BMC Neuroscience, ISSN 1471-2202, 12/2007, Volume 8, Issue 1, pp. 108 - 108
Background: Nitric oxide synthase 2 (NOS2) contributes to neural death in some settings, but its role in glaucoma remains controversial. NOS2 is implicated in...
RETINAL GANGLION-CELLS | OCULAR HYPERTENSION TREATMENT | IRIS ATROPHY | OPEN-ANGLE GLAUCOMA | RISK-FACTORS | AXONAL-TRANSPORT | NERVE HEAD ASTROCYTES | PIGMENTARY GLAUCOMA | INTRAOCULAR-PRESSURE ELEVATION | NEUROSCIENCES | INHERITED GLAUCOMA | Intraocular Pressure | Optic Nerve Diseases - pathology | Retinal Diseases - enzymology | Animals | Optic Disk - enzymology | Retinal Diseases - pathology | Mice, Inbred DBA | Glaucoma - pathology | Mice | Glaucoma - metabolism | Optic Nerve Diseases - enzymology | Optic Disk - pathology | Disease Models, Animal | Nitric Oxide Synthase Type II - metabolism | Glaucoma | Polymerase chain reaction | Aminoguanidine | Care and treatment | Dosage and administration | Genetic aspects | Diagnosis | Health aspects
RETINAL GANGLION-CELLS | OCULAR HYPERTENSION TREATMENT | IRIS ATROPHY | OPEN-ANGLE GLAUCOMA | RISK-FACTORS | AXONAL-TRANSPORT | NERVE HEAD ASTROCYTES | PIGMENTARY GLAUCOMA | INTRAOCULAR-PRESSURE ELEVATION | NEUROSCIENCES | INHERITED GLAUCOMA | Intraocular Pressure | Optic Nerve Diseases - pathology | Retinal Diseases - enzymology | Animals | Optic Disk - enzymology | Retinal Diseases - pathology | Mice, Inbred DBA | Glaucoma - pathology | Mice | Glaucoma - metabolism | Optic Nerve Diseases - enzymology | Optic Disk - pathology | Disease Models, Animal | Nitric Oxide Synthase Type II - metabolism | Glaucoma | Polymerase chain reaction | Aminoguanidine | Care and treatment | Dosage and administration | Genetic aspects | Diagnosis | Health aspects
Journal Article
Cell, ISSN 0092-8674, 2007, Volume 131, Issue 6, pp. 1164 - 1178
During development, the formation of mature neural circuits requires the selective elimination of inappropriate synaptic connections. Here we show that C1q,...
HUMDISEASE | MOLNEURO | CELLIMMUNO | DBA/2J MICE | CELLS | C1Q | ACTIVATION | VISUAL-CORTEX | ALZHEIMERS-DISEASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | CENTRAL-NERVOUS-SYSTEM | GLAUCOMA | EXPRESSION | PLASTICITY | CELL BIOLOGY | Animals, Newborn | Up-Regulation | Retina - metabolism | Complement Activation | Complement C3 - metabolism | Complement C1q - genetics | Geniculate Bodies - physiology | RNA, Messenger - metabolism | Retinal Ganglion Cells - metabolism | Complement C1q - metabolism | Long-Term Synaptic Depression | Mice, Knockout | Central Nervous System - physiology | Retina - physiology | Animals | Mice, Inbred DBA | Mice | Glaucoma - metabolism | Synapses | Astrocytes - metabolism | Glaucoma | Ophthalmology | Neurons | Analysis
HUMDISEASE | MOLNEURO | CELLIMMUNO | DBA/2J MICE | CELLS | C1Q | ACTIVATION | VISUAL-CORTEX | ALZHEIMERS-DISEASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | CENTRAL-NERVOUS-SYSTEM | GLAUCOMA | EXPRESSION | PLASTICITY | CELL BIOLOGY | Animals, Newborn | Up-Regulation | Retina - metabolism | Complement Activation | Complement C3 - metabolism | Complement C1q - genetics | Geniculate Bodies - physiology | RNA, Messenger - metabolism | Retinal Ganglion Cells - metabolism | Complement C1q - metabolism | Long-Term Synaptic Depression | Mice, Knockout | Central Nervous System - physiology | Retina - physiology | Animals | Mice, Inbred DBA | Mice | Glaucoma - metabolism | Synapses | Astrocytes - metabolism | Glaucoma | Ophthalmology | Neurons | Analysis
Journal Article
Nature, ISSN 0028-0836, 09/2016, Volume 537, Issue 7621, pp. 508 - 514
Approximately one-third of all mammalian genes are essential for life. Phenotypes resulting from knockouts of these genes in mice have provided tremendous...
MICRO-CT | MULTIDISCIPLINARY SCIENCES | DISEASE | GENOME-WIDE | MAMMALIAN GENE-FUNCTION | SCREENS | GLYCOGENIN-1 DEFICIENCY | IDENTIFICATION | EXPRESSION | MOUSE EMBRYO | RESOURCE | Genetic research | Phenotype | Research | High-throughput screening (Biochemical assaying) | Methods | Genotype & phenotype | Disease | Developmental biology | Genes | Genomes | Mutation | Embryos | knockout | embryonic lethal | mouse | KOMP | IMPC | EUCOMM
MICRO-CT | MULTIDISCIPLINARY SCIENCES | DISEASE | GENOME-WIDE | MAMMALIAN GENE-FUNCTION | SCREENS | GLYCOGENIN-1 DEFICIENCY | IDENTIFICATION | EXPRESSION | MOUSE EMBRYO | RESOURCE | Genetic research | Phenotype | Research | High-throughput screening (Biochemical assaying) | Methods | Genotype & phenotype | Disease | Developmental biology | Genes | Genomes | Mutation | Embryos | knockout | embryonic lethal | mouse | KOMP | IMPC | EUCOMM
Journal Article
RNA, ISSN 1355-8382, 2017, Volume 23, Issue 4, pp. 457 - 465
Editing of the human and murine ApoB mRNA by APOBEC1, the catalytic enzyme of the protein complex that catalyzes C-to-U RNA editing, creates an internal stop...
APOBEC1 | RNA editing | ACF | APOB | Kidney | PROTEIN | BIOCHEMISTRY & MOLECULAR BIOLOGY | B MESSENGER-RNA | IDENTIFICATION | kidney | ENZYME | GENE | MOLECULAR-CLONING | MICE | BINDING | EXPRESSION | REVEALS | Apolipoproteins B - metabolism | RNA Editing | Liver - metabolism | RNA, Messenger - genetics | APOBEC-1 Deaminase - genetics | Water-Electrolyte Imbalance | Male | APOBEC-1 Deaminase - metabolism | Apolipoproteins B - genetics | Kidney Glomerulus - pathology | Organ Specificity | RNA, Messenger - metabolism | Mice, Knockout | Heterogeneous-Nuclear Ribonucleoproteins - genetics | Heterogeneous-Nuclear Ribonucleoproteins - deficiency | Animals | Protein Isoforms - metabolism | Base Sequence | Sex Factors | Kidney Glomerulus - metabolism | Female | Mice | Intestine, Small - metabolism | Protein Isoforms - genetics
APOBEC1 | RNA editing | ACF | APOB | Kidney | PROTEIN | BIOCHEMISTRY & MOLECULAR BIOLOGY | B MESSENGER-RNA | IDENTIFICATION | kidney | ENZYME | GENE | MOLECULAR-CLONING | MICE | BINDING | EXPRESSION | REVEALS | Apolipoproteins B - metabolism | RNA Editing | Liver - metabolism | RNA, Messenger - genetics | APOBEC-1 Deaminase - genetics | Water-Electrolyte Imbalance | Male | APOBEC-1 Deaminase - metabolism | Apolipoproteins B - genetics | Kidney Glomerulus - pathology | Organ Specificity | RNA, Messenger - metabolism | Mice, Knockout | Heterogeneous-Nuclear Ribonucleoproteins - genetics | Heterogeneous-Nuclear Ribonucleoproteins - deficiency | Animals | Protein Isoforms - metabolism | Base Sequence | Sex Factors | Kidney Glomerulus - metabolism | Female | Mice | Intestine, Small - metabolism | Protein Isoforms - genetics
Journal Article
Human Molecular Genetics, ISSN 0964-6906, 09/2003, Volume 12, Issue 17, pp. 2179 - 2189
Mutations within the CRB1 gene have been shown to cause human retinal diseases including retinitis pigmentosa and Leber congenital amaurosis. We have recently...
LEBER CONGENITAL AMAUROSIS | PROTEIN | GENE | EPITHELIAL-CELL POLARITY | MYOSIN-VIIA | BIOCHEMISTRY & MOLECULAR BIOLOGY | GENETICS & HEREDITY | HOMOLOG | PIGMENTOSA | MUTATIONS | DROSOPHILA-CRUMBS | DEGENERATION | Frameshift Mutation | Retina - growth & development | Alternative Splicing | Retina - embryology | Retinal Degeneration - metabolism | Morphogenesis | Cell Cycle Proteins - immunology | Gene Expression Regulation, Developmental | Peptide Fragments - immunology | Schizosaccharomyces pombe Proteins - metabolism | Nerve Tissue Proteins - physiology | Nerve Tissue Proteins - immunology | Mice, Inbred C57BL | Cell Cycle Proteins - metabolism | Nuclear Proteins - metabolism | Photoreceptor Cells, Vertebrate - cytology | Chromosome Mapping | Nuclear Proteins - immunology | Basement Membrane - metabolism | Nerve Tissue Proteins - genetics | Schizosaccharomyces pombe Proteins - immunology | Animals | Protein Isoforms | Mice | Photoreceptor Cells, Vertebrate - metabolism | Retinal Degeneration - pathology
LEBER CONGENITAL AMAUROSIS | PROTEIN | GENE | EPITHELIAL-CELL POLARITY | MYOSIN-VIIA | BIOCHEMISTRY & MOLECULAR BIOLOGY | GENETICS & HEREDITY | HOMOLOG | PIGMENTOSA | MUTATIONS | DROSOPHILA-CRUMBS | DEGENERATION | Frameshift Mutation | Retina - growth & development | Alternative Splicing | Retina - embryology | Retinal Degeneration - metabolism | Morphogenesis | Cell Cycle Proteins - immunology | Gene Expression Regulation, Developmental | Peptide Fragments - immunology | Schizosaccharomyces pombe Proteins - metabolism | Nerve Tissue Proteins - physiology | Nerve Tissue Proteins - immunology | Mice, Inbred C57BL | Cell Cycle Proteins - metabolism | Nuclear Proteins - metabolism | Photoreceptor Cells, Vertebrate - cytology | Chromosome Mapping | Nuclear Proteins - immunology | Basement Membrane - metabolism | Nerve Tissue Proteins - genetics | Schizosaccharomyces pombe Proteins - immunology | Animals | Protein Isoforms | Mice | Photoreceptor Cells, Vertebrate - metabolism | Retinal Degeneration - pathology
Journal Article
6.
Full Text
GpnmbR150X allele must be present in bone marrow derived cells to mediate DBA/2J glaucoma
BMC Genetics, ISSN 1471-2156, 04/2008, Volume 9, Issue 1, pp. 30 - 30
The Gpnmb gene encodes a transmembrane protein whose function(s) remain largely unknown. Here, we assess if a mutant allele of Gpnmb confers susceptibility to...
Interleukin-18 - immunology | Disease Susceptibility | Mice, Inbred C57BL | Bone Marrow Cells - physiology | Genotype | Antigen-Presenting Cells - immunology | Aqueous Humor - immunology | Membrane Glycoproteins - genetics | Animals | Intraocular Pressure - genetics | Bone Marrow Cells - immunology | Alleles | Glaucoma - immunology | Mice, Inbred DBA | Mice | Mice, Congenic | Eye Proteins - genetics | Mutation | Glaucoma - genetics | Glaucoma - physiopathology
Interleukin-18 - immunology | Disease Susceptibility | Mice, Inbred C57BL | Bone Marrow Cells - physiology | Genotype | Antigen-Presenting Cells - immunology | Aqueous Humor - immunology | Membrane Glycoproteins - genetics | Animals | Intraocular Pressure - genetics | Bone Marrow Cells - immunology | Alleles | Glaucoma - immunology | Mice, Inbred DBA | Mice | Mice, Congenic | Eye Proteins - genetics | Mutation | Glaucoma - genetics | Glaucoma - physiopathology
Journal Article
BMC Genetics, ISSN 1471-2156, 04/2008, Volume 9, p. 30
The Gpnmb gene encodes a transmembrane protein whose function(s) remain largely unknown. Here, we assess if a mutant allele of Gpnmb confers susceptibility to...
Glaucoma | Care and treatment | Dendritic cells | Genetic aspects | Research | Gene expression | Health aspects
Glaucoma | Care and treatment | Dendritic cells | Genetic aspects | Research | Gene expression | Health aspects
Journal Article
Human Molecular Genetics, ISSN 0964-6906, 09/2003, Volume 12, Issue 17, p. 2179
Mutations within the CRB1 gene have been shown to cause human retinal diseases including retinitis pigmentosa and Leber congenital amaurosis. We have...
Journal Article
No results were found for your search.
Cannot display more than 1000 results, please narrow the terms of your search.