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  • 1
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    Tbx5 and the retinotectum projection (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-30
    Description: Dorsal and ventral aspects of the eye are distinct from the early stages of development. The developing eye cup grows dorsally, and the choroidal fissure is formed on its ventral side. Retinal axons from the dorsal and ventral retina project to the ventral and dorsal tectum, respectively. Misexpression of the Tbx5 gene induced dorsalization of the ventral side of the eye and altered projections of retinal ganglion cell axons. Thus, Tbx5 is involved in eye morphogenesis and is a topographic determinant of the visual projections between retina and tectum.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koshiba-Takeuchi, K -- Takeuchi, J K -- Matsumoto, K -- Momose, T -- Uno, K -- Hoepker, V -- Ogura, K -- Takahashi, N -- Nakamura, H -- Yasuda, K -- Ogura, T -- New York, N.Y. -- Science. 2000 Jan 7;287(5450):134-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate School of Biological Sciences, Nara Institute of Science and Technology, 8916-5, Takayama, Ikoma, Nara, Japan 630-0101.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10615048" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Avian Proteins ; Axons/*ultrastructure ; Body Patterning ; Bone Morphogenetic Protein 4 ; Bone Morphogenetic Proteins/genetics/physiology ; Chick Embryo ; DNA-Binding Proteins/genetics ; Electroporation ; Ephrin-B1 ; Ephrin-B2 ; Eye/*embryology ; Gene Expression ; Homeodomain Proteins/genetics ; Membrane Proteins/genetics/physiology ; Morphogenesis ; PAX2 Transcription Factor ; Pigment Epithelium of Eye/embryology/metabolism ; Retina/*embryology/metabolism ; Retinal Ganglion Cells/ultrastructure ; Superior Colliculi/*embryology ; T-Box Domain Proteins/genetics/*physiology ; Transcription Factors/genetics ; Transfection ; Transgenes
    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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    Regulation of spermatogenesis by testis-specific, cytoplasmic poly(A) polymerase TPAP (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-12-10
    Description: Spermatogenesis is a highly specialized process of cellular differentiation to produce spermatozoa. This differentiation process accompanies morphological changes that are controlled by a number of genes expressed in a stage-specific manner during spermatogenesis. Here we show that in mice, the absence of a testis-specific, cytoplasmic polyadenylate [poly(A)] polymerase, TPAP, results in the arrest of spermiogenesis. TPAP-deficient mice display impaired expression of haploid-specific genes that are required for the morphogenesis of germ cells. The TPAP deficiency also causes incomplete elongation of poly(A) tails of particular transcription factor messenger RNAs. Although the overall cellular level of the transcription factor TAF10 is unaffected, TAF10 is insufficiently transported into the nucleus of germ cells. We propose that TPAP governs germ cell morphogenesis by modulating specific transcription factors at posttranscriptional and posttranslational levels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kashiwabara, Shin-Ichi -- Noguchi, Junko -- Zhuang, Tiangang -- Ohmura, Ko -- Honda, Arata -- Sugiura, Shin -- Miyamoto, Kiyoko -- Takahashi, Satoru -- Inoue, Kimiko -- Ogura, Atsuo -- Baba, Tadashi -- New York, N.Y. -- Science. 2002 Dec 6;298(5600):1999-2002.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Applied Biochemistry, Institute of Basic Medical Sciences, University of Tsukuba, Tsukuba Science City, Ibaraki 305-8572, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12471261" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Cytoplasm/enzymology ; Female ; Gene Expression Regulation, Developmental ; Gene Targeting ; In Situ Nick-End Labeling ; Male ; Mice ; Mice, Inbred C57BL ; Mutation ; Nuclear Proteins/genetics/metabolism ; Organ Size ; Poly A/metabolism ; Polynucleotide Adenylyltransferase/genetics/*metabolism ; Protein Biosynthesis ; RNA, Messenger/*metabolism ; Spermatids/physiology ; Spermatocytes/physiology ; *Spermatogenesis ; Spermatozoa/*physiology ; Testis/*enzymology/metabolism ; Transcription Factors/genetics/metabolism ; Transcription, Genetic ; mRNA Cleavage and Polyadenylation 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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    Altered cochlear fibrocytes in a mouse model of DFN3 nonsyndromic deafness (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-28
    Description: DFN3, an X chromosome-linked nonsyndromic mixed deafness, is caused by mutations in the BRN-4 gene, which encodes a POU transcription factor. Brn-4-deficient mice were created and found to exhibit profound deafness. No gross morphological changes were observed in the conductive ossicles or cochlea, although there was a dramatic reduction in endocochlear potential. Electron microscopy revealed severe ultrastructural alterations in cochlear spiral ligament fibrocytes. The findings suggest that these fibrocytes, which are mesenchymal in origin and for which a role in potassium ion homeostasis has been postulated, may play a critical role in auditory function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Minowa, O -- Ikeda, K -- Sugitani, Y -- Oshima, T -- Nakai, S -- Katori, Y -- Suzuki, M -- Furukawa, M -- Kawase, T -- Zheng, Y -- Ogura, M -- Asada, Y -- Watanabe, K -- Yamanaka, H -- Gotoh, S -- Nishi-Takeshima, M -- Sugimoto, T -- Kikuchi, T -- Takasaka, T -- Noda, T -- New York, N.Y. -- Science. 1999 Aug 27;285(5432):1408-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, The Cancer Institute, Japanese Foundation for Cancer Research, 1-37-1 Kami-ikebukuro, Toshima-ku, Tokyo 170-8455, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10464101" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cochlear Duct/*metabolism/pathology ; *DNA-Binding Proteins ; Deafness/genetics/*metabolism/pathology ; Ear, Inner/metabolism/pathology ; Ear, Middle/pathology ; Endolymph/metabolism ; Evoked Potentials, Auditory, Brain Stem ; Female ; Gene Expression ; Gene Targeting ; Genetic Linkage ; In Situ Hybridization ; Ion Transport ; Male ; Membrane Potentials ; Mice ; Mice, Inbred C57BL ; Mutagenesis ; *Nerve Tissue Proteins ; POU Domain Factors ; Potassium/*metabolism ; Transcription Factors/genetics/*metabolism ; X Chromosome
    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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    Requirement of CD9 on the egg plasma membrane for fertilization (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-01-15
    Description: CD9 is an integral membrane protein associated with integrins and other membrane proteins. Mice lacking CD9 were produced by homologous recombination. Both male and female CD9-/- mice were born healthy and grew normally. However, the litter size from CD9-/- females was less than 2% of that of the wild type. In vitro fertilization experiments indicated that the cause of this infertility was due to the failure of sperm-egg fusion. When sperm were injected into oocytes with assisted microfertilization techniques, however, the fertilized eggs developed to term. These results indicate that CD9 has a crucial role in sperm-egg fusion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miyado, K -- Yamada, G -- Yamada, S -- Hasuwa, H -- Nakamura, Y -- Ryu, F -- Suzuki, K -- Kosai, K -- Inoue, K -- Ogura, A -- Okabe, M -- Mekada, E -- New York, N.Y. -- Science. 2000 Jan 14;287(5451):321-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Life Science, Kurume University, Kurume, Fukuoka 839-0861, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10634791" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/*physiology ; Antigens, CD9 ; Cell Membrane/immunology/metabolism ; Crosses, Genetic ; Embryonic and Fetal Development ; Female ; Fertilization/physiology ; Fertilization in Vitro ; Gene Targeting ; Infertility, Female/*physiopathology ; Integrin alpha6beta1 ; Integrins/physiology ; Litter Size ; Male ; *Membrane Glycoproteins ; Mice ; Mice, Inbred C57BL ; Oocytes/immunology/*physiology ; Ovulation ; Sperm-Ovum Interactions/*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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    CCR3 is a target for age-related macular degeneration diagnosis and therapy (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-06-16
    Description: Age-related macular degeneration (AMD), a leading cause of blindness worldwide, is as prevalent as cancer in industrialized nations. Most blindness in AMD results from invasion of the retina by choroidal neovascularisation (CNV). Here we show that the eosinophil/mast cell chemokine receptor CCR3 is specifically expressed in choroidal neovascular endothelial cells in humans with AMD, and that despite the expression of its ligands eotaxin-1, -2 and -3, neither eosinophils nor mast cells are present in human CNV. Genetic or pharmacological targeting of CCR3 or eotaxins inhibited injury-induced CNV in mice. CNV suppression by CCR3 blockade was due to direct inhibition of endothelial cell proliferation, and was uncoupled from inflammation because it occurred in mice lacking eosinophils or mast cells, and was independent of macrophage and neutrophil recruitment. CCR3 blockade was more effective at reducing CNV than vascular endothelial growth factor A (VEGF-A) neutralization, which is in clinical use at present, and, unlike VEGF-A blockade, is not toxic to the mouse retina. In vivo imaging with CCR3-targeting quantum dots located spontaneous CNV invisible to standard fluorescein angiography in mice before retinal invasion. CCR3 targeting might reduce vision loss due to AMD through early detection and therapeutic angioinhibition.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2712122/" 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/PMC2712122/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takeda, Atsunobu -- Baffi, Judit Z -- Kleinman, Mark E -- Cho, Won Gil -- Nozaki, Miho -- Yamada, Kiyoshi -- Kaneko, Hiroki -- Albuquerque, Romulo J C -- Dridi, Sami -- Saito, Kuniharu -- Raisler, Brian J -- Budd, Steven J -- Geisen, Pete -- Munitz, Ariel -- Ambati, Balamurali K -- Green, Martha G -- Ishibashi, Tatsuro -- Wright, John D -- Humbles, Alison A -- Gerard, Craig J -- Ogura, Yuichiro -- Pan, Yuzhen -- Smith, Justine R -- Grisanti, Salvatore -- Hartnett, M Elizabeth -- Rothenberg, Marc E -- Ambati, Jayakrishna -- AI039759/AI/NIAID NIH HHS/ -- AI45898/AI/NIAID NIH HHS/ -- DK076893/DK/NIDDK NIH HHS/ -- EY010572/EY/NEI NIH HHS/ -- EY015130/EY/NEI NIH HHS/ -- EY015422/EY/NEI NIH HHS/ -- EY017011/EY/NEI NIH HHS/ -- EY017182/EY/NEI NIH HHS/ -- EY017950/EY/NEI NIH HHS/ -- EY018350/EY/NEI NIH HHS/ -- EY018836/EY/NEI NIH HHS/ -- R01 DK076893/DK/NIDDK NIH HHS/ -- R01 EY015422/EY/NEI NIH HHS/ -- R01 EY015422-04/EY/NEI NIH HHS/ -- R01 EY018350/EY/NEI NIH HHS/ -- R01 EY018350-02/EY/NEI NIH HHS/ -- R01 EY018836/EY/NEI NIH HHS/ -- R01 EY018836-02/EY/NEI NIH HHS/ -- England -- Nature. 2009 Jul 9;460(7252):225-30. doi: 10.1038/nature08151. Epub 2009 Jun 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ophthalmology & Visual Science, University of Kentucky, Lexington, Kentucky 40506, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19525930" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Movement ; Cell Proliferation ; Cells, Cultured ; Chemokine CCL11/antagonists & inhibitors/metabolism ; Chemokine CCL24/antagonists & inhibitors/metabolism ; Chemokines, CC/antagonists & inhibitors/metabolism ; Choroid/blood supply/cytology/metabolism ; Choroidal Neovascularization/diagnosis/metabolism ; Disease Models, Animal ; Endothelial Cells/cytology/metabolism ; Humans ; Inflammation ; Leukocytes ; Ligands ; Macular Degeneration/*diagnosis/metabolism/*therapy ; Mice ; Mice, Inbred C57BL ; Quantum Dots ; Receptors, CCR3/analysis/*antagonists & ; inhibitors/genetics/immunology/*metabolism ; Retina/drug effects/pathology ; Vascular Endothelial Growth Factor A/antagonists & inhibitors/immunology
    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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    The dynamic genome of Hydra (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-03-17
    Description: The freshwater cnidarian Hydra was first described in 1702 and has been the object of study for 300 years. Experimental studies of Hydra between 1736 and 1744 culminated in the discovery of asexual reproduction of an animal by budding, the first description of regeneration in an animal, and successful transplantation of tissue between animals. Today, Hydra is an important model for studies of axial patterning, stem cell biology and regeneration. Here we report the genome of Hydra magnipapillata and compare it to the genomes of the anthozoan Nematostella vectensis and other animals. The Hydra genome has been shaped by bursts of transposable element expansion, horizontal gene transfer, trans-splicing, and simplification of gene structure and gene content that parallel simplification of the Hydra life cycle. We also report the sequence of the genome of a novel bacterium stably associated with H. magnipapillata. Comparisons of the Hydra genome to the genomes of other animals shed light on the evolution of epithelia, contractile tissues, developmentally regulated transcription factors, the Spemann-Mangold organizer, pluripotency genes and the neuromuscular junction.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4479502/" 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/PMC4479502/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chapman, Jarrod A -- Kirkness, Ewen F -- Simakov, Oleg -- Hampson, Steven E -- Mitros, Therese -- Weinmaier, Thomas -- Rattei, Thomas -- Balasubramanian, Prakash G -- Borman, Jon -- Busam, Dana -- Disbennett, Kathryn -- Pfannkoch, Cynthia -- Sumin, Nadezhda -- Sutton, Granger G -- Viswanathan, Lakshmi Devi -- Walenz, Brian -- Goodstein, David M -- Hellsten, Uffe -- Kawashima, Takeshi -- Prochnik, Simon E -- Putnam, Nicholas H -- Shu, Shengquiang -- Blumberg, Bruce -- Dana, Catherine E -- Gee, Lydia -- Kibler, Dennis F -- Law, Lee -- Lindgens, Dirk -- Martinez, Daniel E -- Peng, Jisong -- Wigge, Philip A -- Bertulat, Bianca -- Guder, Corina -- Nakamura, Yukio -- Ozbek, Suat -- Watanabe, Hiroshi -- Khalturin, Konstantin -- Hemmrich, Georg -- Franke, Andre -- Augustin, Rene -- Fraune, Sebastian -- Hayakawa, Eisuke -- Hayakawa, Shiho -- Hirose, Mamiko -- Hwang, Jung Shan -- Ikeo, Kazuho -- Nishimiya-Fujisawa, Chiemi -- Ogura, Atshushi -- Takahashi, Toshio -- Steinmetz, Patrick R H -- Zhang, Xiaoming -- Aufschnaiter, Roland -- Eder, Marie-Kristin -- Gorny, Anne-Kathrin -- Salvenmoser, Willi -- Heimberg, Alysha M -- Wheeler, Benjamin M -- Peterson, Kevin J -- Bottger, Angelika -- Tischler, Patrick -- Wolf, Alexander -- Gojobori, Takashi -- Remington, Karin A -- Strausberg, Robert L -- Venter, J Craig -- Technau, Ulrich -- Hobmayer, Bert -- Bosch, Thomas C G -- Holstein, Thomas W -- Fujisawa, Toshitaka -- Bode, Hans R -- David, Charles N -- Rokhsar, Daniel S -- Steele, Robert E -- P 21108/Austrian Science Fund FWF/Austria -- R24 RR015088/RR/NCRR NIH HHS/ -- England -- Nature. 2010 Mar 25;464(7288):592-6. doi: 10.1038/nature08830. Epub 2010 Mar 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉US Department of Energy Joint Genome Institute, Walnut Creek, California 94598, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20228792" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anthozoa/genetics ; Comamonadaceae/genetics ; DNA Transposable Elements/genetics ; Gene Transfer, Horizontal/genetics ; Genome/*genetics ; Genome, Bacterial/genetics ; Hydra/*genetics/microbiology/ultrastructure ; Molecular Sequence Data ; Neuromuscular Junction/ultrastructure
    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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    Neurotransmitter release from synaptotagmin-deficient clonal variants of PC12 cells (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-06-26
    Description: Synaptotagmin (p65) is an abundant synaptic vesicle protein of neurons and contains regions similar to the regulatory domain of protein kinase C. These domains are thought to be involved in calcium-dependent interaction with membrane phospholipids during exocytosis. To assess the functional role of synaptotagmin, synaptotagmin-deficient clonal variants of PC12 cells were isolated. All of the variant cells released catecholamine and adenosine triphosphate in response to elevated intracellular concentrations of calcium, which suggests that synaptotagmin is not essential for secretion of catecholamine and adenosine triphosphate from PC12 cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shoji-Kasai, Y -- Yoshida, A -- Sato, K -- Hoshino, T -- Ogura, A -- Kondo, S -- Fujimoto, Y -- Kuwahara, R -- Kato, R -- Takahashi, M -- New York, N.Y. -- Science. 1992 Jun 26;256(5065):1821-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mitsubishi Kasel Institute of Life Sciences, Tokyo, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1352065" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/secretion ; Animals ; Blotting, Northern ; Blotting, Western ; Calcium/pharmacology ; *Calcium-Binding Proteins ; Cerebellum/metabolism ; Dopamine/secretion ; Ionomycin/pharmacology ; Membrane Glycoproteins/*physiology ; Nerve Tissue Proteins/*physiology ; Neurotransmitter Agents/*secretion ; PC12 Cells ; Prosencephalon/metabolism ; RNA, Messenger/analysis ; Rats ; Synaptotagmin I ; Synaptotagmins
    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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    Identification of a primary target of thalidomide teratogenicity (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-03-13
    Description: Half a century ago, thalidomide was widely prescribed to pregnant women as a sedative but was found to be teratogenic, causing multiple birth defects. Today, thalidomide is still used in the treatment of leprosy and multiple myeloma, although how it causes limb malformation and other developmental defects is unknown. Here, we identified cereblon (CRBN) as a thalidomide-binding protein. CRBN forms an E3 ubiquitin ligase complex with damaged DNA binding protein 1 (DDB1) and Cul4A that is important for limb outgrowth and expression of the fibroblast growth factor Fgf8 in zebrafish and chicks. Thalidomide initiates its teratogenic effects by binding to CRBN and inhibiting the associated ubiquitin ligase activity. This study reveals a basis for thalidomide teratogenicity and may contribute to the development of new thalidomide derivatives without teratogenic activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ito, Takumi -- Ando, Hideki -- Suzuki, Takayuki -- Ogura, Toshihiko -- Hotta, Kentaro -- Imamura, Yoshimasa -- Yamaguchi, Yuki -- Handa, Hiroshi -- New York, N.Y. -- Science. 2010 Mar 12;327(5971):1345-50. doi: 10.1126/science.1177319.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Integrated Research Institute, Tokyo Institute of Technology, Yokohama 226-8503, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20223979" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carrier Proteins/metabolism ; Chick Embryo ; Cullin Proteins/metabolism ; DNA-Binding Proteins/*metabolism ; Embryo, Nonmammalian/drug effects ; Embryonic Development/drug effects ; Fibroblast Growth Factors/genetics/metabolism ; Forelimb/abnormalities/embryology ; Gene Expression Regulation, Developmental ; HeLa Cells ; Humans ; Mutant Proteins/metabolism ; Peptide Hydrolases/genetics/*metabolism ; Teratogens/metabolism/*toxicity ; Thalidomide/metabolism/*toxicity ; Ubiquitin-Protein Ligases/antagonists & inhibitors/*metabolism ; Ubiquitination ; Zebrafish/embryology/genetics ; Zebrafish Proteins/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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  • 9
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    Epigenetic regulation of mouse sex determination by the histone demethylase Jmjd1a (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-09-07
    Description: Developmental gene expression is defined through cross-talk between the function of transcription factors and epigenetic status, including histone modification. Although several transcription factors play crucial roles in mammalian sex determination, how epigenetic regulation contributes to this process remains unknown. We observed male-to-female sex reversal in mice lacking the H3K9 demethylase Jmjd1a and found that Jmjd1a regulates expression of the mammalian Y chromosome sex-determining gene Sry. Jmjd1a directly and positively controls Sry expression by regulating H3K9me2 marks. These studies reveal a pivotal role of histone demethylation in mammalian sex determination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kuroki, Shunsuke -- Matoba, Shogo -- Akiyoshi, Mika -- Matsumura, Yasuko -- Miyachi, Hitoshi -- Mise, Nathan -- Abe, Kuniya -- Ogura, Atsuo -- Wilhelm, Dagmar -- Koopman, Peter -- Nozaki, Masami -- Kanai, Yoshiakira -- Shinkai, Yoichi -- Tachibana, Makoto -- New York, N.Y. -- Science. 2013 Sep 6;341(6150):1106-9. doi: 10.1126/science.1239864.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Experimental Research Center for Infectious Diseases, Institute for Virus Research, Kyoto University, 53 Shogoin, Kawara-cho, Sakyo-ku, Kyoto, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24009392" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Epididymis/abnormalities ; *Epigenesis, Genetic ; Female ; *Gene Expression Regulation, Developmental ; Histones/*metabolism ; Jumonji Domain-Containing Histone Demethylases/genetics/*metabolism ; Male ; Methylation ; Mice ; Mice, Mutant Strains ; Mice, Transgenic ; Ovary/abnormalities/enzymology ; *Protein Processing, Post-Translational ; Sex Determination Processes/*genetics ; Testis/abnormalities/enzymology ; Uterus/abnormalities
    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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    Nod2-dependent regulation of innate and adaptive immunity in the intestinal tract (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-02-05
    Description: The gene encoding the Nod2 protein is frequently mutated in Crohn's disease (CD) patients, although the physiological function of Nod2 in the intestine remains elusive. Here we show that protective immunity mediated by Nod2 recognition of bacterial muramyl dipeptide is abolished in Nod2-deficient mice. These animals are susceptible to bacterial infection via the oral route but not through intravenous or peritoneal delivery. Nod2 is required for the expression of a subgroup of intestinal anti-microbial peptides, known as cryptdins. The Nod2 protein is thus a critical regulator of bacterial immunity within the intestine, providing a possible mechanism for Nod2 mutations in CD.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kobayashi, Koichi S -- Chamaillard, Mathias -- Ogura, Yasunori -- Henegariu, Octavian -- Inohara, Naohiro -- Nunez, Gabriel -- Flavell, Richard A -- New York, N.Y. -- Science. 2005 Feb 4;307(5710):731-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Immunobiology, 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/15692051" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylmuramyl-Alanyl-Isoglutamine/*immunology ; Animals ; *Antibody Formation ; Female ; Gene Expression ; Gene Targeting ; Ileum/*immunology/microbiology ; *Immunity, Innate ; Immunity, Mucosal ; Immunoglobulins/biosynthesis ; Interleukins/biosynthesis ; Intestinal Diseases/immunology/microbiology ; Intestinal Mucosa/immunology/microbiology ; Intracellular Signaling Peptides and Proteins/*physiology ; Ligands ; Lipopolysaccharides/toxicity ; Listeria monocytogenes/growth & development/immunology/isolation & purification ; Listeriosis/*immunology/microbiology ; Liver/microbiology ; Macrophages/immunology ; Male ; Membrane Glycoproteins/physiology ; Mice ; Nod2 Signaling Adaptor Protein ; Oligonucleotide Array Sequence Analysis ; Protein Precursors/biosynthesis/genetics ; Receptors, Cell Surface/physiology ; Serum Albumin/immunology ; Signal Transduction ; Spleen/microbiology ; Toll-Like Receptors ; Tumor Necrosis Factor-alpha/biosynthesis ; alpha-Defensins/*biosynthesis/genetics
    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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