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  • 1
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    Reovirus therapy of tumors with activated Ras pathway (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-11-13
    Description: Human reovirus requires an activated Ras signaling pathway for infection of cultured cells. To investigate whether this property can be exploited for cancer therapy, severe combined immune deficient mice bearing tumors established from v-erbB-transformed murine NIH 3T3 cells or human U87 glioblastoma cells were treated with the virus. A single intratumoral injection of virus resulted in regression of tumors in 65 to 80 percent of the mice. Treatment of immune-competent C3H mice bearing tumors established from ras-transformed C3H-10T1/2 cells also resulted in tumor regression, although a series of injections were required. These results suggest that, with further work, reovirus may have applicability in the treatment of cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Coffey, M C -- Strong, J E -- Forsyth, P A -- Lee, P W -- New York, N.Y. -- Science. 1998 Nov 13;282(5392):1332-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Biology Research Group and Department of Microbiology and Infectious Diseases, University of Calgary Health Science Centre, Calgary, Alberta, T2N 4N1, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9812900" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Antibodies, Viral/immunology ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Cell Line, Transformed ; Genes, erbB ; *Genes, ras ; Humans ; Male ; Mammalian orthoreovirus 3/immunology/*physiology ; Mice ; Mice, Inbred C3H ; Mice, SCID ; Neoplasm Transplantation ; Neoplasms, Experimental/metabolism/pathology/*therapy/virology ; Signal Transduction ; Tumor Cells, Cultured ; Virus Replication ; ras Proteins/*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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    Role of T-bet in commitment of TH1 cells before IL-12-dependent selection (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-06-09
    Description: How cytokines control differentiation of helper T (TH) cells is controversial. We show that T-bet, without apparent assistance from interleukin 12 (IL-12)/STAT4, specifies TH1 effector fate by targeting chromatin remodeling to individual interferon-gamma (IFN-gamma) alleles and by inducing IL-12 receptor beta2 expression. Subsequently, it appears that IL-12/STAT4 serves two essential functions in the development of TH1 cells: as growth signal, inducing survival and cell division; and as trans-activator, prolonging IFN-gamma synthesis through a genetic interaction with the coactivator, CREB-binding protein. These results suggest that a cytokine does not simply induce TH fate choice but instead may act as an essential secondary stimulus that mediates selective survival of a lineage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mullen, A C -- High, F A -- Hutchins, A S -- Lee, H W -- Villarino, A V -- Livingston, D M -- Kung, A L -- Cereb, N -- Yao, T P -- Yang, S Y -- Reiner, S L -- AI-42370/AI/NIAID NIH HHS/ -- EY-07131/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 2001 Jun 8;292(5523):1907-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Abramson Family Cancer Research Institute and Department of Medicine, University of Pennsylvania, Philadelphia, PA 19104-6160, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11397944" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; CREB-Binding Protein ; Cell Differentiation ; Cell Division ; Cell Lineage ; Cells, Cultured ; DNA-Binding Proteins/metabolism ; Gene Expression Regulation ; Histones/metabolism ; Interferon-gamma/*biosynthesis/genetics ; Interleukin-12/*metabolism ; Lymphocyte Activation ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Nuclear Proteins/metabolism ; RNA, Messenger/genetics/metabolism ; Receptors, Interleukin/metabolism ; Receptors, Interleukin-12 ; STAT4 Transcription Factor ; Signal Transduction ; T-Box Domain Proteins ; Th1 Cells/cytology/*immunology/metabolism ; Trans-Activators/metabolism ; Transcription Factors/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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  • 3
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    A subclass of Ras proteins that regulate the degradation of IkappaB (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-02-05
    Description: Small guanosine triphosphatases, typified by the mammalian Ras proteins, play major roles in the regulation of numerous cellular pathways. A subclass of evolutionarily conserved Ras-like proteins was identified, members of which differ from other Ras proteins in containing amino acids at positions 12 and 61 that are similar to those present in the oncogenic forms of Ras. These proteins, kappaB-Ras1 and kappaB-Ras2, interact with the PEST domains of IkappaBalpha and IkappaBbeta [inhibitors of the transcription factor nuclear factor kappa B (NF-kappaB)] and decrease their rate of degradation. In cells, kappaB-Ras proteins are associated only with NF-kappaB:IkappaBbeta complexes and therefore may provide an explanation for the slower rate of degradation of IkappaBbeta compared with IkappaBalpha.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fenwick, C -- Na, S Y -- Voll, R E -- Zhong, H -- Im, S Y -- Lee, J W -- Ghosh, S -- New York, N.Y. -- Science. 2000 Feb 4;287(5454):869-73.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Immunobiology and Department of Molecular Biophysics and Biochemistry, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10657303" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Amino Acid Motifs ; Amino Acid Sequence ; Animals ; Binding Sites ; Cell Line ; Guanosine Triphosphate/metabolism ; Humans ; I-kappa B Proteins/*metabolism ; Mice ; Molecular Sequence Data ; NF-kappa B/metabolism ; Phosphorylation ; Recombinant Fusion Proteins/chemistry/metabolism ; Signal Transduction ; Transcription Factor RelA ; Transfection ; Tumor Necrosis Factor-alpha/metabolism/pharmacology ; Two-Hybrid System Techniques ; ras Proteins/chemistry/*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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  • 4
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    Secretion of activin by interstitial cells in the testis (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-01-20
    Description: Activin, a dimer formed by the beta subunits of inhibin, has an effect that is opposite to that of inhibin in a number of biological systems. Which cell types secrete activin in vivo is not known. TM3 cells, a Leydig-derived cell line, contained messenger RNAs that hybridized with human beta A and beta B complementary DNA probes and were similar in size to the porcine messenger RNA for the beta subunits of inhibin. No hybridization to the inhibin alpha subunit was detectable in the TM3 cells. Conditioned medium from TM3 cells and from primary cultures of rat and porcine interstitial cells stimulated the release of follicle-stimulating hormone in a pituitary cell culture assay. It is likely that, in the testis, the Leydig cells secrete activin and the Sertoli cells produce inhibin, or a combination of both.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, W -- Mason, A J -- Schwall, R -- Szonyi, E -- Mather, J P -- New York, N.Y. -- Science. 1989 Jan 20;243(4889):396-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Culture, Genentech, South San Francisco, CA 94080.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2492117" target="_blank"〉PubMed〈/a〉
    Keywords: Activins ; Animals ; Cell Line ; Follicle Stimulating Hormone/secretion ; Inhibins/*physiology/*secretion ; Leydig Cells/*physiology ; Male ; Mice ; Rats ; Sertoli Cells/physiology ; Swine ; Testis/cytology/*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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  • 5
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    Prolyl 4-hydroxylation regulates Argonaute 2 stability (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-08-12
    Description: Human Argonaute (Ago) proteins are essential components of the RNA-induced silencing complexes (RISCs). Argonaute 2 (Ago2) has a P-element-induced wimpy testis (PIWI) domain, which folds like RNase H and is responsible for target RNA cleavage in RNA interference. Proteins such as Dicer, TRBP, MOV10, RHA, RCK/p54 and KIAA1093 associate with Ago proteins and participate in small RNA processing, RISC loading and localization of Ago proteins in the cytoplasmic messenger RNA processing bodies. However, mechanisms that regulate RNA interference remain obscure. Here we report physical interactions between Ago2 and the alpha-(P4H-alpha(I)) and beta-(P4H-beta) subunits of the type I collagen prolyl-4-hydroxylase (C-P4H(I)). Mass spectrometric analysis identified hydroxylation of the endogenous Ago2 at proline 700. In vitro, both Ago2 and Ago4 seem to be more efficiently hydroxylated than Ago1 and Ago3 by recombinant human C-P4H(I). Importantly, human cells depleted of P4H-alpha(I) or P4H-beta by short hairpin RNA and P4H-alpha(I) null mouse embryonic fibroblast cells showed reduced stability of Ago2 and impaired short interfering RNA programmed RISC activity. Furthermore, mutation of proline 700 to alanine also resulted in destabilization of Ago2, thus linking Ago2 P700 and hydroxylation at this residue to its stability regulation. These findings identify hydroxylation as a post-translational modification important for Ago2 stability and effective RNA interference.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661850/" 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/PMC2661850/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Qi, Hank H -- Ongusaha, Pat P -- Myllyharju, Johanna -- Cheng, Dongmei -- Pakkanen, Outi -- Shi, Yujiang -- Lee, Sam W -- Peng, Junmin -- Shi, Yang -- AG025688/AG/NIA NIH HHS/ -- GM53874/GM/NIGMS NIH HHS/ -- R01 GM053874/GM/NIGMS NIH HHS/ -- R01 GM053874-15/GM/NIGMS NIH HHS/ -- England -- Nature. 2008 Sep 18;455(7211):421-4. doi: 10.1038/nature07186. Epub 2008 Aug 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Harvard Medical School, New Research Building 854, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18690212" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Argonaute Proteins ; Enzyme Stability ; Eukaryotic Initiation Factor-2/*chemistry/genetics/*metabolism ; HeLa Cells ; Humans ; Hydroxylation ; Mice ; MicroRNAs/genetics ; Proline/*metabolism ; Protein Binding ; Protein Subunits ; RNA-Induced Silencing Complex/genetics/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
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    Skp2 targeting suppresses tumorigenesis by Arf-p53-independent cellular senescence (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-03-20
    Description: Cellular senescence has been recently shown to have an important role in opposing tumour initiation and promotion. Senescence induced by oncogenes or by loss of tumour suppressor genes is thought to critically depend on induction of the p19(Arf)-p53 pathway. The Skp2 E3-ubiquitin ligase can act as a proto-oncogene and its aberrant overexpression is frequently observed in human cancers. Here we show that although Skp2 inactivation on its own does not induce cellular senescence, aberrant proto-oncogenic signals as well as inactivation of tumour suppressor genes do trigger a potent, tumour-suppressive senescence response in mice and cells devoid of Skp2. Notably, Skp2 inactivation and oncogenic-stress-driven senescence neither elicit activation of the p19(Arf)-p53 pathway nor DNA damage, but instead depend on Atf4, p27 and p21. We further demonstrate that genetic Skp2 inactivation evokes cellular senescence even in oncogenic conditions in which the p19(Arf)-p53 response is impaired, whereas a Skp2-SCF complex inhibitor can trigger cellular senescence in p53/Pten-deficient cells and tumour regression in preclinical studies. Our findings therefore provide proof-of-principle evidence that pharmacological inhibition of Skp2 may represent a general approach for cancer prevention and therapy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2928066/" 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/PMC2928066/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, Hui-Kuan -- Chen, Zhenbang -- Wang, Guocan -- Nardella, Caterina -- Lee, Szu-Wei -- Chan, Chia-Hsin -- Yang, Wei-Lei -- Wang, Jing -- Egia, Ainara -- Nakayama, Keiichi I -- Cordon-Cardo, Carlos -- Teruya-Feldstein, Julie -- Pandolfi, Pier Paolo -- R01 CA082328/CA/NCI NIH HHS/ -- R01 CA082328-13/CA/NCI NIH HHS/ -- R01 MD004038/MD/NIMHD NIH HHS/ -- England -- Nature. 2010 Mar 18;464(7287):374-9. doi: 10.1038/nature08815.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Biology and Genetics Program, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, New York 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20237562" target="_blank"〉PubMed〈/a〉
    Keywords: Activating Transcription Factor 4/metabolism ; Adenovirus E1A Proteins/genetics/metabolism ; Animals ; *Cell Aging/drug effects ; *Cell Transformation, Neoplastic/drug effects ; Cells, Cultured ; Cyclin-Dependent Kinase Inhibitor p16/deficiency/genetics/metabolism ; Cyclin-Dependent Kinase Inhibitor p21/metabolism ; Cyclin-Dependent Kinase Inhibitor p27/metabolism ; Fibroblasts ; Male ; Mice ; PTEN Phosphohydrolase/deficiency/genetics/metabolism ; Prostate/cytology/metabolism ; Prostatic Neoplasms/drug therapy/pathology/prevention & control ; Proto-Oncogene Proteins p21(ras)/genetics/metabolism ; S-Phase Kinase-Associated Proteins/antagonists & inhibitors/genetics/*metabolism ; SKP Cullin F-Box Protein Ligases/metabolism ; Tumor Suppressor Protein p53/deficiency/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
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    Identification of small molecule activators of cryptochrome (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-07-17
    Description: Impairment of the circadian clock has been associated with numerous disorders, including metabolic disease. Although small molecules that modulate clock function might offer therapeutic approaches to such diseases, only a few compounds have been identified that selectively target core clock proteins. From an unbiased cell-based circadian phenotypic screen, we identified KL001, a small molecule that specifically interacts with cryptochrome (CRY). KL001 prevented ubiquitin-dependent degradation of CRY, resulting in lengthening of the circadian period. In combination with mathematical modeling, our studies using KL001 revealed that CRY1 and CRY2 share a similar functional role in the period regulation. Furthermore, KL001-mediated CRY stabilization inhibited glucagon-induced gluconeogenesis in primary hepatocytes. KL001 thus provides a tool to study the regulation of CRY-dependent physiology and aid development of clock-based therapeutics of diabetes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3589997/" 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/PMC3589997/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hirota, Tsuyoshi -- Lee, Jae Wook -- St John, Peter C -- Sawa, Mariko -- Iwaisako, Keiko -- Noguchi, Takako -- Pongsawakul, Pagkapol Y -- Sonntag, Tim -- Welsh, David K -- Brenner, David A -- Doyle, Francis J 3rd -- Schultz, Peter G -- Kay, Steve A -- GM074868/GM/NIGMS NIH HHS/ -- GM085764/GM/NIGMS NIH HHS/ -- GM096873/GM/NIGMS NIH HHS/ -- MH051573/MH/NIMH NIH HHS/ -- MH082945/MH/NIMH NIH HHS/ -- P50 GM085764/GM/NIGMS NIH HHS/ -- R01 GM041804/GM/NIGMS NIH HHS/ -- R01 GM074868/GM/NIGMS NIH HHS/ -- R01 GM096873/GM/NIGMS NIH HHS/ -- R01 MH051573/MH/NIMH NIH HHS/ -- R01 MH082945/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2012 Aug 31;337(6098):1094-7. doi: 10.1126/science.1223710. Epub 2012 Jul 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biological Sciences, University of California San Diego, La Jolla, CA 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22798407" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Amino Acid Sequence ; Animals ; Carbazoles/chemistry/isolation & purification/*pharmacology ; Cell Line, Tumor ; Circadian Clocks/*drug effects ; Cryptochromes/*agonists/metabolism ; Gluconeogenesis/drug effects/genetics ; Glucose-6-Phosphatase/genetics ; HEK293 Cells ; Hepatocytes/drug effects/metabolism ; Humans ; Liver/cytology/drug effects/metabolism ; Mice ; Molecular Sequence Data ; Phosphoenolpyruvate Carboxykinase (GTP)/genetics ; Protein Stability/drug effects ; Proteolysis/drug effects ; *Small Molecule Libraries ; Sulfonamides/chemistry/isolation & purification/*pharmacology
    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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  • 8
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    Hematopoietic cell regulation by Rac1 and Rac2 guanosine triphosphatases (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-18
    Description: The Rho guanosine triphosphatases (GTPases) Rac1 and Rac2 are critical signaling regulators in mammalian cells. The deletion of both Rac1 and Rac2 murine alleles leads to a massive egress of hematopoietic stem/progenitor cells (HSC/Ps) into the blood from the marrow, whereas Rac1-/- but not Rac2-/- HSC/Ps fail to engraft in the bone marrow of irradiated recipient mice. In contrast, Rac2, but not Rac1, regulates superoxide production and directed migration in neutrophils, and in each cell type, the two GTPases play distinct roles in actin organization, cell survival, and proliferation. Thus, Rac1 and Rac2 regulate unique aspects of hematopoietic development and function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gu, Yi -- Filippi, Marie-Dominique -- Cancelas, Jose A -- Siefring, Jamie E -- Williams, Emily P -- Jasti, Aparna C -- Harris, Chad E -- Lee, Andrew W -- Prabhakar, Rethinasamy -- Atkinson, Simon J -- Kwiatkowski, David J -- Williams, David A -- DK62757/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2003 Oct 17;302(5644):445-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Experimental Hematology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14564009" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Animals ; Apoptosis ; Bone Marrow Transplantation ; Cell Adhesion ; Cell Cycle ; Cell Movement ; Cell Size ; Colony-Forming Units Assay ; Cyclin D1/metabolism ; Fibronectins/metabolism ; Hematopoiesis ; Hematopoietic Stem Cell Mobilization ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/*physiology ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Mitogen-Activated Protein Kinases/metabolism ; Neutrophils/*physiology ; *Protein-Serine-Threonine Kinases ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-akt ; Recombination, Genetic ; Signal Transduction ; Stem Cell Factor/pharmacology ; Superoxides/metabolism ; rac GTP-Binding Proteins/genetics/*metabolism ; rac1 GTP-Binding Protein/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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  • 9
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    Biomimetic self-templating supramolecular structures (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-10-21
    Description: In nature, helical macromolecules such as collagen, chitin and cellulose are critical to the morphogenesis and functionality of various hierarchically structured materials. During tissue formation, these chiral macromolecules are secreted and undergo self-templating assembly, a process whereby multiple kinetic factors influence the assembly of the incoming building blocks to produce non-equilibrium structures. A single macromolecule can form diverse functional structures when self-templated under different conditions. Collagen type I, for instance, forms transparent corneal tissues from orthogonally aligned nematic fibres, distinctively coloured skin tissues from cholesteric phase fibre bundles, and mineralized tissues from hierarchically organized fibres. Nature's self-templated materials surpass the functional and structural complexity achievable by current top-down and bottom-up fabrication methods. However, self-templating has not been thoroughly explored for engineering synthetic materials. Here we demonstrate the biomimetic, self-templating assembly of chiral colloidal particles (M13 phage) into functional materials. A single-step process produces long-range-ordered, supramolecular films showing multiple levels of hierarchical organization and helical twist. Three distinct supramolecular structures are created by this approach: nematic orthogonal twists, cholesteric helical ribbons and smectic helicolidal nanofilaments. Both chiral liquid crystalline phase transitions and competing interfacial forces at the interface are found to be critical factors in determining the morphology of the templated structures during assembly. The resulting materials show distinctive optical and photonic properties, functioning as chiral reflector/filters and structural colour matrices. In addition, M13 phages with genetically incorporated bioactive peptide ligands direct both soft and hard tissue growth in a hierarchically organized manner. Our assembly approach provides insight into the complexities of hierarchical assembly in nature and could be expanded to other chiral molecules to engineer sophisticated functional helical-twisted structures.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chung, Woo-Jae -- Oh, Jin-Woo -- Kwak, Kyungwon -- Lee, Byung Yang -- Meyer, Joel -- Wang, Eddie -- Hexemer, Alexander -- Lee, Seung-Wuk -- R21DE018360/DE/NIDCR NIH HHS/ -- England -- Nature. 2011 Oct 19;478(7369):364-8. doi: 10.1038/nature10513.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bioengineering, University of California, Berkeley, California 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22012394" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteriophage M13/chemistry/*physiology ; Biomimetic Materials/chemical synthesis/*chemistry ; Cell Line ; Macromolecular Substances/chemistry ; Mice ; Optical Rotation ; Tissue Culture Techniques/instrumentation ; Virion/chemistry
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
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    Wnt activation in nail epithelium couples nail growth to digit regeneration (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-06-14
    Description: The tips of mammalian digits can regenerate after amputation, like those of amphibians. It is unknown why this capacity is limited to the area associated with the nail. Here we show that nail stem cells (NSCs) reside in the proximal nail matrix and that the mechanisms governing NSC differentiation are coupled directly with their ability to orchestrate digit regeneration. Early nail progenitors undergo Wnt-dependent differentiation into the nail. After amputation, this Wnt activation is required for nail regeneration and also for attracting nerves that promote mesenchymal blastema growth, leading to the regeneration of the digit. Amputations proximal to the Wnt-active nail progenitors result in failure to regenerate the nail or digit. Nevertheless, beta-catenin stabilization in the NSC region induced their regeneration. These results establish a link between NSC differentiation and digit regeneration, and suggest that NSCs may have the potential to contribute to the development of novel treatments for amputees.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3936678/" 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/PMC3936678/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takeo, Makoto -- Chou, Wei Chin -- Sun, Qi -- Lee, Wendy -- Rabbani, Piul -- Loomis, Cynthia -- Taketo, M Mark -- Ito, Mayumi -- 1R01AR059768-01A1/AR/NIAMS NIH HHS/ -- 5P30CA0016087-32/CA/NCI NIH HHS/ -- P30 CA016087-30/CA/NCI NIH HHS/ -- R01 AR059768/AR/NIAMS NIH HHS/ -- S10 RR023704-01A1/RR/NCRR NIH HHS/ -- England -- Nature. 2013 Jul 11;499(7457):228-32. doi: 10.1038/nature12214. Epub 2013 Jun 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Ronald O. Perelman Department of Dermatology, New York University, School of Medicine, New York, New York 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23760480" target="_blank"〉PubMed〈/a〉
    Keywords: Amputation ; Animals ; Bone and Bones/cytology/metabolism ; Cell Differentiation ; Cells, Cultured ; Epithelium/metabolism ; Extremities/growth & development/innervation/*physiology ; Hoof and Claw/cytology/*growth & development/metabolism ; Mesoderm/cytology/metabolism ; Mice ; Regeneration/*physiology ; Stem Cells/cytology/metabolism ; Wnt Proteins/*metabolism ; Wnt Signaling Pathway ; beta Catenin/genetics/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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