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  • 1
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    EGFR phosphorylation and resistance to gefitinib [Biochemistry] (2015)
    National Academy of Sciences
    Details
    Publication Date: 2015-06-03
    Description: Epidermal growth factor receptor (EGFR) is a heavily glycosylated transmembrane receptor tyrosine kinase. Upon EGF-binding, EGFR undergoes conformational changes to dimerize, resulting in kinase activation and autophosphorylation and downstream signaling. Tyrosine kinase inhibitors (TKIs) have been used to treat lung cancer by inhibiting EGFR phosphorylation. Previously, we demonstrated that EGFR...
    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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    GGGGCC repeat expansion in C9orf72 compromises nucleocytoplasmic transport (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-08-27
    Description: The GGGGCC (G4C2) repeat expansion in a noncoding region of C9orf72 is the most common cause of sporadic and familial forms of amyotrophic lateral sclerosis and frontotemporal dementia. The basis for pathogenesis is unknown. To elucidate the consequences of G4C2 repeat expansion in a tractable genetic system, we generated transgenic fly lines expressing 8, 28 or 58 G4C2-repeat-containing transcripts that do not have a translation start site (AUG) but contain an open-reading frame for green fluorescent protein to detect repeat-associated non-AUG (RAN) translation. We show that these transgenic animals display dosage-dependent, repeat-length-dependent degeneration in neuronal tissues and RAN translation of dipeptide repeat (DPR) proteins, as observed in patients with C9orf72-related disease. This model was used in a large-scale, unbiased genetic screen, ultimately leading to the identification of 18 genetic modifiers that encode components of the nuclear pore complex (NPC), as well as the machinery that coordinates the export of nuclear RNA and the import of nuclear proteins. Consistent with these results, we found morphological abnormalities in the architecture of the nuclear envelope in cells expressing expanded G4C2 repeats in vitro and in vivo. Moreover, we identified a substantial defect in RNA export resulting in retention of RNA in the nuclei of Drosophila cells expressing expanded G4C2 repeats and also in mammalian cells, including aged induced pluripotent stem-cell-derived neurons from patients with C9orf72-related disease. These studies show that a primary consequence of G4C2 repeat expansion is the compromise of nucleocytoplasmic transport through the nuclear pore, revealing a novel mechanism of neurodegeneration.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4631399/" 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/PMC4631399/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Freibaum, Brian D -- Lu, Yubing -- Lopez-Gonzalez, Rodrigo -- Kim, Nam Chul -- Almeida, Sandra -- Lee, Kyung-Ha -- Badders, Nisha -- Valentine, Marc -- Miller, Bruce L -- Wong, Philip C -- Petrucelli, Leonard -- Kim, Hong Joo -- Gao, Fen-Biao -- Taylor, J Paul -- AG019724/AG/NIA NIH HHS/ -- N079725/PHS HHS/ -- NS079725/NS/NINDS NIH HHS/ -- P01 AG019724/AG/NIA NIH HHS/ -- R01 NS057553/NS/NINDS NIH HHS/ -- R01 NS079725/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2015 Sep 3;525(7567):129-33. doi: 10.1038/nature14974. Epub 2015 Aug 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Molecular Biology, St Jude Children's Research Hospital, Memphis, Tennessee 38105, USA. ; Department of Neurology, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA. ; Memory and Aging Center, Department of Neurology, University of California San Francisco, San Francisco, California 94158, USA. ; Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. ; Department of Neuroscience, Mayo Clinic Florida, Jacksonville, Florida 32224, USA. ; Howard Hughes Medical Institute, Department of Cell and Molecular Biology, St Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26308899" target="_blank"〉PubMed〈/a〉
    Keywords: Active Transport, Cell Nucleus/*genetics ; Amyotrophic Lateral Sclerosis/genetics/pathology ; Animals ; Animals, Genetically Modified ; DNA Repeat Expansion/*genetics ; Drosophila melanogaster/*cytology/genetics/*metabolism ; Eye/metabolism ; Female ; Frontotemporal Dementia/genetics/pathology ; HeLa Cells ; Humans ; Induced Pluripotent Stem Cells/cytology/metabolism ; Male ; Muscles/cytology/metabolism ; Neurons/cytology/metabolism ; Nuclear Pore/genetics/metabolism/pathology ; Open Reading Frames/*genetics ; Phenotype ; Protein Biosynthesis ; Proteins/*genetics ; RNA/genetics/metabolism ; RNA Transport/*genetics ; Salivary Glands/cytology/metabolism/pathology
    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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    TDP-43 repression of nonconserved cryptic exons is compromised in ALS-FTD (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-08-08
    Description: Cytoplasmic aggregation of TDP-43, accompanied by its nuclear clearance, is a key common pathological hallmark of amyotrophic lateral sclerosis and frontotemporal dementia (ALS-FTD). However, a limited understanding of this RNA-binding protein (RBP) impedes the clarification of pathogenic mechanisms underlying TDP-43 proteinopathy. In contrast to RBPs that regulate splicing of conserved exons, we found that TDP-43 repressed the splicing of nonconserved cryptic exons, maintaining intron integrity. When TDP-43 was depleted from mouse embryonic stem cells, these cryptic exons were spliced into messenger RNAs, often disrupting their translation and promoting nonsense-mediated decay. Moreover, enforced repression of cryptic exons prevented cell death in TDP-43-deficient cells. Furthermore, repression of cryptic exons was impaired in ALS-FTD cases, suggesting that this splicing defect could potentially underlie TDP-43 proteinopathy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ling, Jonathan P -- Pletnikova, Olga -- Troncoso, Juan C -- Wong, Philip C -- P50AG05146/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2015 Aug 7;349(6248):650-5. doi: 10.1126/science.aab0983.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205-2196, USA. ; Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205-2196, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205-2196, USA. ; Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205-2196, USA. Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205-2196, USA. wong@jhmi.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26250685" target="_blank"〉PubMed〈/a〉
    Keywords: Amyotrophic Lateral Sclerosis/*genetics ; Animals ; Base Sequence ; Cells, Cultured ; Cysteine Endopeptidases/genetics ; DNA-Binding Proteins/genetics/*physiology ; Embryonic Stem Cells ; Exons/*genetics ; Frontotemporal Dementia/*genetics ; Gene Knockout Techniques ; HeLa Cells ; Humans ; Mice ; Molecular Sequence Data ; Protein Isoforms/genetics ; *RNA Splicing ; RNA Stability ; RNA, Messenger/metabolism ; Sequence Analysis, DNA
    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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  • 4
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    Mitochondrial uncoupling reveals a novel therapeutic opportunity for p53-defective cancers (2018)
    Springer Nature
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    Publication Date: 2018-09-27
    Description: Mitochondrial uncoupling reveals a novel therapeutic opportunity for p53-defective cancers Mitochondrial uncoupling reveals a novel therapeutic opportunity for p53-defective cancers, Published online: 26 September 2018; doi:10.1038/s41467-018-05805-1 Several challenges are involved in direct targeting of mutant p53, while targeting altered fitness of cells with loss of wild type p53 is an alternative approach. Here they identify niclosamide to be selectively toxic to p53 deficient cells through a previously unknown mitochondrial uncoupling mechanism.
    Electronic ISSN: 2041-1723
    Topics: Biology , Chemistry and Pharmacology , Natural Sciences in General , Physics
    Published by Springer Nature
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  • 5
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    Meaningful Share Generation for (2, 2)-Multiple Visual Secret Sharing Scheme Without Pixel Expansion (2015)
    Oxford University Press
    Details
    Publication Date: 2015-06-27
    Description: In ( k , n )-threshold visual secret sharing (VSS) schemes, the secret holder can base a group of n participants with n shares to reconstruct secret message by stacking shares. The secret messages are identified directly without any computation with only k ( k ≤ n ) or more shares using the human eye. Recently, many researchers have devoted themselves to studying how more secret images can be encrypted into the same quantity of shares. An extended random-grid VSS scheme that can embed four secret images without pixel expansion under the (2,2)-visual secret-sharing scheme was proposed by Chen et al . The secrets can be recovered by directly stacking and rotating one of the two shares at 90°, 180° and 270°, respectively. However, the used shares are meaningless, causing the attacker to become doubtful by looking at meaningless shares and trying to steal secret messages. The meaningless shares lead to difficult encryption management. This paper proposes an improved black-and-white (2,2)-visual secret sharing scheme that adapts square shares to embed three secret images via two camouflaged images. Compared with other related VSS schemes, this technique has more flexibility, efficiency and security.
    Print ISSN: 0010-4620
    Electronic ISSN: 1460-2067
    Topics: Computer Science
    Published by Oxford University Press
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  • 6
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    Low dietary protein content alleviates motor symptoms in mice with mutant dynactin/dynein-mediated neurodegeneration (2015)
    Oxford University Press
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    Publication Date: 2015-03-20
    Description: Mutations in components of the molecular motor dynein/dynactin lead to neurodegenerative diseases of the motor system or atypical parkinsonism. These mutations are associated with prominent accumulation of vesicles involved in autophagy and lysosomal pathways, and with protein inclusions. Whether alleviating these defects would affect motor symptoms remain unknown. Here, we show that a mouse model expressing low levels of disease linked-G59S mutant dynactin p150 Glued develops motor dysfunction 〉8 months before loss of motor neurons or dopaminergic degeneration is observed. Abnormal accumulation of autophagosomes and protein inclusions were efficiently corrected by lowering dietary protein content, and this was associated with transcriptional upregulations of key players in autophagy. Most importantly this dietary modification partially rescued overall neurological symptoms in these mice after onset. Similar observations were made in another mouse strain carrying a point mutation in the dynein heavy chain gene. Collectively, our data suggest that stimulating the autophagy/lysosomal system through appropriate nutritional intervention has significant beneficial effects on motor symptoms of dynein/dynactin diseases even after symptom onset.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
    Published by Oxford University Press
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  • 7
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    Combinatorial morphogenetic and mechanical cues to mimic bone development for defect repair (2019)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2019
    Description: 〈p〉Endochondral ossification during long bone development and natural fracture healing initiates by mesenchymal cell condensation, directed by local morphogen signals and mechanical cues. Here, we aimed to mimic development for regeneration of large bone defects. We hypothesized that engineered human mesenchymal condensations presenting transforming growth factor–β1 (TGF-β1) and/or bone morphogenetic protein-2 (BMP-2) from encapsulated microparticles promotes endochondral defect regeneration contingent on in vivo mechanical cues. Mesenchymal condensations induced bone formation dependent on morphogen presentation, with BMP-2 + TGF-β1 fully restoring mechanical function. Delayed in vivo ambulatory loading significantly enhanced the bone formation rate in the dual morphogen group. In vitro, BMP-2 or BMP-2 + TGF-β1 initiated robust endochondral lineage commitment. In vivo, however, extensive cartilage formation was evident predominantly in the BMP-2 + TGF-β1 group, enhanced by mechanical loading. Together, this study demonstrates a biomimetic template for recapitulating developmental morphogenic and mechanical cues in vivo for tissue engineering.〈/p〉
    Electronic ISSN: 2375-2548
    Topics: Natural Sciences in General
    Published by American Association for the Advancement of Science (AAAS)
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  • 8
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    Combinatorial morphogenetic and mechanical cues to mimic bone development for defect repair (2019)
    American Association for the Advancement of Science
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    Publication Date: 2019-08-07
    Electronic ISSN: 2375-2548
    Topics: Natural Sciences in General
    Published by American Association for the Advancement of Science
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