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| 1 | Cellular mechanisms of connexin32mutations associated with CNS manifestations显示文摘 | Kleopa KA Yum SW Scherer SS | 2002 | J Neurosci Res2002，68，5： | 1 |
| 2 | Unique distributions of the gap junction proteins connexin29, connexin32, and connexin47 in ohgodendrocytes显示文摘 | Kleopa K A Orthmann J L Enriquez A | 2004 | Glia2004，47，4： | 1 |
| 3 | Connexin29 is uniquely distributed within myelinating glial cells of the central and peripheral nervous systems 显示文摘 | Altevogt B M Kleopa K A Postma F R | 2002 | J Neurosci2002，22，15： | 1 |
| 4 | Autoimmune channelopathies and related neurological disorders显示文摘 | Vincent A Lang B Kleopa KA | 2006 | Neuron2006，52，： | 1 |
| 5 | Acute cervical radiculopathies in spontaneous intracranial hypotension显示文摘 | Kleopa KA Natsiopoulos K | 2009 | Neurol2009，256，3： | 1 |
| 6 | Naturally occurring utrophin correlates with disease severity in Duchenne muscular dystrophy显示文摘 | Kleopa KA Drousiotou A Mavrikiou E | 2006 | Hum Mol Genet2006，15，10： | 1 |
| 7 | BiPAP improves survival and rate of pulmonary function decline in patients with ALS显示文摘 | Kleopa KA Sherman M Neal B | | Journal of the Neurological Sciences0，，： | 1 |
| 8 | Autoimmune limbicencephalitis in 39patients:immunophenotypes and outcomes显示文摘 | Bataller L Kleopa KA Wu GF | 2007 | J Neurol Neurosurg Psychiatry2007，78，4： | 1 |
| 9 | Autoimmune limbic en?cephalitis in 39 patients: immunophenotypes and outcomes显示文摘 | Bataller L Kleopa KA Wu GF | 2007 | J Neurol Neurosurg Psychiatry2007，78，： | 1 |
| 10 | Naturally occurring utrophin correlates with disease severity in Duchenne muscular dystrophy显示文摘 | Kleopa KA Drousiotou A Mavrikiou E | 2006 | Human Molecular Genetics2006，15，： | 1 |
| 11 | Human GLUD2 glutamate dehydrogenase is expressed in neural and testicular supporting cells显示文摘 | Spanaki C Zaganas I Kleopa KA | 2010 | J Biol Chem2010，285，16： | 1 |
| 12 | Bipap improves survival and rate of pulmonary function decline in patients with ALS显示文摘 | Kleopa KA Sherman M Neal B | 1999 | J Neurol Sci1999，164，1： | 1 |
| 13 | Bipap improves survival and rate of pulmonary function decline in patients with ALS显示文摘 | Kleopa KA Sherman M Neal B | 1999 | J Neurol Sci1999，164，1： | 1 |
| 14 | KCNQ2 is a nodal K+ channel显示文摘 | Kleopa KA Cooper EC Scherer SS | 2004 | J Neurosci2004，24，： | 1 |
| 15 | Morvan syndrome: clinical and serological observations in 29 cases 显示文摘 | Irani SIR PettingilI P Kleopa KA | 2012 | Ann Neurol2012，72，2： | 1 |
| 16 | Autoimmune limbic encephalitis in 39 patiens:immunopheno types and outcomes显示文摘 | BatallerL Kleopa KA Wu GF | 2007 | Neurol Neurosurge Psychiatry2007，78，4： | 1 |
| 17 | Conuexins, gap junctions and peripheral neuropathy显示文摘 | Kleopa KA Sargiannidou I | 2014 | Neurosci Lett2014，24，2： | 1 |
| 18 | A novel PMP22 mutation Ser22Phe in a family with hereditary neuropathy with liability to pressure palsies and CMT1A phenotypes显示文摘 | Kleopa KA Georgioa DM Nicolaou P | 2004 | Neurogenetics2004，5，： | 1 |
| 19 | CMT1A current gene therapy approaches and promising biomarkers显示文摘Charcot-Marie-Tooth neuropathies(CMT)constitute a group of common but highly heterogeneous,non-syndromic genetic disorders affecting predominantly the peripheral nervous system.CMT type 1A(CMT1A)is the most frequent type and accounts for almost~50%of all diagnosed CMT cases.CMT1A results from the duplication of the peripheral myelin protein 22(PMP22)gene.Overexpression of PMP22 protein overloads the protein folding apparatus in Schwann cells and activates the unfolded protein response.This leads to Schwann cell apoptosis,dys-and de-myelination and secondary axonal degeneration,ultimately causing neurological disabilities.During the last decades,several different gene therapies have been developed to treat CMT1A.Almost all of them remain at the pre-clinical stage using CMT1A animal models overexpressing PMP22.The therapeutic goal is to achieve gene silencing,directly or indirectly,thereby reversing the CMT1A genetic mechanism allowing the recovery of myelination and prevention of axonal loss.As promising treatments are rapidly emerging,treatment-responsive and clinically relevant biomarkers are becoming necessary.These biomarkers and sensitive clinical evaluation tools will facilitate the design and successful completion of future clinical trials for CMT1A. | Marina Stavrou Kleopas AKleopa | 2023 | Neural Regeneration Research2023，18，7： | 1 |
| 20 | Autoimmune Channelopathies and Related Neurological Disorders显示文摘 | Angela Vincent Bethan Lang Kleopas A. Kleopa | 2006 | Neuron2006，，1： | 1 |
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