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1. Full Text Zika Virus Disrupts Neural Progenitor Development and Leads to Microcephaly in Mice
by Li, Cui and Xu, Dan and Xu, Zhiheng and Ye, Qing and Hong, Shuai and Jiang, Yisheng and Liu, Xinyi and Zhang, Nana and Shi, Lei and Qin, Cheng-Feng
Cell Stem Cell, ISSN 1934-5909, 07/2016, Volume 19, Issue 1, pp. 120 - 126
The link between Zika virus (ZIKV) infection and microcephaly has raised urgent global alarm. The historical African ZIKV MR766 was recently shown to infect... 
STEM | CELL & TISSUE ENGINEERING | CELL BIOLOGY | Cell Cycle - genetics | Brain - embryology | Microcephaly - genetics | Brain - virology | Immunity | Microcephaly - virology | Cell Differentiation - genetics | Zika Virus Infection - virology | Microcephaly - immunology | Cell Death - genetics | Microcephaly - pathology | Embryo, Mammalian - virology | Cell Lineage - genetics | Embryo, Mammalian - pathology | Zika Virus Infection - pathology | Neural Stem Cells - virology | Zika Virus - physiology | Gene Expression Regulation | Neural Stem Cells - pathology | Mice, Inbred ICR | Animals | Zika Virus Infection - genetics | Virus Replication | Embryo, Mammalian - immunology | Brain - pathology | Zika Virus Infection - immunology | Index Medicus
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2. Full Text Correction of a pathogenic gene mutation in human embryos
by Ma, Hong and Marti-Gutierrez, Nuria and Park, Sang-Wook and Wu, Jun and Lee, Yeonmi and Suzuki, Keiichiro and Koski, Amy and Ji, Dongmei and Hayama, Tomonari and Ahmed, Riffat and Darby, Hayley and Van Dyken, Crystal and Li, Ying and Kang, Eunju and Park, A.-Reum and Kim, Daesik and Kim, Sang-Tae and Gong, Jianhui and Gu, Ying and Xu, Xun and Battaglia, David and Krieg, Sacha A and Lee, David M and Wu, Diana H and Wolf, Don P and Heitner, Stephen B and Belmonte, Juan Carlos Izpisua and Amato, Paula and Kim, Jin-Soo and Kaul, Sanjiv and Mitalipov, Shoukhrat
Nature, ISSN 0028-0836, 08/2017, Volume 548, Issue 7668, pp. 413 - 419
Genome editing has potential for the targeted correction of germline mutations. Here we describe the correction of the heterozygous MYBPC3 mutation in human... 
PRIMATE EMBRYOS | HUMAN-CELLS | DNA | ZYGOTES | MULTIDISCIPLINARY SCIENCES | MOUSE | DIGENOME-SEQ | RNA-GUIDED ENDONUCLEASES | CRISPR-CAS9 | CAS9 | NUCLEASES | Gene Targeting | Embryo, Mammalian - pathology | Recombinational DNA Repair - genetics | Humans | Blastocyst - metabolism | Zygote - metabolism | Templates, Genetic | Male | Blastocyst - pathology | Mutation - genetics | DNA Breaks, Double-Stranded | Genetic Complementation Test | Embryo, Mammalian - metabolism | Zygote - pathology | Carrier Proteins - genetics | Homozygote | Cell Division | S Phase | Alleles | Adult | Heterozygote | Mosaicism | Clustered Regularly Interspaced Short Palindromic Repeats - genetics | Gene Editing - methods | Care and treatment | Gene targeting | Gene mutations | Genetic aspects | Genetic engineering | Human embryo | Methods | Heart failure | CRISPR | Cardiomyopathy | Therapeutic applications | Genomics | Homology | Genomes | Double-strand break repair | Embryos | DNA repair | Genetic screening | Proteins | Point mutation | Cell cycle | Mutation | Gene therapy | Deoxyribonucleic acid--DNA | Index Medicus
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3. Full Text Upregulated function of mitochondria-associated ER membranes in Alzheimer disease
by Area-Gomez, E and Del Carmen Lara Castillo, M and Tambini, M.D and Guardia-Laguarta, C and Groof, A.J.C. de and Maa, M and Ikenouchi, J and Umeda, M and Bird, T.D and Sturley, S.L and Schon, E.A
EMBO Journal, ISSN 0261-4189, 2012, Volume 31, Issue 21, pp. 4106 - 4123
Alzheimer disease (AD) is associated with aberrant processing of the amyloid precursor protein (APP) by gamma-secretase, via an unknown mechanism. We recently... 
MAM | APP | cholesterol | phospholipids | presenilin | BIOCHEMISTRY & MOLECULAR BIOLOGY | SUBCELLULAR-LOCALIZATION | PRESENILIN 2 | AMYLOID PRECURSOR PROTEIN | BLOOD MONONUCLEAR-CELLS | CELL BIOLOGY | C-TERMINAL FRAGMENT | LIPID RAFTS | A-BETA | GAMMA-SECRETASE ACTIVITY | ENDOPLASMIC-RETICULUM | INTRACELLULAR DOMAIN | RNA, Small Interfering - genetics | Membrane Microdomains - metabolism | Humans | Endoplasmic Reticulum - metabolism | Presenilin-1 - physiology | Presenilin-2 - physiology | Embryo, Mammalian - metabolism | Alzheimer Disease - pathology | Endoplasmic Reticulum - pathology | Presenilin-1 - antagonists & inhibitors | Real-Time Polymerase Chain Reaction | Fibroblasts - metabolism | Embryo, Mammalian - pathology | Presenilin-2 - antagonists & inhibitors | RNA, Messenger - genetics | Cells, Cultured | Mitochondria - metabolism | Mitochondria - pathology | Fibroblasts - pathology | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | Mice, Knockout | Mitochondrial Membranes - metabolism | Animals | Mitochondrial Membranes - pathology | Alzheimer Disease - metabolism | Mice | Subcellular Fractions | Membrane Microdomains - pathology | Proteins | Membranes | Mitochondria | Pathogenesis | Lipids | Alzheimers disease | Gene expression | Molecular biology | Index Medicus
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4. Full Text High Fat Diet Induced Developmental Defects in the Mouse: Oocyte Meiotic Aneuploidy and Fetal Growth Retardation/Brain Defects
by Luzzo, Kerri M and Wang, Qiang and Purcell, Scott H and Chi, Maggie and Jimenez, Patricia T and Grindler, Natalia and Schedl, Tim and Moley, Kelle H
PLoS ONE, ISSN 1932-6203, 11/2012, Volume 7, Issue 11, pp. e49217 - e49217
Background: Maternal obesity is associated with poor outcomes across the reproductive spectrum including infertility, increased time to pregnancy, early... 
DIABETES-MELLITUS | OXIDATIVE STRESS | MATERNAL OBESITY | MULTIDISCIPLINARY SCIENCES | MITOCHONDRIA | BODY-MASS INDEX | PREPREGNANCY | RISK | DISORDERS | OCCURS | PREGNANCY | Oocytes - ultrastructure | Uterus - pathology | Brain - embryology | Humans | Diet, High-Fat - adverse effects | Aneuploidy | Brain - abnormalities | Oocytes - pathology | Mitochondria - ultrastructure | Cumulus Cells - ultrastructure | Cumulus Cells - metabolism | Female | Cumulus Cells - pathology | Embryo, Mammalian - pathology | Oocytes - metabolism | Fetal Development | Organ Size | Feeding Behavior | Meiosis | Mitochondria - pathology | Embryo, Mammalian - abnormalities | Fetal Growth Retardation - pathology | Mice, Inbred ICR | Obesity - pathology | Pregnancy | Phenotype | Animals | Models, Biological | Placenta - pathology | Brain - pathology | Mice | Chromosomes, Mammalian - metabolism | Women | Complications and side effects | Obesity | Embryonic development | Genetic disorders | Diet | Growth | Fetus | Health aspects | Neonates | Brain | Oxidative stress | Growth rate | Pregnancy complications | Abortion | Oocytes | Defects | High fat diet | Mitochondria | Uterus | Rodents | Complications | Abnormalities | Fetuses | Gynecology | Metabolism | Embryos | Obstetrics | Insulin | Medicine | Embryo transfer | Brain research | Maternal effects | Infertility | Weight reduction | Diabetes | Laboratory animals | Females | Apoptosis | Index Medicus
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5. Full Text Caspase 8 inhibits programmed necrosis by processing CYLD
by O'Donnell, Marie Anne and Perez-Jimenez, Eva and Oberst, Andrew and Ng, Aylwin and Massoumi, Ramin and Xavier, Ramnik and Green, Douglas R and Ting, Adrian T
Nature Cell Biology, ISSN 1465-7392, 12/2011, Volume 13, Issue 12, pp. 1437 - 1442
Caspase 8 initiates apoptosis downstream of TNF death receptors by undergoing autocleavage and processing the executioner caspase 3 (ref. 1). However, the... 
UBIQUITINATION | APOPTOSIS | REGULATOR | PHAGOCYTOSIS | RECEPTOR-INTERACTING PROTEIN | ALPHA | IDENTIFICATION | PHOSPHATIDYLSERINE | RIP1 | CELL-DEATH | CELL BIOLOGY | Fibroblasts - enzymology | Tumor Suppressor Proteins - metabolism | Embryo, Mammalian - pathology | Deubiquitinating Enzyme CYLD | Jurkat Cells | Humans | Protein Processing, Post-Translational - genetics | Caspase 8 - metabolism | Cells, Cultured | Cell Survival - genetics | Signal Transduction - genetics | Fibroblasts - pathology | Necrosis | Caspase 8 - genetics | Animals | Embryo, Mammalian - cytology | Tumor Suppressor Proteins - genetics | HEK293 Cells | Female | Embryo, Mammalian - enzymology | Fibroblasts - cytology | Mice | Care and treatment | Genetic aspects | Research | Diagnosis | Risk factors | Apoptosis | Index Medicus
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6. Full Text Essential role of the zinc finger transcription factor Casz1 for mammalian cardiac morphogenesis and development
by Liu, Zhihui and Li, Wenling and Ma, Xuefei and Ding, Nancy and Spallotta, Francesco and Southon, Eileen and Tessarollo, Lino and Gaetano, Carlo and Mukouyama, Yoh-Suke and Thiele, Carol J
Journal of Biological Chemistry, ISSN 0021-9258, 10/2014, Volume 289, Issue 43, pp. 29801 - 29816
Background: The CASZ1 (castor zinc finger 1) gene localizes to chromosome 1p36, and 1p36 deletion syndrome is related to congenital heart disease (CHD).... 
Cardiovascular | BIOCHEMISTRY & MOLECULAR BIOLOGY | CARDIOMYOPATHY | CASTOR | Heart Development | MYOPATHIES | GENE | CONGENITAL HEART-DISEASE | GROWTH | Development | Heart Failure | CELL-CYCLE | MUTATIONS | DIFFERENTIATION | EXPRESSION | Cardiac Development | Cell Cycle - genetics | Cell Proliferation | Lymphatic System - pathology | Heart - embryology | Humans | Transcription Factors - deficiency | Sarcomeres - pathology | Gene Expression Regulation, Developmental | Myocardium - metabolism | Reproducibility of Results | Zinc Fingers | Embryo, Mammalian - pathology | Morphogenesis - genetics | Sarcomeres - metabolism | Embryonic Development - genetics | Myocardium - pathology | Transcription Factors - genetics | Embryo, Mammalian - abnormalities | Transcription Factors - metabolism | Myocytes, Cardiac - pathology | Phenotype | Animals | Models, Biological | Myocytes, Cardiac - metabolism | Mice | Lymphatic System - abnormalities | Lymphatic System - embryology | Index Medicus | Developmental Biology
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7. Full Text Mammalian tumor xenografts induce neovascularization in zebrafish embryos
by Nicoli, Stefania and Ribatti, Domenico and Cotelli, Franco and Presta, Marco
Cancer Research, ISSN 0008-5472, 04/2007, Volume 67, Issue 7, pp. 2927 - 2931
The zebrafish (Danio rerio)/tumor xenograft model represents a powerful new model system in cancer. Here, we describe a novel exploitation of the zebrafish... 
CADHERIN | FIBROBLAST GROWTH FACTOR-2 | ANGIOGENESIS | ONCOLOGY | EXPRESSION | Neoplasm Transplantation | Embryo, Mammalian - pathology | Animals, Genetically Modified | Endothelial Cells - metabolism | Embryo, Mammalian - blood supply | Humans | Fibroblast Growth Factor 2 - biosynthesis | Angiogenesis Inhibitors - pharmacology | Neoplasms - blood supply | Transplantation, Heterologous | Xenograft Model Antitumor Assays - methods | Zebrafish - embryology | Zebrafish - genetics | Neoplasms - drug therapy | Animals | Neovascularization, Pathologic - drug therapy | Embryo, Nonmammalian | Cell Line, Tumor | Neovascularization, Pathologic - genetics | Mice | Endothelial Cells - pathology | Index Medicus
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8. Full Text A mouse model of ATR-Seckel shows embryonic replicative stress and accelerated aging
by Soria, Rebeca and Mulero, Francisca and Montaña, Maria F and Fernandez-Capetillo, Oscar and Murga, Matilde and Bunting, Samuel and McKinnon, Peter J and Lee, Youngsoo and Cañamero, Marta and Nussenzweig, Andre
Nature Genetics, ISSN 1061-4036, 08/2009, Volume 41, Issue 8, pp. 891 - 898
Although DNA damage is considered a driving force for aging, the nature of the damage that arises endogenously remains unclear. Replicative stress, a source of... 
CHROMOSOME INSTABILITY | GENE ATR | DNA-DAMAGE RESPONSE | HEMATOPOIETIC STEM-CELLS | GENETICS & HEREDITY | LEADS | CHECKPOINT | DEFICIENT MICE | ATAXIA-TELANGIECTASIA | AGE | P53 | Abnormalities, Multiple - pathology | Embryo, Mammalian - drug effects | Protein-Serine-Threonine Kinases - deficiency | Fibroblasts - enzymology | Apoptosis - drug effects | DNA Replication - drug effects | Humans | Aging - drug effects | Brain - enzymology | Embryo, Mammalian - metabolism | DNA-Binding Proteins - metabolism | Aging - genetics | Progeria - embryology | DNA-Activated Protein Kinase - metabolism | Progeria - pathology | Embryo, Mammalian - enzymology | Stress, Physiological - drug effects | Abnormalities, Multiple - genetics | Protein-Serine-Threonine Kinases - metabolism | Disease Models, Animal | DNA Repair - drug effects | Embryo, Mammalian - pathology | Progeria - enzymology | Cell Cycle Proteins - metabolism | Tumor Suppressor Protein p53 - metabolism | Nuclear Proteins - metabolism | Ataxia Telangiectasia Mutated Proteins | Fibroblasts - pathology | Tumor Suppressor Protein p53 - deficiency | Syndrome | Aging - pathology | Phenotype | Animals | Fibroblasts - drug effects | Alleles | Abnormalities, Multiple - enzymology | Brain - pathology | Mice | Protein Kinase Inhibitors - pharmacology | DNA Damage | Embryonic development | Usage | Control | Animal models in research | DNA damage | Causes of | Physiological aspects | Genetic aspects | Research | Proteins | Dwarfism | Studies | Genotype & phenotype | Cell cycle | Kinases | Molecular biology | Cancer | Index Medicus
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9. Full Text RNAi screens in mice identify physiological regulators of oncogenic growth
by Beronja, Slobodan and Janki, Peter and Heller, Evan and Lien, Wen-Hui and Keyes, Brice E and Oshimori, Naoki and Fuchs, Elaine
Nature, ISSN 0028-0836, 2013, Volume 501, Issue 7466, pp. 185 - 190
Tissue growth is the multifaceted outcome of a cell's intrinsic capabilities and its interactions with the surrounding environment. Decoding these complexities... 
CANCER-CELLS | STEM-CELLS | HOMEOSTASIS | ACTIVATION | TGF-BETA | EPIDERMAL DIFFERENTIATION | MULTIDISCIPLINARY SCIENCES | HAIR FOLLICLE MORPHOGENESIS | LEUKEMIA | BETA-CATENIN | MOUSE SKIN | Neoplasms - metabolism | Cell Proliferation | Humans | Genome - genetics | Male | Neoplasm Proteins - metabolism | Wnt Proteins - metabolism | Carcinogenesis - metabolism | DNA-Binding Proteins - deficiency | Embryo, Mammalian - metabolism | Oncogene Protein p21(ras) - metabolism | DNA-Binding Proteins - metabolism | Hyperplasia - genetics | Neoplasms - genetics | RNA Interference | Time Factors | Female | Neoplasm Proteins - genetics | Hyperplasia - metabolism | Wnt Signaling Pathway | Skin Neoplasms - pathology | Epidermis - metabolism | Oncogenes - genetics | Epidermis - pathology | Reproducibility of Results | Embryo, Mammalian - pathology | Signal Transduction | beta Catenin - deficiency | Carcinogenesis - genetics | DNA-Binding Proteins - genetics | Cell Adhesion | beta Catenin - metabolism | beta Catenin - genetics | Skin Neoplasms - metabolism | Carcinogenesis - pathology | Hyperplasia - pathology | Animals | Embryo, Mammalian - embryology | Skin Neoplasms - genetics | Epidermis - embryology | Mice | Neoplasm Proteins - deficiency | Neoplasms - pathology | Physiological aspects | Genome-wide association studies | Cell physiology | Research | Carcinogenesis | Proteins | Keratin | Rodents | Cyclin-dependent kinases | Cloning | Genomes | Kinases | Gene expression | Embryos | Cancer | Index Medicus
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10. Full Text Tet1 controls meiosis by regulating meiotic gene expression
by Yamaguchi, Shinpei and Hong, Kwonho and Liu, Rui and Shen, Li and Inoue, Azusa and Diep, Dinh and Zhang, Kun and Zhang, Yi
Nature, ISSN 0028-0836, 12/2012, Volume 492, Issue 7429, pp. 443 - 447
Meiosis is a germ-cell-specific cell division process through which haploid gametes are produced for sexual reproduction(1). Before the initiation of meiosis,... 
DNA METHYLATION | MAMMALIAN DNA | 5-METHYLCYTOSINE | MULTIDISCIPLINARY SCIENCES | MOUSE | MICE | PLURIPOTENCY | EPIGENETIC EVENTS | SPECIFICATION | PRIMORDIAL GERM-CELLS | 5-CARBOXYLCYTOSINE | Animal experimentation | Usage | Germ cells | Physiological aspects | Meiosis | Research | Gene expression | Methylation | Proteins | Studies | DNA methylation | Genetics | Amino acids | Mass spectrometry | Apoptosis | Defects | Index Medicus
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