Affiliation: Philipps University
- The expression of transforming growth factor-beta1 (TGF-beta1) in hippocampal neurons: a temporary upregulated protein level after transient forebrain ischemia in the ratY Zhu
Institut fur Pharmakologie und Toxikologie, Philipps Universitat, Marburg, Germany
Brain Res 866:286-98. 2000..The endogenous TGF-beta1 expressed in neurons may play a role in the pathological process of DNA degradation and delayed neuronal death after transient forebrain ischemia...
- TGF-beta1 inhibits caspase-3 activation and neuronal apoptosis in rat hippocampal culturesY Zhu
Institut fur Pharmakologie und Toxikologie, Philipps Universitat Marburg, Ketzerbach 63, D 35032, Marburg, Germany
Neurochem Int 38:227-35. 2001..This study provides evidence that TGF-beta1 is able to efficiently inhibit caspase-3 activation, and thereby protects cultured hippocampal neurons against apoptosis...
- Beta(2)-adrenoceptor stimulation enhances latent transforming growth factor-beta-binding protein-1 and transforming growth factor-beta1 expression in rat hippocampus after transient forebrain ischemiaY Zhu
Institut fur Pharmakologie und Toxikologie, Philipps Universitat, Marburg, Germany
Neuroscience 107:593-602. 2001..Our data demonstrate a concomitant increase in LTBP-1 and TGF-beta1 expression in the ischemic hippocampus after stimulation of beta(2)-adrenoceptors...
- Transforming growth factor-beta 1 increases bad phosphorylation and protects neurons against damageYuan Zhu
Institut für Pharmakologie und Toxikologie and Pharmazeutische Chemie, Philipps Universitat, D 35032 Marburg, Germany
J Neurosci 22:3898-909. 2002..Together, we demonstrate that TGF-beta1 suppresses Bad expression under lesion conditions, increases Bad phosphorylation, and activates the MAPK/Erk pathway, which may contribute to its neuroprotective activity...
- Neuroprotection by transforming growth factor-beta1 involves activation of nuclear factor-kappaB through phosphatidylinositol-3-OH kinase/Akt and mitogen-activated protein kinase-extracellular-signal regulated kinase1,2 signaling pathwaysY Zhu
Institut fuer Pharmakologie und Toxikologie, Philipps Universitaet, Ketzerbach 63, D 35032 Marburg, Germany
Neuroscience 123:897-906. 2004....
- Cytosine arabinofuranoside-induced activation of astrocytes increases the susceptibility of neurons to glutamate due to the release of soluble factorsBarbara Ahlemeyer
Institut fur Pharmakologie und Toxikologie, Fachbereich Pharmazie der Philipps Universität Marburg, Ketzerbach 63, 35032 Marburg, Germany
Neurochem Int 42:567-81. 2003..Our findings provide evidence that activation of astrocytes impairs their ability to protect neurons after excitotoxic injury due to changes in the release of soluble and heat-sensitive factors...
- Oleic acid causes apoptosis and dephosphorylates BadYuan Zhu
Philipps Universitat Marburg, Institut fur Pharmakologie und Toxikologie, Ketzerbach 63, 35032 Marburg, Germany
Neurochem Int 46:127-35. 2005..We conclude that oleic acid induces neuronal apoptosis through a caspase-3-independent mechanism involving dephosphorylation of Bad...
- Involvement of PTEN promoter methylation in cerebral cavernous malformationsYuan Zhu
Department of Neurosurgery, University of Marburg, Marburg, Germany
Stroke 40:820-6. 2009..PTEN promoter hypermethylation is a major epigenetic silencing mechanism leading to activation of angiogenesis in tumors. The present study aimed to investigate whether PTEN promoter methylation was involved in CCMs...
- Increase in glutamate-induced neurotoxicity by activated astrocytes involves stimulation of protein kinase CBarbara Ahlemeyer
Institut fur Pharmakologie und Toxikologie, Fachbereich Pharmazie der Philipps Universität Marburg, Germany
J Neurochem 82:504-15. 2002....
- Implication of PTEN in production of reactive oxygen species and neuronal death in in vitro models of stroke and Parkinson's diseaseYuan Zhu
Institut fur Pharmakologie und Toxikologie, Philipps Universitat Marburg, Baldingerstrasse, D 35032 Marburg, Germany
Neurochem Int 50:507-16. 2007..The present study highlights PTEN as a crucial and common mediator of ROS generation and neuronal death and suggests that PTEN could become a potential therapeutic target for interfering with neurodegeneration...
- Biological activity of paediatric cerebral cavernomas: an immunohistochemical study of 28 patientsWuttipong Tirakotai
Department of Neurosurgery, Philipps University, Baldingerstrasse, 35033, Marburg, Germany
Childs Nerv Syst 22:685-91. 2006..According to the hypothesis that paediatric cerebral cavernomas may have different biological activity compared to adult cavernomas, immunohistochemical analysis was used to elucidate the biological nature of paediatric cavernomas...
- Phosphatase and tensin homolog in cerebral cavernous malformation: a potential role in pathological angiogenesisYuan Zhu
Departments of Neurosurgery, University of Marburg, Marburg, Germany
J Neurosurg 110:530-9. 2009..Phosphatase and tensin homolog (PTEN) plays a crucial role in regulating angiogenesis. The authors attempted to determine whether PTEN is involved in the pathological angiogenesis of CCM...
- Protein kinase CK2 phosphorylates BAD at threonine-117Susanne Klumpp
Institut für Pharmazeutische and Medizinische Chemie, Westfalische Wilhelms Universitat, Hittorfstr 58 62, D 48149 Munster, Germany
Neurochem Int 45:747-52. 2004..The discovery of the constitutively active CK2 phosphorylating BAD is shedding an unexpected light in the otherwise strictly signal-regulated phosphorylation events on BAD...
- Transplantation of vascular endothelial growth factor-transfected neural stem cells into the rat brain provides neuroprotection after transient focal cerebral ischemiaWei Zhu
Institution of Neurosurgery, Hua Shan Hospital, Fudan University, Shanghai, China
Neurosurgery 57:325-33; discussion 325-33. 2005....
- The loss of Nf1 transiently promotes self-renewal but not tumorigenesis by neural crest stem cellsNancy M Joseph
Center for Stem Cell Biology, Howard Hughes Medical Institute, Life Sciences Institute, University of Michigan, Ann Arbor, MI 48109 2216, USA
Cancer Cell 13:129-40. 2008..Tumors appeared to arise from differentiated glia, not NCSCs...
- Induction of abnormal proliferation by nonmyelinating schwann cells triggers neurofibroma formationHuarui Zheng
Division of Molecular Medicine and Genetics, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109, USA
Cancer Cell 13:117-28. 2008..Subsequent degeneration of abnormal Remak bundles was accompanied by initial expansion of nonmyelinating Schwann cells. We suggest abnormally differentiated Remak bundles as a cell of origin for plexiform neurofibroma...
- Inactivation of NF1 in CNS causes increased glial progenitor proliferation and optic glioma formationYuan Zhu
Center for Developmental Biology and Kent Waldrep Foundation Center for Basic Research on Nerve Growth and Regeneration, University of Texas Southwestern Medical Center, Dallas, TX 75390 9133, USA
Development 132:5577-88. 2005..These data point to hyperproliferative glial progenitors as the source of the optic tumors and provide a genetic model for NF1-associated astrogliosis and optic glioma...
- Synthesis and structure-activity relationship of novel 6-aryl-1,4-dihydrobenzo[d][1,3]oxazine-2-thiones as progesterone receptor modulators leading to the potent and selective nonsteroidal progesterone receptor agonist tanaprogetAndrew Fensome
Chemical and Screening Sciences, Women s Health Research Institute, Wyeth Research, 500 Arcola Road, Collegeville, PA 19426, USA
J Med Chem 48:5092-5. 2005..Additional SAR, biological activity, and structural information from a tanaproget/hPR-LBD (hPR-LBD = human progesterone receptor ligand binding domain) cocrystal structure will also be presented...
- Potent nonsteroidal progesterone receptor agonists: synthesis and SAR study of 6-aryl benzoxazinesPuwen Zhang
Medicinal Chemistry I, Chemical Sciences, Wyeth Research, 500 Arcola Road, Collegeville, PA 19426, USA
Bioorg Med Chem Lett 12:787-90. 2002..20-0.35nM). Compound 6a was more potent than progesterone (P4) in the in vivo decidualization assay in an ovariectomized female rat model by subcutaneous administration with an ED(50) of 1.5mg/kg (vs 5.62mg/kg for P4)...
- Astrocyte-specific inactivation of the neurofibromatosis 1 gene (NF1) is insufficient for astrocytoma formationMichaela Livia Bajenaru
Department of Neurology, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO 63110, USA
Mol Cell Biol 22:5100-13. 2002..Collectively, our results suggest that loss of neurofibromin is not sufficient for astrocytoma formation in mice and that other genetic or environmental factors might influence NF1-associated glioma tumorigenesis...
- Optic nerve glioma in mice requires astrocyte Nf1 gene inactivation and Nf1 brain heterozygosityM Livia Bajenaru
Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63110, USA
Cancer Res 63:8573-7. 2003..This mouse model demonstrates that Nf1+/- cells contribute to the pathogenesis of gliomas in NF1 and provides a tool for the preclinical evaluation of potential therapeutic interventions for these tumors...