John D Ash
University Of Florida
Project start date: 2012-02-01
Project end date: 2012-08-31
Sponsored Links Excellgen http://Excellgen.com
Grants awarded to John D Ash
ROLE OF THE INTERLEUKIN 6 CYTOKINE FAMILY RECEPTOR GP130 IN DIABETES
John D Ash
University Of Oklahoma Hlth Sciences Ctr, Health Sciences Center, Oklahoma City, Ok 73117-1213
Abstract: This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Inflammatory cytokines, such as Interleukin 6 (IL-6) has been shown to be involved in the progression of both type 1 and type 2 diabetes. IL-6 levels are elevated in the retina during diabetes. In the central nervous system other IL-6 family members, including ciliary neurotrophic factor (CNTF) and Leukemia Inhibitory Factor (LIF), are elevated during ischemic stress and injury. Members of the IL-6 family of cytokines do not share sequence homology, but are grouped together based on activation of a common signaling receptor, gp130. Because multiple ligands signal through gp130, there is significant overlap in their biological activity, and since ligands of gp130 are present during multiple stages of disease it is possible that multiple ligands of the same receptor may play multiple roles in disease progression. To demonstrate the complete involvement of the gp130 pathway in disease progression we are proposing to two complimentary approaches to block gp130 signaling in vascular endothelial cells and in adult animals. In the first aim we will use mice with gp130 inactivated in vascular endothelial cells using the tie2-cre transgenic mouse and the loxP targeted gp130 mouse. These mice will undergo development without gp130 in vascular endothelial cells and bone marrow derived cells. In the second aim we will use a protein antagonist of LIFRb to block the activity of neurotrophic IL-6 family members (LIF and CNTF) in adult animals. In both aims we will determine whether or not blocking gp130 signaling reduces the severity and progression of diabetic complications in the eye
Keywords: B cell differentiation factor; B cell stimulating factor 2; B-Cell Differentiation Factor-2; B-Cell Stimulatory Factor-2; BCDF; BSF-2; BSF2; BSF2 (B cell stimulating factor 2); Biological; Bone Marrow; CNTF; CRISP; Cell Communication and Signaling; Cell Signaling; Cells; Central Nervous System; Cholinergic Differentiation Factor; Ciliary Neuronotrophic Factor; Ciliary Neurotrophic Factor; Complications of Diabetes Mellitus; Computer Retrieval of Information on Scientific Projects Database; D-Factor; Development; Diabetes Complications; Diabetes Mellitus; Diabetes-Related Complications; Diabetic Complications; Differentiation Factor, B-Cell; Disease; Disease Progression; Disorder; Eye; Eyeball; Family; Family member; Funding; Grant; HPGF; Hepatocyte-Stimulating Factor; Human Interleukin in DA Cells; Hybridoma Growth Factor; IFN-beta 2; IFNB2; IL-6; IL6 Protein; Inflammatory; Injury; Institution; Interleukin 6 (Interferon, Beta 2); Interleukin-6; Intracellular Communication and Signaling; Investigators; LIF; Ligands; MGI-2; MLPLI; Mammals, Mice; Melanoma-Derived LPL Inhibitor; Mentors; Mice; Murine; Mus; Myeloid Differentiation-Inducing Protein; NIH; National Institutes of Health; National Institutes of Health (U.S.); Nervous System, CNS; Neuraxis; Oklahoma; Pathway interactions; Plasmacytoma Growth Factor; Play; Proteins; Receptor Protein; Receptor Signaling; Research; Research Personnel; Research Resources; Researchers; Resources; Reticuloendothelial System, Bone Marrow; Retina; Role; Sequence Homology; Severities; Signal Transduction; Signal Transduction Systems; Signaling; Source; Staging; Stress; Transgenic Mice; United States National Institutes of Health; Vascular Endothelial Cell; Vision research; adult animal; base; biological signal transduction; cytokine; diabetes; disease/disorder; gene product; homology (molecular); interferon beta 2; leukemia inhibitory factor; mature animal; member; pathway; receptor; social role; type I and type II diabetes
Project start date: 2009-07-01
Project end date: 2010-06-30
Budget start date: 1-JUL-2009
Budget end date: 30-JUN-2010
PFA/PA: RFA-RR-06-001
5P20RR017703-08_6144 (2009): $209946
John D Ash
University Of Oklahoma Hlth Sciences Ctr, Health Sciences Center, Oklahoma City, Ok 73117-1213
Abstract: This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The Molecular Biology Module has supported investigators of the Vision COBRE in their research programs primarily through DNA purification from tissues and PCR-based genotyping. The module also supports investigators through maintenance of equipment used for gene expression analysis by real-time PCR, and Western blots. Dr. Ash is the director of this module and he oversees its day to day operation. Dr Ash is qualified to supervise this module based on his extensive experience in real-time PCR, Western blot analysis, DNA purification, and PCR genotyping. Dr Ash has worked with genetically modified mice since 1994. During this 14 year period, Dr Ash has maintained approximately 30 lines of genetically modified mice. His lab currently genotypes 5 to 10,000 samples per year. Dr. Carr is the assistant director. Dr Carr has extensive experience in animal genotyping, as well as analysis by Real-Time PCR and ELISA. Operations of the Molecular Biology Module are conduced by a full time research assistant Fatemeh Shariati. Projects are initiated by a service request. Following completion of service Mrs. Shariati completes a report describing the completion of the job and all results. The report will contain a gel picture documenting accurate PCR reactions, and an assessment of positive and negative results. All reports are approved by the module director before they are returned to the users. If the results are not satisfactory, Mrs. Shariati will repeat the analysis. The module is operating at a rate of 10,000 reactions per year with and accuracy rate of 80 to 90%
Keywords: Animals; Blotting, Western; Body Tissues; COBRE; CRISP; Center of Biomedical Research Excellence; Centers of Research Excellence; Computer Retrieval of Information on Scientific Projects Database; DNA Molecular Biology; DNA purification; ELISA; Enzyme-Linked Immunosorbent Assay; Equipment; Funding; Gel; Gene Expression; Genotype; Grant; Institution; Investigators; Jobs; Maintenance; Maintenances; Mammals, Mice; Mentors; Mice; Molecular Biology; Murine; Mus; NIH; National Institutes of Health; National Institutes of Health (U.S.); Occupations; Oklahoma; Operation; Operative Procedures; Operative Surgical Procedures; Professional Postions; Programs (PT); Programs [Publication Type]; Qualifying; Reaction; Reporting; Research; Research Personnel; Research Resources; Researchers; Resources; Sampling; Services; Sight; Source; Surgical; Surgical Interventions; Surgical Procedure; Time; Tissues; United States National Institutes of Health; Vision; Vision research; Western Blotting; Western Blottings; Western Immunoblotting; Work; base; experience; programs; protein blotting; surgery
Project start date: 2009-07-01
Project end date: 2010-06-30
Budget start date: 1-JUL-2009
Budget end date: 30-JUN-2010
PFA/PA: RFA-RR-06-001
5P20RR017703-08_6149 (2009): $127448
CYTOKINE REGULATION OF PHOTORECEPTOR GENE EXPRESSION
John D Ash
University Of Oklahoma Hlth Sciences Ctr, Health Sciences Center, Oklahoma City, Ok 73117-1213
Grant 3R01EY016459-04S1 from National Eye Institute
Abstract: This proposal is made in response to notice number NOT-OD-09-058 entitled NIH Announces the Availability of Recovery Act Funds for Competitive Revision Applications. This application is therefore intended to revise the currently funded project EY016459. Neurological cytokines have shown tremendous therapeutic potential for preventing or delaying neurodegenerations, including those causing retinitis pigmentosa and dry macular degeneration. The broad-spectrum protective activity of leukemia inhibitory factor (LIF) and ciliary neurotrophic factor (CNTF) have a clear therapeutic advantage when the genetic mutation or environmental factors are diverse or unknown. Because of this advantage, CNTF is in phase II clinical trials to prevent photoreceptor cell death in patients suffering from retinitis pigmentosa (RP). Almost all drugs have unwanted side effects, which are usually manifested when drugs are used well above their therapeutic range. Unfortunately, at high concentrations, CNTF and LIF have the unwanted side effect of reducing photoreceptor function thus potentially limiting their therapeutic value. LIF is not homologous to CNTF but is functionally related. Our studies have shown that at moderate doses LIF is protective without reducing function over a 5 fold range, thus establishing a large therapeutic range. At higher doses LIF inhibits function. The inhibition of function at high concentrations is an impediment to future therapies and may limit the usefulness of the molecules. We would like to further refine the therapeutic value of LIF by determining the mechanism by which LIF induces survival versus its mechanism for inhibiting function. This would allow us to develop new therapies which would give broad spectrum protection without inhibiting function. The identification of intracellular targets would open the pathway for the development of small molecules that can be used instead of bulky and labile proteins. Neurological cytokines have shown tremendous therapeutic potential for preventing or delaying neurodegenerations, including those causing retinitis pigmentosa and dry macular degeneration. The broad- spectrum protective activity of ciliary neurotrophic factor (CNTF) has a clear therapeutic advantage when the genetic mutation or environmental factors causing the disease are diverse or unknown. Because of this advantage, CNTF is in phase II clinical trials to prevent photoreceptor cell death in patients suffering from retinitis pigmentosa (RP). Almost all drugs have unwanted side effects, which are usually manifested when drugs are used well above their therapeutic range. Unfortunately, at high concentrations, CNTF has the unwanted side effect of reducing photoreceptor function, thus potentially limiting its therapeutic value. Leukemia inhibitory factor (LIF) is not homologous to CNTF but is functionally related. Our studies have shown that LIF provides protection from cell death without reducing photoreceptor function over a 5-fold range of dosages. Nevertheless, the inhibition of function at high concentrations has resulted in severe adverse consequences when LIF is applied at high concentrations. It is anticipated that this is an impediment to future therapies and may limit the usefulness of this important molecule. One goal of this project is to further define the therapeutic value of LIF by determining the mechanism by which LIF induces survival versus its mechanism for inhibiting function. This knowledge would allow development of new therapies which would give broad spectrum protection without inhibiting function. The identification of intracellular targets would open the pathway for the development of small molecules that can be used instead of bulky and labile proteins. We and others have identified STAT3 as a transcription factor downstream of LIF that is required for protection. The specific aims of this revision are to identify genes regulated by LIF that specifically require STAT3. This will identify the mechanism by which LIF induces protection. One candidate gene that we have identified in preliminary work is a member of the PIM serine/theronine kinase family. We will use knockout mice for these kinases to determine if they are essential for LIF induced protection
Keywords: Adverse effects; Antibodies; Blindness; CNTF; Cancer Genes; Cancer-Promoting Gene; Candidate Disease Gene; Candidate Gene; Cell Death; Cell Growth in Number; Cell Multiplication; Cell Proliferation; Cell Survival; Cell Viability; Cells; Cellular Proliferation; Cholinergic Differentiation Factor; Ciliary Neuronotrophic Factor; Ciliary Neurotrophic Factor; Clinical Trials; Clinical Trials, Phase II; Clinical Trials, Unspecified; D-Factor; DNA; DNA Alteration; DNA Chips; DNA Microarray; DNA Microarray Chip; DNA Microchips; DNA mutation; Data; Deoxyribonucleic Acid; Development; Disease; Disorder; Dose; Drug usage; Drugs; EC 2.7; Environmental Factor; Environmental Risk Factor; Family; Funding; Future; Gene Alteration; Gene Expression; Gene Mutation; Genes; Genetic Alteration; Genetic Change; Genetic defect; Genetic mutation; Goals; Hereditary; Human Interleukin in DA Cells; IL-6 receptor signal transducer gp130; IL6ST gp130; Inherited; Injection of therapeutic agent; Injections; Kinases; Knock-out; Knockout; Knockout Mice; Knowledge; L-Serine; LIF; Light; MLPLI; Macular degeneration; Macular degenerative disease; Malignant Cell; Mammals, Mice; Measures; Mediating; Medication; Melanoma-Derived LPL Inhibitor; Mice; Mice, Knock-out; Mice, Knockout; Murine; Mus; Mutation; NIH; National Institutes of Health; National Institutes of Health (U.S.); Nerve Degeneration; Neurologic; Neurological; Neuron Degeneration; Null Mouse; Oncogenes; PIM; PIM1; PIM1 gene; Pathway interactions; Patients; Pharmaceutic Preparations; Pharmaceutical Preparations; Phase 2 Clinical Trials; Phase II Clinical Trials; Phosphotransferases; Photoradiation; Photoreceptor Cell; Photoreceptors; Photosensitive Cell; Pigmentary Retinopathy; Play; Protein-Serine Kinase; Protein-Serine-Threonine Kinases; Protein-Threonine Kinase; Proteins; Provirus Insertion Site Gene-1; RNA analysis; Recovery; Regulation; Retina; Retinal Degeneration; Retinitis Pigmentosa; Rod; Rod Photoreceptors; Rod-Cone Dystrophy; Rods (Eye); Rods (Retina); Role; STAT3; STAT3 gene; Sequence Alteration; Serine; Serine Kinase; Serine-Threonine Kinases; Signal Pathway; System; System, LOINC Axis 4; Tapetoretinal Degeneration; Testing; Therapeutic; Threonine Kinase; Time; Transforming Genes; Transphosphorylases; Treatment Side Effects; Tumor Cell; United States; United States National Institutes of Health; Up-Regulation; Up-Regulation (Physiology); Upregulation; Visual Receptor; Work; age dependent; age related; base; cancer cell; clinical investigation; cytokine; cytokine receptor gp130; design; designing; disease/disorder; dosage; drug use; drug/agent; environmental risk; gene product; genome mutation; gp130 IL-6 family receptor; gp130 protein; gp130 transducing protein; inherited retinal degeneration; leukemia inhibitory factor; member; necrocytosis; neoplastic cell; neural degeneration; neurodegeneration; neuronal degeneration; neuroprotection; overexpression; pathway; phase 2 study; phase 2 trial; phase II trial; prevent; preventing; protocol, phase II; public health relevance; response; retina degeneration; retinal degenerative; retinal neuron; rod cell; side effect; signal transducer gp130; signal-transducing receptor gp130; small molecule; social role; study, phase II; therapy adverse effect; transcription factor; treatment adverse effect
Relevance: 7. Neurological cytokines have shown tremendous therapeutic potential for preventing or delaying neurodegenerations, including those causing retinitis pigmentosa and dry macular degeneration. The broad- spectrum protective activity of ciliary neurotrophic factor (CNTF) has a clear therapeutic advantage when the genetic mutation or environmental factors causing the disease are diverse or unknown. Because of this advantage, CNTF is in phase II clinical trials to prevent photoreceptor cell death in patients suffering from retinitis pigmentosa (RP). Almost all drugs have unwanted side effects, which are usually manifested when drugs are used well above their therapeutic range. Unfortunately, at high concentrations, CNTF has the unwanted side effect of reducing photoreceptor function, thus potentially limiting its therapeutic value. Leukemia inhibitory factor (LIF) is not homologous to CNTF but is functionally related. Our studies have shown that LIF provides protection from cell death without reducing photoreceptor function over a 5-fold range of dosages. Nevertheless, the inhibition of function at high concentrations has resulted in severe adverse consequences when LIF is applied at high concentrations. It is anticipated that this is an impediment to future therapies and may limit the usefulness of this important molecule. One goal of this project is to further define the therapeutic value of LIF by determining the mechanism by which LIF induces survival versus its mechanism for inhibiting function. This knowledge would allow development of new therapies which would give broad spectrum protection without inhibiting function. The identification of intracellular targets would open the pathway for the development of small molecules that can be used instead of bulky and labile proteins. We and others have identified STAT3 as a transcription factor downstream of LIF that is required for protection. The specific aims of this revision are to identify genes regulated by LIF that specifically require STAT3. This will identify the mechanism by which LIF induces protection. One candidate gene that we have identified in preliminary work is a member of the PIM serine/theronine kinase family. We will use knockout mice for these kinases to determine if they are essential for LIF induced protection
Project start date: 2009-09-30
Project end date: 2010-09-29
Budget start date: 30-SEP-2009
Budget end date: 29-SEP-2010
PFA/PA: PA-07-070
3R01EY016459-04S1 (2009): $366250
CELL CYCLE REGULATION IN THE DEVELOPING LENS
John D Ash
Baylor College Of Medicine 1 Baylor Plaza Houston, Tx 770303498
Grant 5F32EY006708-03 from National Eye Institute IRG: VISA
Abstract: The overall objective of this research is to develop an in vivo understanding of the molecular events controlling the differentiation of proliferating lens epithelial cells as they become post-mitotic lens fiber cells. In particular the research described in this proposal is aimed at identifying the role of cell cycle regulators in the differentiation process. In situ hybridization and immunohistochemistry will be employed to observe the expression patterns of endogenous cell cycle regulators as lens cells differentiate. Transgenic mice will be generated with expression vectors which will allow the lens specific over expression of cell cycle regulatory proteins.
Keywords: cell cycle protein, cell differentiation, cell growth regulation, developmental genetics, lens
5F32EY006708-03 (1998): $29160
5F32EY006708-02 (1997): $24420
Gene Expression And Retinal Vascularization
John D Ash
University Of Oklahoma Hlth Sciences Ctr Health Sciences Center Oklahoma City, Ok 731171213
Grant 5R03EY014206-03 from National Eye Institute IRG: ZEY1
Abstract: Proliferative retinopathies are a classification of diseases that include sickle cell retinopathy, diabetic retinopathy, branch vein occlusion retinopathy, and retinopathy of prematurity. An interesting paradox in these retinopathies is that the hypoxia in the retina triggers growth of blood vessels in the vitreous but not in the retina itself. If we could identify the mechanism of this inhibition we may be able to temporarily suppress the inhibition and stimulate vessel growth within the retina. In order to develop strategies to prevent proliferative retinopathies we must understand the changes in gene expression that are responsible for disease progression. We propose to utilize proteomics and DNA-microarrays to identify differential expressed genes between normal retinas and retinas from two mouse models of proliferative retinopathy. The proposed experiments will determine the gene expression profile of the retinas during the course of these disease models. We anticipate that such knowledge will significantly increase our understanding of human retinopathy of prematurity. Some of the differentially expressed proteins are likely to be essential regulators for normal retinal vascular development, while other proteins may be inhibitors of vascular development. By identifying new candidate proteins, this project would feed into our long-range goals of identifying proteins that are essential regulators of retinal vascular development.
Keywords: angiogenesis, gene expression, oxygen tension, pathologic process, retina, retina disorder, age difference, hyperoxia, hypoxia, protein structure function, computer program /software, immunocytochemistry, in situ hybridization, laboratory mouse, mass spectrometry, matrix assisted laser desorption ionization, microarray technology, polymerase chain reaction, proteomics, western blotting
Project start date: 2002-09-01
Project end date: 2006-08-31
5R03EY014206-03 (2004): $146500
5R03EY014206-02 (2003): $146500
REGULATION OF VASCULAR DEVELOPMENT IN THE MOUSE RETINA
John D Ash
University Of Oklahoma Hlth Sciences Ctr Health Sciences Center Oklahoma City, Ok 731171213
Grant 1P20RR017703-010001 from National Center For Research Resources IRG: ZRR1
Abstract: Proliferative retinopathies (PRs) are a classification of diseases that include sickle cell retinopathy, diabetic retinopathy, branch vein occlusion retinopathy, and retinopathy of prematurity. These diseases all are characterized by the loss of normal blood vessels in the retina and subsequent uncontrolled growth of abnormal blood vessels in the vitreous of the eye. As in humans, retinal ischemia in mice induces growth of abnormal vessels in the vitreous. In contrast to humans, mice are only transiently affected by the growth of abnormal blood vessels in the vitreous. Within a short period, normal blood vessels will re-grow within the mouse retina and the abnormal vessels in the vitreous will spontaneously resolve. The regrowth of normal retinal vessels provide mice with an endogenous mechanism for long-term protection from proliferative retinopathy. We hypothesize that the rodent retina is competent to promote retinal vascular regrowth through the expression of genes that are essential regulators and effectors of blood vessel growth and stability. Our goal is to identify the molecular regulators and effectors of vascular growth in the mouse retina. We have previously demonstrated that transgenic expression of either activated transforming growth factor 131(TGF-131) or leukemia inhibitory factor (LIF) in the lens alters the environment within the retina so that it is no longer competent for vascular development. Our strategy is to identify the genes that are expressed in wild type retinas which can promote vascular development, but that are not expressed in retinas which have lost the ability to support vascular development. In the current proposal, we will use transgenic mice in which we can induce the expression of TGF-131 (aim 1), or LIF (aim 2) in retinal photoreceptors, so that we can turn off retinal competence for vascular development at ages corresponding to the beginning, to the middle, and to completion of normal retinal vascular development (aims 1 and 2). With these mice, we will test the hypothesis that cytokines reduce growth of vascular endothelial cells or increase vascular degeneration. We will also test the hypothesis that cytokines down-regulate the expression of specific genes that are necessary for retinal vascularization (aim 3). This will allow us to identify genes that are regulators and effectors of retinal vascular development in mice.
Keywords: angiogenesis, blood vessel, developmental genetics, gene expression, leukemia inhibitory factor, retina, transforming growth factor, diabetic retinopathy, genetic promoter element, genetic regulation, proliferative vitreoretinopathy, proteomics, retina circulation, retina degeneration, retinopathy of prematurity, vascular endothelial growth factor, vascular endothelium, vision, informatics, laboratory mouse, mass spectrometry, microarray technology, transgenic animal
Project start date: 2002-09-16
Project end date: 2007-08-31
CYTOKINE REGULATION OF PHOTORECEPTOR GENE EXPRESSION
John D Ash
University Of Oklahoma Hlth Sciences Ctr, Health Sciences Center, Oklahoma City, Ok 73117-1213
Grant 5R01EY016459-04 from National Eye Institute
Abstract: Neurological cytokines have shown tremendous therapeutic potential for preventing or delaying blindness. Several of these cytokines stimulate the receptor gp130. Stimulation with either leukemia inhibitory factor (LIF) or ciliary neurotrophic factor (CNTF) has three profound effects on retinal cells inhibition of differentiation; neuroprotection from retinal degeneration; and reduced light response of photoreceptors. Despite the interest in these effects, little is known about the role of gp130 in normal retinal development or its role in preventing photoreceptor death. In this study we will use tissue specific inactivation of gp130 to address three important questions. 1.What is the role gp130 in normal differentiation of the retina? 2. Is gp130 expression in photoreceptors or Muller cells responsible for neuroprotection and function loss? 3. Is the PI3K/Akt pathway responsible for gp130 induced neuroprotection?
Keywords: 21+ years old; Address; Adult; Adverse effects; Bipolar Neuron; Blindness; Body Tissues; CNTF; Cell Communication and Signaling; Cell Death; Cell Differentiation Inhibition; Cell Signaling; Cell Survival; Cell Viability; Cessation of life; Cholinergic Differentiation Factor; Ciliary Neuronotrophic Factor; Ciliary Neurotrophic Factor; Clinical Trials; Clinical Trials, Unspecified; Cone; Cones (Eye); Cones (Retina); D-Factor; Data; Death; Development; Event; Eye; Eyeball; Gene Expression; Genes; Human Interleukin in DA Cells; Human, Adult; Intracellular Communication and Signaling; Investigators; Knockout Mice; LIF; Ligands; Light; MLPLI; Mammals, Mice; Measures; Melanoma-Derived LPL Inhibitor; Mice; Mice, Knock-out; Mice, Knockout; Modeling; Muller`s cell; Murine; Mus; Nervous; Neurologic; Neurological; Null Mouse; Opsin; Pathway interactions; Patients; Photoradiation; Photoreceptor Cell; Photoreceptors; Photoreceptors, Cone; Photoreceptors, Vertebrate; Photosensitive Cell; Pigmentary Retinopathy; Problem Solving; Progenitor Cell Transplantation; Programs (PT); Programs [Publication Type]; Receptor Protein; Regulation; Research Personnel; Researchers; Retina; Retinal; Retinal Cone; Retinal Degeneration; Retinitis Pigmentosa; Rod; Rod Photoreceptors; Rod-Cone Dystrophy; Rod-Opsin; Rods (Eye); Rods (Retina); Rods and Cones; Role; Signal Transduction; Signal Transduction Systems; Signaling; Stem Cell Transplantation; Stem cell transplant; Tapetoretinal Degeneration; Technology; Testing; Therapeutic; Tissues; Transgenic Mice; Transplantation; Treatment Side Effects; Vertebrate Photoreceptors; Visual Receptor; adult human (21+); biological signal transduction; cell type; clinical investigation; cone cell; cytokine; experiment; experimental research; experimental study; inherited retinal degeneration; interest; leukemia inhibitory factor; loss of function; necrocytosis; neural; neuroblast; neuroprotection; pathway; prevent; preventing; programs; receptor; recombinase; relating to nervous system; research study; response; retina degeneration; retinal degenerative; retinal neuron; rod cell; side effect; social role; synapse formation; synaptogenesis; theories; therapy adverse effect; transplant; treatment adverse effect
Project start date: 2006-02-02
Project end date: 2011-01-31
Budget start date: 1-FEB-2009
Budget end date: 31-JAN-2011
5R01EY016459-04 (2009): $282657
5R01EY016459-02 (2007): $282657
Sponsored Links Excellgen http://Excellgen.com
1R01EY016459-01A1 (2006): $291099
COBRE:REGULATION OF VASCULAR DEVELOPMENT IN MOUSE RETINA
John D Ash
University Of Oklahoma Hlth Sciences Ctr Health Sciences Center Oklahoma City, Ok 731171213
Grant 5P20RR017703-030006 from National Center For Research Resources IRG: ZRR1
Keywords: angiogenesis, health science research, retina, vision, laboratory mouse
Project start date: 2004-07-01
Project end date: 2005-06-30