Tönges, Lars

[["dc.bibliographiccitation.firstpage","1297"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","STEM CELLS"],["dc.bibliographiccitation.lastpage","1310"],["dc.bibliographiccitation.volume","30"],["dc.contributor.author","Doeppner, T. R."],["dc.contributor.author","Ewert, T. A. S."],["dc.contributor.author","Tönges, L."],["dc.contributor.author","Herz, J."],["dc.contributor.author","Zechariah, A."],["dc.contributor.author","Elali, A."],["dc.contributor.author","Ludwig, A.-K."],["dc.contributor.author","Giebel, B."],["dc.contributor.author","Nagel, F."],["dc.contributor.author","Dietz, G. P. H."],["dc.contributor.author","Weise, J."],["dc.contributor.author","Hermann, D. M."],["dc.contributor.author","Bähr, M."],["dc.date.accessioned","2017-09-07T11:48:52Z"],["dc.date.available","2017-09-07T11:48:52Z"],["dc.date.issued","2012"],["dc.description.abstract","Novel therapeutic concepts against cerebral ischemia focus on cell-based therapies in order to overcome some of the side effects of thrombolytic therapy. However, cell-based therapies are hampered because of restricted understanding regarding optimal cell transplantation routes and due to low survival rates of grafted cells. We therefore transplanted adult green fluorescence protein positive neural precursor cells (NPCs) either intravenously (systemic) or intrastriatally (intracerebrally) 6 hours after stroke in mice. To enhance survival of NPCs, cells were in vitro protein-transduced with TAT-heat shock protein 70 (Hsp70) before transplantation followed by a systematic analysis of brain injury and underlying mechanisms depending on cell delivery routes. Transduction of NPCs with TAT-Hsp70 resulted in increased intracerebral numbers of grafted NPCs after intracerebral but not after systemic transplantation. Whereas systemic delivery of either native or transduced NPCs yielded sustained neuroprotection and induced neurological recovery, only TAT-Hsp70-transduced NPCs prevented secondary neuronal degeneration after intracerebral delivery that was associated with enhanced functional outcome. Furthermore, intracerebral transplantation of TAT-Hsp70-transduced NPCs enhanced postischemic neurogenesis and induced sustained high levels of brain-derived neurotrophic factor, glial cell line-derived neurotrophic factor, and vascular endothelial growth factor in vivo. Neuroprotection after intracerebral cell delivery correlated with the amount of surviving NPCs. On the contrary, systemic delivery of NPCs mediated acute neuroprotection via stabilization of the blood-brain-barrier, concomitant with reduced activation of matrix metalloprotease 9 and decreased formation of reactive oxygen species. Our findings imply two different mechanisms of action of intracerebrally and systemically transplanted NPCs, indicating that systemic NPC delivery might be more feasible for translational stroke concepts, lacking a need of in vitro manipulation of NPCs to induce long-term neuroprotection. STEM CELLS2012;30:12971310"],["dc.identifier.doi","10.1002/stem.1098"],["dc.identifier.gro","3142531"],["dc.identifier.isi","000304087300026"],["dc.identifier.pmid","22593021"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8892"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1066-5099"],["dc.title","Transduction of Neural Precursor Cells with TAT-Heat Shock Protein 70 Chaperone: Therapeutic Potential Against Ischemic Stroke after Intrastriatal and Systemic Transplantation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Der Nervenarzt"],["dc.contributor.author","Jost, Wolfgang H."],["dc.contributor.author","Buhmann, Carsten"],["dc.contributor.author","Classen, Joseph"],["dc.contributor.author","Eggert, Karla"],["dc.contributor.author","Kohl, Zacharias"],["dc.contributor.author","Outeiro, Tiago"],["dc.contributor.author","Tönges, Lars"],["dc.contributor.author","Woitalla, Dirk"],["dc.contributor.author","Reichmann, Heinz"],["dc.date.accessioned","2022-03-01T11:44:20Z"],["dc.date.available","2022-03-01T11:44:20Z"],["dc.date.issued","2022"],["dc.identifier.doi","10.1007/s00115-021-01237-3"],["dc.identifier.pii","1237"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/102996"],["dc.language.iso","de"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.eissn","1433-0407"],["dc.relation.issn","0028-2804"],["dc.rights.uri","https://www.springer.com/tdm"],["dc.title","Stellenwert der COMT-Hemmer in der Therapie motorischer Fluktuationen"],["dc.title.translated","Relevance of COMT inhibitors in the treatment of motor fluctuations"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Pharmacology & Therapeutics"],["dc.bibliographiccitation.lastpage","21"],["dc.bibliographiccitation.volume","189"],["dc.contributor.author","Koch, Jan Christoph"],["dc.contributor.author","Tatenhorst, Lars"],["dc.contributor.author","Roser, Anna-Elisa"],["dc.contributor.author","Saal, Kim-Ann"],["dc.contributor.author","Tönges, Lars"],["dc.contributor.author","Lingor, Paul"],["dc.date.accessioned","2020-12-10T15:20:44Z"],["dc.date.available","2020-12-10T15:20:44Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1016/j.pharmthera.2018.03.008"],["dc.identifier.issn","0163-7258"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72778"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","ROCK inhibition in models of neurodegeneration and its potential for clinical translation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","13"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Brain Pathology"],["dc.bibliographiccitation.lastpage","25"],["dc.bibliographiccitation.volume","27"],["dc.contributor.author","Saal, Kim-Ann"],["dc.contributor.author","Galter, Dagmar"],["dc.contributor.author","Roeber, Sigrun"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Tönges, Lars"],["dc.contributor.author","Lingor, Paul"],["dc.date.accessioned","2018-02-22T13:10:28Z"],["dc.date.available","2018-02-22T13:10:28Z"],["dc.date.issued","2017"],["dc.description.abstract","Causative treatment strategies for Parkinson's disease (PD) will have to address multiple underlying pathomechanisms to attenuate neurodegeneration. Additionally, the intrinsic regenerative capacity of the central nervous system is also an important factor contributing to restoration. Extracellular cues can limit sprouting and regrowth of adult neurons, but even aged neurons have a low intrinsic regeneration capacity. Whether this capacity has been lost or if growth inhibitory cues are increased during PD progression has not been resolved yet. In this study, we assessed the regenerative potential in the nigrostriatal system in post-mortem brain sections of PD patients compared to age-matched and young controls. Investigation of the expression pattern of the regeneration-associated protein GAP-43 suggested a lower regenerative capacity in nigral dopaminergic neurons of PD patients. Furthermore, the increase in protein expression of the growth-inhibitory protein ROCK2 in astrocytes and a similar trend in microglia, suggests an important role for ROCK2 in glial PD pathology, which is initiated already in normal aging. Considering the role of astro- and microglia in PD pathogenesis as well as beneficial effects of ROCK inhibition on neuronal survival and regeneration in neurodegenerative disease models, our data strengthens the importance of the ROCK pathway as a therapeutic target in PD."],["dc.identifier.doi","10.1111/bpa.12346"],["dc.identifier.pmid","26748453"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/12431"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.doi","10.1111/bpa.12346"],["dc.relation.eissn","1750-3639"],["dc.relation.issn","1015-6305"],["dc.title","Altered Expression of Growth Associated Protein-43 and Rho Kinase in Human Patients with Parkinson's Disease"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","853"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Neurochemistry"],["dc.bibliographiccitation.lastpage","864"],["dc.bibliographiccitation.volume","105"],["dc.contributor.author","Nagel, F."],["dc.contributor.author","Falkenburger, B. H."],["dc.contributor.author","Tönges, L."],["dc.contributor.author","Kowsky, S."],["dc.contributor.author","Pöppelmeyer, C."],["dc.contributor.author","Schulz, J. B."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Dietz, G. P. H."],["dc.date.accessioned","2017-09-07T11:48:44Z"],["dc.date.available","2017-09-07T11:48:44Z"],["dc.date.issued","2008"],["dc.description.abstract","Parkinson's disease is characterized by the progressive loss of dopaminergic (DA) neurons in the substantia nigra. The heat-shock protein 70 (Hsp70) reduces protein misfolding and aggregation. It has been shown to protect cells against oxidative stress and apoptotic stimuli in various neurodegenerative disease models. To deliver Hsp70 across cellular membranes and into the brain, we linked it to a cell-penetrating peptide derived from the HIV trans-activator of transcription (Tat) protein. In vitro, Tat-Hsp70 transduced neuroblastoma cells and protected primary mesencephalic DA neurons and their neurites against MPP+-mediated degeneration. In vivo, the systemic application of cell-permeable Hsp70 protected DA neurons of the substantia nigra pars compacta against subacute toxicity of MPTP. Furthermore, Tat-Hsp70 diminished the MPTP induced decrease in DA striatal fiber density. Thus, we demonstrate that systemically applied Tat-Hsp70 effectively prevents neuronal cell death in in vitro and in vivo models of Parkinson's disease. The use of Tat-fusion proteins might therefore be a valuable tool to deliver molecular chaperones like Hsp70 into the brain and may be the starting point for new protective strategies in neurodegenerative diseases."],["dc.identifier.doi","10.1111/j.1471-4159.2007.05204.x"],["dc.identifier.gro","3143309"],["dc.identifier.isi","000255139200025"],["dc.identifier.pmid","18182047"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/809"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0022-3042"],["dc.title","Tat-Hsp70 protects dopaminergic neurons in midbrain cultures and in the substantia nigra in models of Parkinson's disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1187"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Cerebral Blood Flow & Metabolism"],["dc.bibliographiccitation.lastpage","1196"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Doeppner, T. R."],["dc.contributor.author","Nagel, F."],["dc.contributor.author","Dietz, G. P. H."],["dc.contributor.author","Weise, J."],["dc.contributor.author","Tönges, L."],["dc.contributor.author","Schwarting, S."],["dc.contributor.author","Bähr, M."],["dc.date.accessioned","2017-09-07T11:47:27Z"],["dc.date.available","2017-09-07T11:47:27Z"],["dc.date.issued","2009"],["dc.description.abstract","Cerebral ischemia stimulates endogenous neurogenesis within the subventricular zone and the hippocampal dentate gyrus of the adult rodent brain. However, such newly generated cells soon die after cerebral ischemia. To enhance postischemic survival of neural precursor cells (NPC) and long-lasting neural regeneration, we applied the antiapoptotic chaperone heat shock protein 70 (Hsp70) fused to a cell-penetrating peptide derived from the HIV TAT to ensure delivery across the blood-brain barrier and the cell membrane. After transient focal cerebral ischemia in mice, TAT-Hsp70 was intravenously injected concomitant with reperfusion and additionally on day 14 after stroke. TAT-Hsp70 treatment resulted in smaller infarct size (27.1 +/- 9.0 versus 109.0 +/- 14.0 and 88.5 +/- 26.0 mm(3) in controls) and in functional improvement as assessed by the rota rod, tight rope, and water maze tests when compared with saline-and TAT-hemagglutinin- treated controls. In addition, postischemic survival of endogenous doublecortin (Dcx)-positive NPC was improved within the lesioned striatum of TAT-Hsp70-treated animals for up to 4 weeks after stroke without changing overall cell proliferation of BrdU(+) cells. Thus, TAT-Hsp70 treatment after stroke may be a promising tool to act neuroprotective and improve postischemic functional outcome, and also to increase survival of endogenous NPC after stroke. Journal of Cerebral Blood Flow & Metabolism (2009) 29, 1187-1196; doi: 10.1038/jcbfm.2009.44; published online 22 April 2009"],["dc.identifier.doi","10.1038/jcbfm.2009.44"],["dc.identifier.gro","3143110"],["dc.identifier.isi","000266451700013"],["dc.identifier.pmid","19384335"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/588"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: BMBF [1362910]"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0271-678X"],["dc.title","TAT-Hsp70-mediated neuroprotection and increased survival of neuronal precursor cells after focal cerebral ischemia in mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","104677"],["dc.bibliographiccitation.journal","Neurobiology of Disease"],["dc.bibliographiccitation.volume","134"],["dc.contributor.author","Maass, Fabian"],["dc.contributor.author","Michalke, Bernhard"],["dc.contributor.author","Willkommen, Desiree"],["dc.contributor.author","Leha, Andreas"],["dc.contributor.author","Schulte, Claudia"],["dc.contributor.author","Tönges, Lars"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Rückamp, Daniel"],["dc.contributor.author","Börger, Matthias"],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Lingor, Paul"],["dc.date.accessioned","2020-12-10T15:20:25Z"],["dc.date.available","2020-12-10T15:20:25Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1016/j.nbd.2019.104677"],["dc.identifier.issn","0969-9961"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72661"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Elemental fingerprint: Reassessment of a cerebrospinal fluid biomarker for Parkinson's disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e3936"],["dc.bibliographiccitation.issue","61"],["dc.bibliographiccitation.journal","Journal of Visualized Experiments"],["dc.contributor.author","Günther, R."],["dc.contributor.author","Suhr, M."],["dc.contributor.author","Koch, J. C."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Lingor, P."],["dc.contributor.author","Tönges, L."],["dc.date.accessioned","2017-09-07T11:48:58Z"],["dc.date.available","2017-09-07T11:48:58Z"],["dc.date.issued","2012"],["dc.description.abstract","Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder resulting in progressive degeneration of motoneurons. Peak of onset is around 60 years for the sporadic disease and around 50 years for the familial disease. Due to its progressive course, 50% of the patients die within 30 months of symptom onset. In order to evaluate novel treatment options for this disease, genetic mouse models of ALS have been generated based on human familial mutations in the SOD gene, such as the SOD1 (G93A) mutation. Most important aspects that have to be evaluated in the model are overall survival, clinical course and motor function. Here, we demonstrate the clinical evaluation, show the conduction of two behavioural motor tests and provide quantitative scoring systems for all parameters. Because an in depth analysis of the ALS mouse model usually requires an immunohistochemical examination of the spinal cord, we demonstrate its preparation in detail applying the dorsal laminectomy method. Exemplary histological findings are demonstrated. The comprehensive application of the depicted examination methods in studies on the mouse model of ALS will enable the researcher to reliably test future therapeutic options which can provide a basis for later human clinical trials."],["dc.identifier.doi","10.3791/3936"],["dc.identifier.gro","3142575"],["dc.identifier.isi","000209222800054"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8941"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1940-087X"],["dc.title","Clinical Testing and Spinal Cord Removal in a Mouse Model for Amyotrophic Lateral Sclerosis (ALS)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2606"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","2619"],["dc.bibliographiccitation.volume","131"],["dc.contributor.author","Planchamp, V."],["dc.contributor.author","Bermel, C."],["dc.contributor.author","Tönges, L."],["dc.contributor.author","Ostendorf, T."],["dc.contributor.author","Kügler, Sebastian"],["dc.contributor.author","Reed, J. C."],["dc.contributor.author","Kermer, Pawel"],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Lingor, P."],["dc.date.accessioned","2017-09-07T11:48:10Z"],["dc.date.available","2017-09-07T11:48:10Z"],["dc.date.issued","2008"],["dc.description.abstract","Improved survival of injured neurons and the inhibition of repulsive environmental signalling are prerequisites for functional regeneration. BAG1 (Bcl-2-associated athanogene-1) is an Hsp70/Hsc70-binding protein, which has been shown to suppress apoptosis and enhance neuronal differentiation. We investigated BAG1 as a therapeutic molecule in the lesioned visual system in vivo. Using an adeno-associated viral vector, BAG1 (AAV.BAG1) was expressed in retinal ganglion cells (RGC) and then tested in models of optic nerve axotomy and optic nerve crush. BAG1 significantly increased RGC survival as compared to adeno-associated viral vector enhanced green fluorescent protein (AAV.EGFP) treated controls and this was independently confirmed in transgenic mice over-expressing BAG1 in neurons. The numbers and lengths of regenerating axons after optic nerve crush were also significantly increased in the AAV.BAG1 group. In pRGC cultures, BAG1-over-expression resulted in a similar to 3-fold increase in neurite length and growth cone surface. Interestingly, BAG1 induced an intracellular translocation of Raf-1 and ROCK2 and ROCK activity was decreased in a Raf-1-dependent manner by BAG1-over-expression. In summary, we show that BAG1 acts in a dual role by inhibition of lesion-induced apoptosis and interaction with the inhibitory ROCK signalling cascade. BAG1 is therefore a promising molecule to be further examined as a putative therapeutic tool in neurorestorative strategies."],["dc.identifier.doi","10.1093/brain/awn196"],["dc.identifier.gro","3143228"],["dc.identifier.isi","000260381300008"],["dc.identifier.pmid","18757464"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/719"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0006-8950"],["dc.subject","BAG1; ROCK2; Raf-1 kinase; retinal ganglion cell; regeneration; apoptosis"],["dc.title","BAG1 promotes axonal outgrowth and regeneration in vivo via Raf-1 and reduction of ROCK activity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","250"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","263"],["dc.bibliographiccitation.volume","131"],["dc.contributor.author","Lingor, Paul"],["dc.contributor.author","Tönges, Lars"],["dc.contributor.author","Pieper, Nicole"],["dc.contributor.author","Bermel, Christina"],["dc.contributor.author","Barski, Elisabeth"],["dc.contributor.author","Planchamp, Veronique"],["dc.contributor.author","Bähr, Mathias"],["dc.date.accessioned","2017-09-07T11:48:48Z"],["dc.date.available","2017-09-07T11:48:48Z"],["dc.date.issued","2008"],["dc.description.abstract","Functional regeneration in the CNS is limited by lesion-induced neuronal apoptosis and an environment inhibiting axonal elongation. A principal, yet unresolved question is the interaction between these two major factors. We thus evaluated the role of pharmacological inhibition of rho kinase (ROCK), a key mediator of myelin-derived axonal growth inhibition and CNTF, a potent neurotrophic factor for retinal ganglion cells (RGC), in models of retinal ganglion cell apoptosis and neurite outgrowth/regeneration in vitro and in vivo. Here, we show for the first time that the ROCK inhibitor Y-27632 significantly enhanced survival of RGC in vitro and in vivo. In vitro, the co-application of CNTF and Y-27632 potentiated the effect of either substance alone. ROCK inhibition resulted in the activation of the intrinsic MAPK pathway, and the combination of CNTF and Y-27632 resulted in even more pronounced MAPK activation. While CNTF also induced STAT3 phosphorylation, the additional application of ROCK inhibitor surprisingly diminished the effects of CNTF on STAT3 phosphorylation. ROCK activity was also decreased in an additive manner by both substances. In vivo, both CNTF and Y-27632 enhanced regeneration of RGC into the non-permissive optic nerve crush model and additive effects were observed after combination treatment. Further evaluation using specific inhibitors delineate STAT3 as a negative regulator of neurite growth and positive regulator of cell survival, while MAPK and Akt support neurite growth. These results show that next to neurotrophic factors ROCK inhibition by Y-27632 potently supports survival of lesioned adult CNS neurons. Co-administration of CNTF and Y-27632 results in additive effects on neurite outgrowth and regeneration. The interaction of intracellular signalling pathways may, however, attenuate more pronounced synergy and has to be taken into account for future treatment strategies."],["dc.identifier.doi","10.1093/brain/awm284"],["dc.identifier.gro","3143369"],["dc.identifier.isi","000251865700021"],["dc.identifier.pmid","18063589"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/875"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0006-8950"],["dc.subject","retinal ganglion cells; CNTF; rho kinase; axotomy; regeneration"],["dc.title","ROCK inhibition and CNTF interact on intrinsic signalling pathways and differentially regulate survival and regeneration in retinal ganglion cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]