a severe radioresistant DNA synthesis phenotype. MLL fusions function as dominant negative mutants that abrogate the ATR-mediated phosphorylation/stabilization of wild-type MLL on damage to DNA, and thus compromise the S-phase checkpoint. Together, our results identify MLL as a key constituent of the mammalian DNA damage response pathway and show that deregulation of the S-phase checkpoint incurred by MLL translocations probably contributes to the pathogenesis of human MLL leukaemias.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2940944/" 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/PMC2940944/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Han -- Takeda, Shugaku -- Kumar, Rakesh -- Westergard, Todd D -- Brown, Eric J -- Pandita, Tej K -- Cheng, Emily H-Y -- Hsieh, James J-D -- CA119008/CA/NCI NIH HHS/ -- CA123232/CA/NCI NIH HHS/ -- CA129537/CA/NCI NIH HHS/ -- R01 CA119008/CA/NCI NIH HHS/ -- R01 CA119008-01/CA/NCI NIH HHS/ -- R01 CA119008-02/CA/NCI NIH HHS/ -- R01 CA119008-03/CA/NCI NIH HHS/ -- R01 CA119008-04/CA/NCI NIH HHS/ -- R01 CA119008-05/CA/NCI NIH HHS/ -- England -- Nature. 2010 Sep 16;467(7313):343-6. doi: 10.1038/nature09350. Epub 2010 Sep 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Washington University School of Medicine, St Louis, Missouri 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20818375" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Ataxia Telangiectasia Mutated Proteins ; Cell Cycle Proteins/*metabolism ; Cell Line ; Chromatin/metabolism ; DNA Damage ; DNA Replication/physiology ; Genes, Dominant/genetics ; Genomic Instability/physiology ; Histone-Lysine N-Methyltransferase ; Histones/chemistry/metabolism ; Humans ; Leukemia/genetics ; Lysine/metabolism ; Methylation ; Mice ; Myeloid Progenitor Cells/metabolism ; Myeloid-Lymphoid Leukemia Protein/chemistry/deficiency/genetics/*metabolism ; Phosphorylation ; Phosphoserine/metabolism ; Protein Binding ; Protein-Serine-Threonine Kinases/*metabolism ; S Phase/*physiology ; S-Phase Kinase-Associated Proteins/metabolism ; Signal Transduction ; Translocation, Genetic/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)
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  • 8
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    BID, BIM, and PUMA are essential for activation of the BAX- and BAK-dependent cell death program (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-12-04
    Description: Although the proteins BAX and BAK are required for initiation of apoptosis at the mitochondria, how BAX and BAK are activated remains unsettled. We provide in vivo evidence demonstrating an essential role of the proteins BID, BIM, and PUMA in activating BAX and BAK. Bid, Bim, and Puma triple-knockout mice showed the same developmental defects that are associated with deficiency of Bax and Bak, including persistent interdigital webs and imperforate vaginas. Genetic deletion of Bid, Bim, and Puma prevented the homo-oligomerization of BAX and BAK, and thereby cytochrome c-mediated activation of caspases in response to diverse death signals in neurons and T lymphocytes, despite the presence of other BH3-only molecules. Thus, many forms of apoptosis require direct activation of BAX and BAK at the mitochondria by a member of the BID, BIM, or PUMA family of proteins.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3163443/" 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/PMC3163443/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ren, Decheng -- Tu, Ho-Chou -- Kim, Hyungjin -- Wang, Gary X -- Bean, Gregory R -- Takeuchi, Osamu -- Jeffers, John R -- Zambetti, Gerard P -- Hsieh, James J-D -- Cheng, Emily H-Y -- P30CA21765/CA/NCI NIH HHS/ -- R01 CA125562/CA/NCI NIH HHS/ -- R01 CA125562-02/CA/NCI NIH HHS/ -- R01 CA125562-03/CA/NCI NIH HHS/ -- R01 CA125562-04/CA/NCI NIH HHS/ -- R01CA125562/CA/NCI NIH HHS/ -- R01GM083159/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Dec 3;330(6009):1390-3. doi: 10.1126/science.1190217.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Oncology, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21127253" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptosis Regulatory Proteins/deficiency/genetics/*metabolism ; BH3 Interacting Domain Death Agonist Protein/deficiency/genetics/*metabolism ; Caspases/metabolism ; Cells, Cultured ; Cerebellum/cytology ; Cytochromes c/metabolism ; Intracellular Membranes/metabolism ; Membrane Proteins/deficiency/genetics/*metabolism ; Mice ; Mice, Knockout ; Mitochondria/metabolism ; Models, Biological ; Neurons/*physiology ; Permeability ; Protein Multimerization ; Proto-Oncogene Proteins/deficiency/genetics/*metabolism ; Stress, Physiological ; T-Lymphocytes/physiology ; Tumor Suppressor Proteins/deficiency/genetics/*metabolism ; bcl-2 Homologous Antagonist-Killer Protein/chemistry/genetics/*metabolism ; bcl-2-Associated X Protein/chemistry/genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 9
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    Neuroscience. Neural stem cells, excited (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-03-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hsieh, Jenny -- Schneider, Jay W -- New York, N.Y. -- Science. 2013 Mar 29;339(6127):1534-5. doi: 10.1126/science.1237576.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. jenny.hsieh@utsouthwestern.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23539589" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*cytology/*physiology ; Calcium Channels/physiology ; Cells, Cultured ; Humans ; Neural Stem Cells/*physiology ; *Neurogenesis ; Receptors, N-Methyl-D-Aspartate/physiology ; *Synaptic Transmission ; gamma-Aminobutyric Acid/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 10
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    Melanopsin signalling in mammalian iris and retina (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-11-05
    Description: Non-mammalian vertebrates have an intrinsically photosensitive iris and thus a local pupillary light reflex (PLR). In contrast, it is thought that the PLR in mammals generally requires neuronal circuitry connecting the eye and the brain. Here we report that an intrinsic component of the PLR is in fact widespread in nocturnal and crepuscular mammals. In mouse, this intrinsic PLR requires the visual pigment melanopsin; it also requires PLCbeta4, a vertebrate homologue of the Drosophila NorpA phospholipase C which mediates rhabdomeric phototransduction. The Plcb4(-/-) genotype, in addition to removing the intrinsic PLR, also essentially eliminates the intrinsic light response of the M1 subtype of melanopsin-expressing, intrinsically photosensitive retinal ganglion cells (M1-ipRGCs), which are by far the most photosensitive ipRGC subtype and also have the largest response to light. Ablating in mouse the expression of both TRPC6 and TRPC7, members of the TRP channel superfamily, also essentially eliminated the M1-ipRGC light response but the intrinsic PLR was not affected. Thus, melanopsin signalling exists in both iris and retina, involving a PLCbeta4-mediated pathway that nonetheless diverges in the two locations.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3270891/" 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/PMC3270891/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xue, T -- Do, M T H -- Riccio, A -- Jiang, Z -- Hsieh, J -- Wang, H C -- Merbs, S L -- Welsbie, D S -- Yoshioka, T -- Weissgerber, P -- Stolz, S -- Flockerzi, V -- Freichel, M -- Simon, M I -- Clapham, D E -- Yau, K-W -- EY14596/EY/NEI NIH HHS/ -- R01 DC006904/DC/NIDCD NIH HHS/ -- R01 DC006904-07/DC/NIDCD NIH HHS/ -- R01 DC006904-08/DC/NIDCD NIH HHS/ -- R01 DC006904-09/DC/NIDCD NIH HHS/ -- R01 EY006837/EY/NEI NIH HHS/ -- R01 EY006837-22/EY/NEI NIH HHS/ -- R01 EY006837-23/EY/NEI NIH HHS/ -- R01 EY006837-24/EY/NEI NIH HHS/ -- R37 EY006837/EY/NEI NIH HHS/ -- R37 EY006837-13/EY/NEI NIH HHS/ -- R37 EY006837-14/EY/NEI NIH HHS/ -- R37 EY006837-15/EY/NEI NIH HHS/ -- R37 EY006837-15S1/EY/NEI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Nov 2;479(7371):67-73. doi: 10.1038/nature10567.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. txue77@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22051675" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Iris/anatomy & histology/cytology/*metabolism/*radiation effects ; Light Signal Transduction/physiology/*radiation effects ; Mammals/*physiology ; Mice ; Phospholipase C beta/metabolism ; Photic Stimulation ; Primates/physiology ; Reflex, Pupillary/physiology/radiation effects ; Retina/cytology/*metabolism/*radiation effects ; Retinal Ganglion Cells/metabolism/radiation effects ; Rod Opsins/*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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