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1. Full Text The ubiquitin kinase PINK1 recruits autophagy receptors to induce mitophagy
by Lazarou, Michael and Sliter, Danielle A and Kane, Lesley A and Sarraf, Shireen A and Wang, Chunxin and Burman, Jonathon L and Sideris, Dionisia P and Fogel, Adam I and Youle, Richard J
Nature, ISSN 0028-0836, 08/2015, Volume 524, Issue 7565, pp. 309 - 314
Protein aggregates and damaged organelles are tagged with ubiquitin chains to trigger selective autophagy. To initiate mitophagy, the ubiquitin kinase PINK1... 
ACTIVATE PARKIN | OPEN-ANGLE GLAUCOMA | COMPLEX | PARKIN-MEDIATED MITOPHAGY | PHOSPHORYLATION | MULTIDISCIPLINARY SCIENCES | P62/SQSTM1 | DEPOLARIZED MITOCHONDRIA | OPTINEURIN | SELECTIVE AUTOPHAGY | BINDING | Protein Kinases - metabolism | Autophagy-Related Proteins | Phosphorylation | Signal Transduction | Microtubule-Associated Proteins - metabolism | Humans | Ubiquitin - metabolism | Ubiquitin-Protein Ligases - metabolism | Nuclear Proteins - metabolism | Autophagy - physiology | Intracellular Signaling Peptides and Proteins - metabolism | Mitochondria - metabolism | Mitochondrial Degradation - physiology | Transcription Factor TFIIIA - metabolism | Autophagy-Related Protein-1 Homolog | Carrier Proteins - metabolism | Mitochondrial Proteins - metabolism | Models, Biological | Membrane Proteins - metabolism | HeLa Cells | Protein-Serine-Threonine Kinases - metabolism | Ubiquitin | Mitochondrial DNA | Research | Ligases | Membrane proteins | Mitochondria | Mutation | Kinases | Autophagy | Index Medicus
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2. Full Text Cross-ancestry genome-wide association analysis of corneal thickness strengthens link between complex and Mendelian eye diseases
by Iglesias, Adriana I and Mishra, Aniket and Vitart, Veronique and Bykhovskaya, Yelena and Höhn, René and Springelkamp, Henriët and Cuellar-Partida, Gabriel and Gharahkhani, Puya and Bailey, Jessica N. Cooke and Willoughby, Colin E and Li, Xiaohui and Yazar, Seyhan and Nag, Abhishek and Khawaja, Anthony P and Polašek, Ozren and Siscovick, David and Mitchell, Paul and Tham, Yih Chung and Haines, Jonathan L and Kearns, Lisa S and Hayward, Caroline and Shi, Yuan and Van Leeuwen, Elisabeth M and Taylor, Kent D and Wang, Jie Jin and Rochtchina, Elena and Attia, John and Scott, Rodney and Holliday, Elizabeth G and Baird, Paul N and Xie, Jing and Inouye, Michael and Viswanathan, Ananth and Sim, Xueling and Bonnemaijer, Pieter and Rotter, Jerome I and Martin, Nicholas G and Zeller, Tanja and Mills, Richard A and Staffieri, Sandra E and Jonas, Jost B and Schmidtmann, Irene and Boutin, Thibaud and Kang, Jae H and Lucas, Sionne E. M and Wong, Tien Yin and Beutel, Manfred E and Wilson, James F and Allingham, R. Rand and Brilliant, Murray H and Budenz, Donald L and Christen, William G and Fingert, John and Friedman, David S and Gaasterland, Douglas and Gaasterland, Terry and Hauser, Michael A and Kraft, Peter and Lee, Richard K and Lichter, Paul R and Liu, Yutao and Loomis, Stephanie J and Moroi, Sayoko E and Pericak-Vance, Margaret A and Realini, Anthony and Richards, Julia E and Schuman, Joel S and Scott, William K and Singh, Kuldev and Sit, Arthur J and Vollrath, Douglas and Weinreb, Robert N and Wollstein, Gadi and Zack, Donald J and Zhang, Kang and Donnelly, Peter and Barroso, Ines and Blackwell, Jenefer M and Bramon, Elvira and Brown, Matthew A and Casas, Juan P and Corvin, Aiden and Deloukas, Panos and Duncanson, Audrey and Jankowski, Janusz and Markus, Hugh S and Mathew, Christopher G and Palmer, Colin N. A and Plomin, Robert and Rautanen, Anna and Sawcer, Stephen J and Trembath, Richard C and Wood, Nicholas W and Spencer, Chris C. A and Band, Gavin and Bellenguez, Céline and Freeman, Colin and Hellenthal, Garrett and Giannoulatou, Eleni and Pirinen, Matti and ... and Blue Mountains Eye Study-GWAS Grp and NEIGHBORHOOD Consortium and Wellcome Trust Case Control Consor and Blue Mountains Eye Study—GWAS group and Wellcome Trust Case Control Consortium 2 (WTCCC2)
Nature Communications, ISSN 2041-1723, 12/2018, Volume 9, Issue 1, pp. 1 - 11
Central corneal thickness (CCT) is a highly heritable trait associated with complex eye diseases such as keratoconus and glaucoma. We perform a genome-wide... 
DECORIN | CHROMATIN STATES | POLYMORPHISMS | RISK-FACTOR | MULTIDISCIPLINARY SCIENCES | MOUSE | GENE-EXPRESSION | MUTATIONS | HERITABILITY | LUMICAN | KERATOCONUS | Glaucoma | Cornea | Genes | Myopia | Association analysis | Genomes | Gene expression | Tissues | Connective tissues | Keratoconus | Collagen | Eye diseases | Extracellular matrix | Index Medicus
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3. Full Text Cross-ancestry genome-wide association analysis of corneal thickness strengthens link between complex and Mendelian eye diseases
by Iglesias, Adriana I and Mishra, Aniket and Vitart, Veronique and Bykhovskaya, Yelena and Höhn, René and Springelkamp, Henriët and Cuellar-Partida, Gabriel and Gharahkhani, Puya and Bailey, Jessica N Cooke and Willoughby, Colin E and Li, Xiaohui and Yazar, Seyhan and Nag, Abhishek and Khawaja, Anthony P and Polašek, Ozren and Siscovick, David and Mitchell, Paul and Tham, Yih Chung and Haines, Jonathan L and Kearns, Lisa S and Hayward, Caroline and Shi, Yuan and van Leeuwen, Elisabeth M and Taylor, Kent D and Bonnemaijer, Pieter and Rotter, Jerome I and Martin, Nicholas G and Zeller, Tanja and Mills, Richard A and Souzeau, Emmanuelle and Staffieri, Sandra E and Jonas, Jost B and Schmidtmann, Irene and Boutin, Thibaud and Kang, Jae H and Lucas, Sionne E M and Wong, Tien Yin and Beutel, Manfred E and Wilson, James F and Uitterlinden, André G and Vithana, Eranga N and Foster, Paul J and Hysi, Pirro G and Hewitt, Alex W and Khor, Chiea Chuen and Pasquale, Louis R and Montgomery, Grant W and Klaver, Caroline C W and Aung, Tin and Pfeiffer, Norbert and Mackey, David A and Hammond, Christopher J and Cheng, Ching-Yu and Craig, Jamie E and Rabinowitz, Yaron S and Wiggs, Janey L and Burdon, Kathryn P and van Duijn, Cornelia M and MacGregor, Stuart and Blue Mountains Eye Study—GWAS group and NEIGHBORHOOD Consortium and Wellcome Trust Case Control Consortium 2 (WTCCC2)
Nature communications, ISSN 2041-1723, 05/2018, Volume 9, Issue 1, p. 1864
Central corneal thickness (CCT) is a highly heritable trait associated with complex eye diseases such as keratoconus and glaucoma. We perform a genome-wide... 
Lumican - metabolism | Glaucoma, Open-Angle - genetics | Humans | Corneal Diseases - metabolism | Corneal Dystrophies, Hereditary - ethnology | Corneal Diseases - genetics | Ehlers-Danlos Syndrome - genetics | Corneal Dystrophies, Hereditary - pathology | Loeys-Dietz Syndrome - metabolism | Mendelian Randomization Analysis | Fibrillin-1 - metabolism | Cornea - pathology | Keratoconus - pathology | Corneal Diseases - pathology | Decorin - genetics | Gene Expression | Eye Diseases, Hereditary - pathology | Lumican - genetics | ADAMTS Proteins - metabolism | Proteoglycans - metabolism | Ehlers-Danlos Syndrome - ethnology | European Continental Ancestry Group | Myopia - pathology | Cornea - metabolism | Myopia - ethnology | Loeys-Dietz Syndrome - pathology | Corneal Diseases - ethnology | Marfan Syndrome - metabolism | Marfan Syndrome - pathology | Cornea - abnormalities | Quantitative Trait Loci | Proteoglycans - genetics | ADAMTS Proteins - genetics | Transforming Growth Factor beta2 - metabolism | Corneal Dystrophies, Hereditary - genetics | Glaucoma, Open-Angle - pathology | Keratoconus - metabolism | Loeys-Dietz Syndrome - ethnology | Glaucoma, Open-Angle - ethnology | Myopia - metabolism | Ehlers-Danlos Syndrome - pathology | Marfan Syndrome - ethnology | Keratoconus - genetics | Glaucoma, Open-Angle - metabolism | Fibrillin-1 - genetics | Eye Diseases, Hereditary - ethnology | Genome-Wide Association Study | Quantitative Trait, Heritable | Corneal Dystrophies, Hereditary - metabolism | Marfan Syndrome - genetics | Eye Diseases, Hereditary - genetics | Myopia - genetics | Asian Continental Ancestry Group | Keratoconus - ethnology | Ehlers-Danlos Syndrome - metabolism | Loeys-Dietz Syndrome - genetics | Polymorphism, Single Nucleotide | Transforming Growth Factor beta2 - genetics | Genome, Human | Decorin - metabolism | Eye Diseases, Hereditary - metabolism | Cornea | Decorin | Corneal Dystrophies, Hereditary | Myopia | Corneal Diseases | Marfan Syndrome | Keratoconus | ADAMTS Proteins | Lumican | Transforming Growth Factor beta2 | Ehlers-Danlos Syndrome | Glaucoma, Open-Angle | Fibrillin-1 | Eye Diseases, Hereditary | Proteoglycans | Wellcome Trust Case Control Consortium 2 (WTCCC2) | Blue Mountains Eye Study—GWAS group | Loeys-Dietz Syndrome | NEIGHBORHOOD Consortium
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4. Full Text Caspase-8 promotes NLRP1/NLRP3 inflammasome activation and IL-1β production in acute glaucoma
by Wei Chi and Fei Li and Hongrui Chen and Yandong Wang and Yingting Zhu and Xuejiao Yang and Jie Zhu and Frances Wu and Hong Ouyang and Jian Ge and Robert N. Weinre and Kang Zhang and Yehong Zhuo
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 7/2014, Volume 111, Issue 30, pp. 11181 - 11186
Acute glaucoma is a sight-threatening condition characterized by a sudden and substantial rise in intraocular pressure (IOP) and consequent retinal ganglion... 
Glaucoma | Reperfusion | Messenger RNA | Ischemia | Toll like receptors | Central nervous system | Retina | Brain damage | Intraocular pressure | Microglia | Retinal ischemia/reperfusion injury | Cell apoptosis | BRAIN-INJURY | MICROGLIA ACTIVATION | INTERLEUKIN-1-BETA | MULTIDISCIPLINARY SCIENCES | REPERFUSION INJURY | POPULATIONS | retinal ischemia/reperfusion injury | ANGLE-CLOSURE GLAUCOMA | cell apoptosis | TOLL-LIKE RECEPTORS | CENTRAL-NERVOUS-SYSTEM | MICE | CEREBRAL-ISCHEMIA | Inflammasomes - metabolism | NLR Family, Pyrin Domain-Containing 3 Protein | Humans | Caspase 8 - metabolism | Caspase 1 - metabolism | Interleukin-1beta - genetics | Caspase 8 - genetics | Interleukin-1beta - metabolism | Apoptosis Regulatory Proteins - genetics | Eye Proteins - genetics | Glaucoma - metabolism | Disease Models, Animal | Acute Disease | Rats | Toll-Like Receptor 4 - genetics | Receptors, Cytoplasmic and Nuclear - genetics | Nerve Tissue Proteins - genetics | Rats, Sprague-Dawley | Toll-Like Receptor 4 - metabolism | Inflammasomes - genetics | Apoptosis Regulatory Proteins - metabolism | Mice, Knockout | Nerve Tissue Proteins - metabolism | Carrier Proteins - genetics | Animals | Carrier Proteins - metabolism | Eye Proteins - metabolism | Caspase 1 - genetics | Adaptor Proteins, Signal Transducing - genetics | Mice | Adaptor Proteins, Signal Transducing - metabolism | Enzyme Activation - genetics | Glaucoma - genetics | Receptors, Cytoplasmic and Nuclear - metabolism | Index Medicus | Biological Sciences | reperfusion injury | retinal ischemia
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5. Full Text Thioredoxin interacting protein is a novel mediator of retinal inflammation and neurotoxicity
by Al‐Gayyar, Mohammed MH and Abdelsaid, Mohammed A and Matragoon, Suraporn and Pillai, Bindu A and El‐Remessy, Azza B
British Journal of Pharmacology, ISSN 0007-1188, 09/2011, Volume 164, Issue 1, pp. 170 - 180
BACKGROUND AND PURPOSE Up‐regulation of thioredoxin interacting protein (TXNIP), an endogenous inhibitor of thioredoxin (Trx), compromises cellular antioxidant... 
peroxynitrite | retina | neuroprotection | verapamil | NMDA | neurodegeneration | TXNIP | apoptosis | retinal ganglion cells | Thioredoxin | DIABETIC-RETINOPATHY | OXIDATIVE STRESS | RAT RETINA | FACTOR-KAPPA-B | CALCIUM-CHANNEL BLOCKERS | NERVE GROWTH-FACTOR | OPEN-ANGLE GLAUCOMA | IN-VIVO | ENDOTHELIAL-CELLS | PHARMACOLOGY & PHARMACY | UP-REGULATED PROTEIN-1 | Retina - drug effects | Tumor Necrosis Factor-alpha - metabolism | Inflammation - pathology | Retina - metabolism | Apoptosis - drug effects | Caspase 3 - metabolism | Male | NF-kappa B - metabolism | Retinal Ganglion Cells - metabolism | Tyrosine - analogs & derivatives | Inflammation - metabolism | MAP Kinase Kinase 4 - metabolism | Neuroprotective Agents - pharmacology | Interleukin-1beta - metabolism | MAP Kinase Kinase 4 - antagonists & inhibitors | Thioredoxins - metabolism | Thioredoxins - antagonists & inhibitors | p38 Mitogen-Activated Protein Kinases - metabolism | MAP Kinase Kinase Kinase 5 - metabolism | MAP Kinase Kinase Kinase 5 - antagonists & inhibitors | Eye Diseases - pathology | Interleukin-1beta - antagonists & inhibitors | NF-kappa B - antagonists & inhibitors | Carrier Proteins - biosynthesis | Carrier Proteins - antagonists & inhibitors | Rats | Eye Diseases - metabolism | Up-Regulation - genetics | Caspase Inhibitors | Poly(ADP-ribose) Polymerase Inhibitors | Rats, Sprague-Dawley | Verapamil - pharmacology | Carrier Proteins - genetics | Poly(ADP-ribose) Polymerases - metabolism | Tyrosine - metabolism | Animals | Carrier Proteins - metabolism | Eye Diseases - genetics | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Inflammation - genetics | Neuroglia - metabolism | Oxidative Stress - drug effects | Retinal Ganglion Cells - drug effects | Tumor Necrosis Factor-alpha - antagonists & inhibitors | Index Medicus | Research Papers
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6. Full Text Mechanistic basis of Rho GTPase-induced extracellular matrix synthesis in trabecular meshwork cells
by Padmanabhan P. Pattabiraman and Ponugoti Vasantha Rao
American Journal of Physiology - Cell Physiology, ISSN 0363-6143, 03/2010, Volume 298, Issue 3, pp. 749 - 763
Elevated intraocular pressure arising from impaired aqueous humor drainage through the trabecular pathway is a major risk factor for glaucoma. To understand... 
Serum response factor | Actomyosin | Extracellular signal-regulated kinases | Fibronectin | extracellular signal-regulated kinases | AQUEOUS-HUMOR OUTFLOW | PHYSIOLOGY | ACTIVATED PROTEIN-KINASE | INTRAOCULAR-PRESSURE | LIGHT-CHAIN PHOSPHORYLATION | CELL BIOLOGY | OPEN-ANGLE GLAUCOMA | fibronectin | actomyosin | GENE-EXPRESSION | SIGNALING MECHANISM | serum response factor | SMOOTH-MUSCLE CONTRACTION | CYTOSKELETAL DYNAMICS | Serum Response Factor - genetics | Lysophospholipids - metabolism | Fibronectins - biosynthesis | Phosphorylation | Extracellular Matrix Proteins - biosynthesis | Transforming Growth Factor beta2 - metabolism | Humans | Actins - metabolism | Extracellular Matrix - metabolism | rhoA GTP-Binding Protein - metabolism | rhoA GTP-Binding Protein - genetics | Recombinant Fusion Proteins - metabolism | Aqueous Humor - metabolism | RNA Interference | Adenoviridae - genetics | Laminin - biosynthesis | Trabecular Meshwork - cytology | Transduction, Genetic | Serum Response Factor - metabolism | Cells, Cultured | Actomyosin - metabolism | Trabecular Meshwork - enzymology | Tenascin - biosynthesis | Mechanotransduction, Cellular | Stress Fibers - metabolism | Mitogen-Activated Protein Kinase 3 - metabolism | Cytoskeleton - metabolism | Myosin Light Chains - metabolism | Enzyme Activation | Genetic Vectors | Mitogen-Activated Protein Kinase 1 - metabolism | Fibronectins | Physiological aspects | Extracellular matrix | Research | Guanosine triphosphatase | Protein kinases | Glaucoma | Cytoskeleton | Kinases | Ribonucleic acid--RNA | Risk factors | Cells | Index Medicus | Extracellular Matrix, Cell Interactions
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7. Full Text Neuroprotection and neuroregeneration of retinal ganglion cells after intravitreal carbon monoxide release
by Stifter, Julia and Ulbrich, Felix and Goebel, Ulrich and Böhringer, Daniel and Lagrèze, Wolf Alexander and Biermann, Julia
PLoS ONE, ISSN 1932-6203, 11/2017, Volume 12, Issue 11, pp. e0188444 - e0188444
Purpose Retinal ischemia induces apoptosis leading to neurodegeneration and vision impairment. Carbon monoxide (CO) in gaseous form showed cell-protective and... 
ISCHEMIA-REPERFUSION INJURY | ADULT-RAT | FIBRILLARY ACIDIC PROTEIN | NEUROTROPHIC FACTOR | MULTIDISCIPLINARY SCIENCES | RAT RETINA | GENE-EXPRESSION | HEME OXYGENASE-1 | CULTURED MULLER CELLS | RADIAL GLIA | III BETA-TUBULIN | Neuroprotective Agents - therapeutic use | Tumor Necrosis Factor-alpha - metabolism | Intravitreal Injections | Tumor Necrosis Factor-alpha - genetics | Caspase 3 - metabolism | Reperfusion Injury - drug therapy | Male | NF-kappa B - metabolism | Carbon Monoxide - metabolism | GAP-43 Protein - genetics | Glial Fibrillary Acidic Protein - metabolism | RNA, Messenger - metabolism | Retinal Ganglion Cells - metabolism | Coordination Complexes - administration & dosage | Neuroprotection - drug effects | Neuroglia - drug effects | Retinal Ganglion Cells - pathology | Tubulin - metabolism | Neuroprotective Agents - pharmacology | Caspase 3 - genetics | Coordination Complexes - pharmacology | Female | Microfilament Proteins - metabolism | Phosphorylation - drug effects | Microfilament Proteins - genetics | Reperfusion Injury - genetics | Calcium-Binding Proteins - metabolism | Reperfusion Injury - pathology | GAP-43 Protein - metabolism | RNA, Messenger - genetics | Cells, Cultured | Axons - drug effects | Axons - metabolism | Rats, Sprague-Dawley | HSP70 Heat-Shock Proteins - metabolism | Coordination Complexes - therapeutic use | Cell Movement - drug effects | Animals | NF-kappa B - genetics | Nerve Regeneration - drug effects | HSP90 Heat-Shock Proteins - metabolism | Neuroglia - metabolism | Retinal Ganglion Cells - drug effects | Calcium-Binding Proteins - genetics | Mitogen-Activated Protein Kinases - metabolism | Prevention | Care and treatment | Usage | Physiological aspects | Research | Carbon monoxide | Ganglion | Retinal diseases | Immunohistochemistry | Glaucoma | Diabetic retinopathy | Nestin | Phosphorylation | Intensive care | Leukocyte migration | Retina | Nervous system | mRNA | Glial cells | Caspase-3 | Neuronal-glial interactions | Laminin | Reperfusion | Ischemia | Neurodegeneration | Rodents | Eye (anatomy) | Ophthalmology | Ganglion cells | GAP-43 protein | Explants | Medical research | Neurons | Glial fibrillary acidic protein | Apoptosis-inducing factor | Rats | Caspase | Cultures | Hsp70 protein | Inflammation | Gene expression | Medicine | Axons | Signaling | Anesthesiology | Viability | Cell migration | Apoptosis | Index Medicus
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8. Full Text Glaucomatous MYOC mutations activate the IL-1/NF-kappa B inflammatory stress response and the glaucoma marker SELE in trabecular meshwork cells
by Itakura, T and Peters, DM and Fini, ME
MOLECULAR VISION, ISSN 1090-0535, 09/2015, Volume 21, pp. 1071 - 1084
Purpose: Activation of the IL-1/NF-kappa B inflammatory stress pathway and induction of SELE expression in the trabecular meshwork (TBM) is a marker for... 
AQUEOUS OUTFLOW PATHWAY | MATRIX METALLOPROTEINASES | WILD-TYPE | OPEN-ANGLE GLAUCOMA | OXIDATIVE STRESS | PROTEIN | GENE | BIOCHEMISTRY & MOLECULAR BIOLOGY | OPHTHALMOLOGY | INTRAOCULAR-PRESSURE | EXPRESSION | CALORIE RESTRICTION | Cytoskeletal Proteins - genetics | Glaucoma, Open-Angle - genetics | Transforming Growth Factor beta2 - metabolism | Humans | Actins - metabolism | Glycoproteins - metabolism | Glaucoma, Open-Angle - pathology | NF-kappa B - metabolism | Interleukin-1beta - genetics | Actins - genetics | E-Selectin - genetics | Forkhead Transcription Factors - metabolism | Interleukin-1beta - metabolism | Cytoskeletal Proteins - metabolism | Glaucoma, Open-Angle - metabolism | Lentivirus - genetics | Eye Proteins - genetics | Interleukin-6 - metabolism | Fibroblasts - metabolism | Glycoproteins - genetics | Trabecular Meshwork - pathology | Mutagenesis, Site-Directed | Genetic Vectors - chemistry | Interleukin-6 - genetics | Signal Transduction | Endothelial Cells - metabolism | Gene Expression Regulation | Genetic Vectors - metabolism | E-Selectin - metabolism | Inflammation | Fibroblasts - pathology | Forkhead Transcription Factors - genetics | Eye Proteins - metabolism | NF-kappa B - genetics | Models, Biological | Trabecular Meshwork - metabolism | Forkhead Box Protein O1 | Primary Cell Culture | Transforming Growth Factor beta2 - genetics | Endothelial Cells - pathology | Cell Line, Transformed | Amino Acid Substitution | Index Medicus
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9. Full Text Mitochondrial DNA Variants Mediate Energy Production and Expression Levels for CFH, C3 and EFEMP1 Genes: Implications for Age-Related Macular Degeneration
by Kenney, M. Cristina and Chwa, Marilyn and Atilano, Shari R and Pavlis, Janelle M and Falatoonzadeh, Payam and Ramirez, Claudio and Malik, Deepika and Hsu, Tiffany and Woo, Grace and Soe, Kyaw and Nesburn, Anthony B and Boyer, David S and Kuppermann, Baruch D and Jazwinski, S. Michal and Miceli, Michael V and Wallace, Douglas C and Udar, Nitin
PLoS ONE, ISSN 1932-6203, 01/2013, Volume 8, Issue 1, pp. e54339 - e54339
Background: Mitochondrial dysfunction is associated with the development and progression of age-related macular degeneration (AMD). Recent studies using... 
DRUSEN FORMATION | POPULATION | OXIDATIVE STRESS | SAUDI PATIENTS | MTDNA | MULTIDISCIPLINARY SCIENCES | FACTOR-H POLYMORPHISM | RISK | MYOSIN VIIA | DYSFUNCTION | HAPLOGROUPS | Haplotypes | Retinal Pigment Epithelium - metabolism | Epithelial Cells - metabolism | Reactive Oxygen Species - metabolism | Humans | Adenosine Triphosphate - biosynthesis | DNA, Mitochondrial - genetics | Mitochondria - genetics | Myosins - metabolism | Epithelial Cells - cytology | Complement C3 - genetics | Extracellular Matrix Proteins - metabolism | Hybrid Cells - metabolism | Gene Expression | DNA, Mitochondrial - metabolism | Complement C3 - metabolism | Reactive Nitrogen Species - metabolism | Extracellular Matrix Proteins - genetics | Lactic Acid - metabolism | Cells, Cultured | Mitochondria - metabolism | Signal Transduction - genetics | Myosins - genetics | Macular Degeneration - metabolism | Complement Factor H - metabolism | Hybrid Cells - pathology | Macular Degeneration - genetics | Models, Biological | Complement Factor H - genetics | Retinal Pigment Epithelium - cytology | Macular Degeneration - pathology | Macular degeneration | Cellular proteins | Care and treatment | Genetic variation | Development and progression | Genetic aspects | Mitochondrial DNA | Health aspects | Glaucoma | Diabetic retinopathy | Cybrids | Disease | Physicians | Epithelial cells | Genes | Retina | Population studies | Arthritis | Proteins | Signal transduction | Mitochondria | Pathways | Energy | Aging | Degeneration | Age | Deoxyribonucleic acid--DNA | Cell division | Metabolism | Gene expression | Signaling | Retinal degeneration | Lactic acid | Index Medicus | Deoxyribonucleic acid | DNA
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10. Full Text Carbonic Anhydrases and Metabolism
by Supuran, Claudiu T
2019, ISBN 9783038978008
Carbonic anhydrases (CAs; EC 4.2.1.1) are metalloenzymes present in all kingdoms of life, as they equilibrate the reaction between three simple but essential... 
antibiotic | inhibitors | glaucoma | metabolic role | inhibitor | engineered bacteria | carbonic anhydrase inhibitors | drug discovery | enzyme inhibition | V-ATPases | photosynthesis | Chlamydomonas reinhardtii | metalloenzymes | CO2 capture | bicarbonate | benzamide | hypoxia | antibody | model alga | cancer therapeutics | CA gene family | resistance | isoforms IX and XII | cancer metabolism | MMP14 | carbonic anhydrase IX | carboxylation | bacterial enzymes | antitumor agent | metabolism | activator | bacterial carbonic anhydrases | amine | amino acid | pH regulation | proton pump inhibitors | pathogens | sulfonamide | metastasis | hypoxic tumor | carbonic anhydrase | carbonic anhydrases | protozoan | integrin | Entamoeba histolytica | tumors | human isoform | acidity | invasion | radiation | tumor | carbonic anhydrase XII | transporter | migration | cancer | tumor microenvironment
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