Research Topics
Genomes and Genes
| Chia Yi KuanSummaryAffiliation: Children's Hospital Medical Center Country: USA Publications
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Detail Information
Publications
A critical role of neural-specific JNK3 for ischemic apoptosisChia Yi Kuan
Department of Pediatrics, Division of Developmental Biology, Children s Hospital Medical Center, Cincinnati, OH 45229, USA
Proc Natl Acad Sci U S A 100:15184-9. 2003..The downstream mechanism of JNK3-mediated apoptosis may include the induction of Bim and Fas and the mitochondrial release of cytochrome c. These results suggest that JNK3 is a potential target for neuroprotection therapies in stroke...- Hypoxia-ischemia induces DNA synthesis without cell proliferation in dying neurons in adult rodent brainChia Yi Kuan
Department of Pediatrics, Children s Hospital Medical Center, Cincinnati, Ohio 45229, USA
J Neurosci 24:10763-72. 2004..Manipulating the aberrant apoptosis-associated DNA synthesis that occurs with hypoxia-ischemia and perhaps neurodegenerative diseases could promote neuronal survival and neurogenesis... - Targeting the JNK signaling pathway for stroke and Parkinson's diseases therapyChia Yi Kuan
Division of Developmental Biology, Cincinnati Children s Hospital Research Foundation, Cincinnati, OH 45229, USA
Curr Drug Targets CNS Neurol Disord 4:63-7. 2005..The mechanisms by which JNK signaling induces apoptosis and evidence of cytoprotective effects of these JNK inhibitors are summarized in the present review... - Rac1 controls the formation of midline commissures and the competency of tangential migration in ventral telencephalic neuronsLei Chen
Division of Experimental Hematology, Cincinnati Children s Hospital Medical Center, Cincinnati, Ohio 45229, USA
J Neurosci 27:3884-93. 2007..Moreover, they indicate that Rac1 has a critical role in axon guidance and in acquisition of migratory competency during differentiation of the progenitors for the ventral telencephalon-derived interneurons... - Cdc42 deficiency causes Sonic hedgehog-independent holoprosencephalyLei Chen
Division of Experimental Hematology, Cincinnati Children s Hospital Medical Center, University of Cincinnati College of Medicine, 3333 Burnet Avenue, Cincinnati, OH 45229, USA
Proc Natl Acad Sci U S A 103:16520-5. 2006..Taken together, these results indicate that Cdc42 has an essential role in establishing the apical-basal polarity of the telencephalic NE, which is needed for the expansion and bifurcation of cerebral hemispheres... - Loss of RhoA in neural progenitor cells causes the disruption of adherens junctions and hyperproliferationKei Ichi Katayama
Division of Developmental Biology, Cincinnati Children s Hospital Medical Center, Cincinnati, OH 45229, USA
Proc Natl Acad Sci U S A 108:7607-12. 2011..These results demonstrate a critical role of RhoA in the maintenance of apical adherens junctions and the regulation of neural progenitor proliferation in the developing mammalian brain... - Nestin-CreER mice reveal DNA synthesis by nonapoptotic neurons following cerebral ischemia hypoxiaKevin A Burns
Divisions of Developmental Biology and Pediatric Neurology, Cincinnati Children s Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH 45229, USA
Cereb Cortex 17:2585-92. 2007..These results suggest that the nestin-CreER system is a useful tool for detecting embryonic and adult neurogensis. They also confirm the existence of nonproliferative DNA synthesis by old neurons after experimental brain injury... - Deleterious effects of plasminogen activators in neonatal cerebral hypoxia-ischemiaFaisal Adhami
Division of Developmental Biology and Division of Neurology, Cincinnati Children s Hospital Research Foundation, Cincinnati, OH 45229, USA
Am J Pathol 172:1704-16. 2008.... - Ex vivo diffusion tensor imaging and neuropathological correlation in a murine model of hypoxia-ischemia-induced thrombotic strokeAhmed Shereen
Department of Radiology, Cincinnati Children s Hospital Medical Center, Cincinnati, Ohio 45229, USA
J Cereb Blood Flow Metab 31:1155-69. 2011..Taken together, these results suggest that cross-evaluation of multiple DTI parameters may provide a fuller picture of axonal and dendritic injury in acute ischemic stroke... - c-Jun N-terminal kinases (JNK) antagonize cardiac growth through cross-talk with calcineurin-NFAT signalingQiangrong Liang
Department of Pediatrics, University of Cincinnati, Children s Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, OH 45229 3039, USA
EMBO J 22:5079-89. 2003..These results also suggest that myocardial JNK activation is primarily dedicated to modulating calcineurin-NFAT signaling in the regulation of differentiated heart growth... - Midgestational lethality in mice lacking the parathyroid hormone (PTH)/PTH-related peptide receptor is associated with abrupt cardiomyocyte deathJin Qian
Department of Medicine, University of Cincinnati, Cincinnati, Ohio 45267, USA
Endocrinology 144:1053-61. 2003..Taken together, these findings indicate that the PTH1R is required for the development of normal cardiomyocyte function... - Cdc42GAP regulates c-Jun N-terminal kinase (JNK)-mediated apoptosis and cell number during mammalian perinatal growthLei Wang
Division of Experimental Hematology, Children s Hospital Medical Center, Molecular Developmental Biology Graduate Program, University of Cincinnati, Cincinnati, OH 45229, USA
Proc Natl Acad Sci U S A 102:13484-9. 2005..These results reveal a role of Cdc42GAP in mammalian perinatal growth and implicate the c-Jun N-terminal kinase-mediated apoptosis machinery as a Cdc42 effector pathway in vivo... - Promiscuous recombination of LoxP alleles during gametogenesis in cornea Cre driver miceDaniel Y Weng
Department of Ophthalmology, University of Cincinnati, Cincinnati, OH 45267 0838, USA
Mol Vis 14:562-71. 2008..To examine whether promiscuous Cre/LoxP recombination happens during gametogenesis in double transgenic mice carrying LoxP modified alleles and Cre transgene driven by tissue-specific promoter outside the gonads of adult mice... - Jun NH2-terminal kinase (JNK) prevents nuclear beta-catenin accumulation and regulates axis formation in Xenopus embryosGuanghong Liao
Department of Pediatrics, Division of Developmental Biology, Children s Hospital Medical Center, Cincinnati, OH 45229, USA
Proc Natl Acad Sci U S A 103:16313-8. 2006..Thus, the high level of sustained maternal JNK activity in early Xenopus embryos may provide a timing mechanism for controlling the dorsal axis formation... - The roles of autophagy in cerebral ischemiaFaisal Adhami
Department of Pediatrics, Children s Hospital Medical Center, Cincinnati, Ohio, USA
Autophagy 3:42-4. 2007..Finally, we suggest autophagy is an important modifier of cell death and survival, interacting with necrosis and apoptosis in determining the outcomes and final morphology of deceased neurons... - Coordinated control of self-renewal and differentiation of neural stem cells by Myc and the p19ARF-p53 pathwayMotoshi Nagao
Division of Developmental Biology, Cincinnati Children s Hospital Research Foundation, Cincinnati, OH 45229, USA
J Cell Biol 183:1243-57. 2008..We propose that opposing actions of Myc and the p19(ARF)-p53 pathway have important functions in coordinated developmental control of self-renewal and cell fate choices in NSCs... - Rac1 deficiency in the forebrain results in neural progenitor reduction and microcephalyLei Chen
Divisios of Experimental Hematology, University of Cincinnati, Cincinnati, OH 45229, USA
Dev Biol 325:162-70. 2009..Together, these results suggest that Rac1 regulates self-renewal, survival, and differentiation of telencephalic neural progenitors, and that dysfunctions of Rac1 may lead to primary microcephaly... - Mannitol-facilitated perfusion staining with 2,3,5-triphenyltetrazolium chloride (TTC) for detection of experimental cerebral infarction and biochemical analysisYu Yo Sun
Division of Developmental Biology, Division of Neurology, Cincinnati Children s Hospital Medical Center, Cincinnati, OH 45229, United States
J Neurosci Methods 203:122-9. 2012..These results demonstrate a fast and inexpensive method that simplifies the task of quantifying cerebral infarction in small or severely injured brains and assists biochemical analysis of experimental cerebral ischemia... - Developmental and post-injury cortical gliogenesis: a genetic fate-mapping study with Nestin-CreER miceKevin A Burns
Division of Developmental Biology, Division of Neurology, Department of Pediatrics, Cincinnati Children s Hospital Medical Center, Cincinnati, Ohio 45229, USA
Glia 57:1115-29. 2009..8% after stab-wound injury. Together, these results suggest NG2+ progenitors, rather than GFAP+ astrocytes, are the primary source of proliferative gliosis after adult brain injury... - Therapeutic administration of plasminogen activator inhibitor-1 prevents hypoxic-ischemic brain injury in newbornsDianer Yang
Division of Developmental Biology and Division of Neurology, Department of Radiology, Cincinnati Children s Hospital Medical Center, Cincinnati, Ohio 45229, USA
J Neurosci 29:8669-74. 2009..Together, these results suggest that the brain PA system plays a pivotal role in neonatal cerebral HI and may be a promising therapeutic target in infants suffering hypoxic-ischemic encephalopathy... - Low doses of bromo- and iododeoxyuridine produce near-saturation labeling of adult proliferative populations in the dentate gyrusKevin A Burns
Department of Pediatrics, Division of Developmental Biology, Room 3464, 3333 Burnet Avenue, Cincinnati, OH 45229, USA
Eur J Neurosci 21:803-7. 2005..These results suggest that the standard dose of BrdU is sufficient to label the majority of proliferative populations in the S-phase in pulse labeling experiments... - Cerebral ischemia-hypoxia induces intravascular coagulation and autophagyFaisal Adhami
Division of Developmental Biology, Cincinnati Children's Hospital Research Foundation, Room 3464, 3333 Burnet Ave, Cincinnati, OH 45229, USA
Am J Pathol 169:566-83. 2006..Together, these results suggest that ischemia-hypoxia is a powerful stimulus for spontaneous coagulation leading to reperfusion deficits and autophagic/lysosomal cell death in brain... - Modulation of germ cell apoptosis with a nitric oxide synthase inhibitor in a murine model of congenital cryptorchidismWilliam R DeFoor
Division of Pediatric Urology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio 45229-3039, USA
J Urol 172:1731-5; discussion 1735. 2004..This finding suggests that early treatment might serve as an adjunct to early surgical intervention to reduce testicular atrophy, although any impact on long-term fertility remains to be determined... - Mixed lineage kinase-c-jun N-terminal kinase signaling pathway: a new therapeutic target in Parkinson's diseaseRobert M Silva
Department of Neurology, The College of Physicians and Surgeons, Columbia University, 650 West 168th Street, New York, NY 10032, USA
Mov Disord 20:653-64. 2005..These studies suggest important future directions for the development of therapies that will target this important cell death pathway... - Specific pathophysiological functions of JNK isoforms in the brainStephan Brecht
Institute of Pharmacology, University Hospital of Schleswig Holstein, Campus Kiel, Hospitalstrasse 4, 24105 Kiel, Germany
Eur J Neurosci 21:363-77. 2005..This comprehensive study provides novel insights into the context-dependent physiological and pathological functions of JNK isoforms... - Requirement of JIP scaffold proteins for NMDA-mediated signal transductionNorman J Kennedy
Howard Hughes Medical Institute and Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA
Genes Dev 21:2336-46. 2007..JIP complexes interact with the SH2 domain of cFyn and may therefore promote tyrosine phosphorylation and activity of the NMDA receptor. We conclude that JIP scaffold proteins are critically required for normal NMDA receptor function...