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  • 1
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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
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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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
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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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
    Published by American Association for the Advancement of Science (AAAS)
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  • 4
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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
    Published by Nature Publishing Group (NPG)
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  • 5
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    Faithful expression of imprinted genes in cloned mice (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-01-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Inoue, Kimiko -- Kohda, Takashi -- Lee, Jiyoung -- Ogonuki, Narumi -- Mochida, Keiji -- Noguchi, Yoko -- Tanemura, Kentaro -- Kaneko-Ishino, Tomoko -- Ishino, Fumitoshi -- Ogura, Atsuo -- New York, N.Y. -- Science. 2002 Jan 11;295(5553):297.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Veterinary Science, National Institute of Infectious Diseases, 1-23-1, Toyama, Shinjuku, Tokyo 162-8640, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11786635" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cloning, Organism ; Embryo Transfer ; Embryonic and Fetal Development ; Female ; Fetus/*metabolism ; Fibroblasts ; *Gene Expression ; Gene Expression Profiling ; *Genomic Imprinting ; Male ; Mice ; Mice, Inbred C57BL ; Nuclear Transfer Techniques ; Ovarian Follicle/cytology ; Placenta/*metabolism ; RNA, Messenger/genetics/metabolism ; Sertoli Cells
    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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