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Genomes and Genes | Abdelhaq RamiSummaryAffiliation: Frankfurt am Main Country: Germany Publications
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Publications
Increased neuronal injury in clock gene per-1 deficient-mice after cerebral ischemiaNina Wiebking
Klinikum der Goethe Universität, Dr Senckenbergische Anatomie, Institut für Anatomie III, Theodor Stern Kai 7, 60590 Frankfurt Main, Germany
Curr Neurovasc Res 10:112-25. 2013..These alterations may be causal for the observed innate vulnerability of Per1(-/-)-mice to cerebral ischemia...
Specific alterations of the HtrA2/HAX-1 ratio in the penumbra upon focal cerebral ischemia in miceA Rami
Dr Senckenbergische Anatomy, Institut für Zelluläre und Molekulare Anatomie Anatomie III, Klinikum der Johann Wolfgang von Goethe Universität, Theodor Stern Kai 7, 60590 Franfurt, Germany
Neurochem Res 37:548-56. 2012..Taken together, these results suggested that HAX-1 is probably involved in the pathophysiology of cell death induced by focal ischemia...- Focal cerebral ischemia induces upregulation of Beclin 1 and autophagy-like cell deathA Rami
Institute of Cellular and Molecular Anatomy Anatomie III, Klinikum der Johann Wolfgang von Goethe Universität, Theodor Stern Kai 7, 60590 Franfurt Main, Germany
Neurobiol Dis 29:132-41. 2008..The upregulation of Beclin 1 and related changes of LC3 in the ischemic penumbra may represent enhanced autophagy either as a mechanism to recycle injured cells and reduce damage or a process leading to cell demise... - Upregulation of Beclin 1 in the ischemic penumbraAbdelhaq Rami
Institute of Cellular and Molecular Anatomy Anatomie III, Dr Senckenbergische Anatomie, Klinikum der Johann Wolfgang von Goethe Universität, Franfurt Main, Germany
Autophagy 4:227-9. 2008..The question that constantly arises, however, is whether autophagic activity in damaged cells is the cause of death or is actually an attempt to prevent it as a part of an endogenous neuroprotective response... - Apoptosis meets autophagy-like cell death in the ischemic penumbra: Two sides of the same coin?Abdelhaq Rami
Institute of Cellular and Molecular Anatomy Anatomie III, Centre for Neurology and Neurosurgery, Johann Wolfgang Goethe University Clinics, Frankfurt Main, Germany
Autophagy 4:422-6. 2008..A profound understanding of the biological effects and the mechanisms underlying ischemia-induced autophagy in neurons might be helpful in seeking effective new treatments for cerebral ischemia... - Exploiting endogenous anti-apoptotic proteins for novel therapeutic strategies in cerebral ischemiaAbdelhaq Rami
Dr Senckenbergische Anatomie, Institute of Cellular and Molecular Anatomy Anatomie III, Johann Wolfgang Goethe University, Theodor Stern Kai 7, D 60590 Frankfurt Main, Germany
Prog Neurobiol 85:273-96. 2008.... - Review: autophagy in neurodegeneration: firefighter and/or incendiarist?A Rami
Dr Senckenbergische Anatomie, Institute of Cellular and Molecular Anatomy Anatomie III, Wolfgang Goethe University, Frankfurt Main, Germany
Neuropathol Appl Neurobiol 35:449-61. 2009..Here, we review the defining characteristics of autophagy with special attention to its role in neurodegenerative disorders, and recent efforts to delineate the pathway of autophagic protein degradation in neurone... - Translocation of the serine protease Omi/HtrA2 from mitochondria into the cytosol upon seizure-induced hippocampal injury in the neonatal rat brainA Rami
Dr Senckenbergische Anatomie, Anatomie III, Universitatsklinikum, Theodor Stern Kai 7, 60590 Frankfurt Main, Germany
Neurochem Res 35:2199-207. 2010.... - beta2-Adrenergic receptor responsiveness of the calpain-calpastatin system and attenuation of neuronal death in rat hippocampus after transient global ischemiaA Rami
Anatomisches Institut III, Dr Senckenbergische Anatomie, Klinikum der JWG Universität, Theodor Stern Kai 7, 60590 Frankfurt Main, Germany
Neurosci Res 47:373-82. 2003..These results provide evidence that CLN is a potent neuroprotective substance, which through the enhancement of calpastatin synthesis attenuates the apoptotic machinery and modulates proteolysis... - Alterations in the expression of the anti-apoptotic factor HAX-1 upon seizures-induced hippocampal injury in the neonatal rat brainA Rami
Institut für Zelluläre und Molekulare Anatomie Anatomie III, Klinikum der Johann Wolfgang von Goethe Universität, Theodor Stern Kai 7, 60590 Franfurt Main, Germany
Neurochem Res 37:116-25. 2012..Taken together, these results suggested that HAX-1 is probably involved in the pathophysiology of cell death induced by epilepsy... - Ischemic neuronal death in the rat hippocampus: the calpain-calpastatin-caspase hypothesisA Rami
Institute of Anatomy III Dr Senckenbergische Anatomie, Faculty of Medicine, Clinic of the Johann Wolfgang Goethe University, Theodor Stern Kai 7, 60590 Frankfurt Main, Germany
Neurobiol Dis 13:75-88. 2003.... - Post-ischemic activation of caspase-3 in the rat hippocampus: evidence of an axonal and dendritic localisationA Rami
Institute of Anatomy III, Dr Senckenbergische Anatomie, Faculty of Medicine, Clinic of the Johann Wolfgang Goethe University, Theodor Ster Kai 7, 60590 Frankfurt Main, Germany
Neurochem Int 43:211-23. 2003.... - Spatial resolution of phospholipid scramblase 1 (PLSCR1), caspase-3 activation and DNA-fragmentation in the human hippocampus after cerebral ischemiaA Rami
Anatomisches Institut III, Universitatsklinikum, Theodor Stern Kai 7, 60590, Frankfurt Main, Germany
Neurochem Int 43:79-87. 2003..This study presents the first evidence that PLSCR1, and probably remodelling of plasma membrane phospholipids (PL), plays a role in ischemic injury in the human hippocampus... - Effective reduction of neuronal death by inhibiting gap junctional intercellular communication in a rodent model of global transient cerebral ischemiaA Rami
Anatomisches Institut III, Dr Senckenbergische Anatomie, Universitatsklinikum, Theodor Stern Kai 7, Frankfurt, 60590, FRG
Exp Neurol 170:297-304. 2001..This provides a novel perspective for analysis of the pathophysiology of cerebral ischemia... - mu-Calpain activation, DNA fragmentation, and synergistic effects of caspase and calpain inhibitors in protecting hippocampal neurons from ischemic damageA Rami
Anatomisches Institut III Dr Senckenbergische Anatomie, Universitatsklinikum, Theodor Stern Kai 7, 60590, Frankfurt, Germany
Brain Res 866:299-312. 2000..Moreover, the synergistic effect of caspase and calpain inhibitors in protecting neurons form ischemic damage suggests that there is a cross-talk between caspase and calpain during apoptosis... - Muscarinic-receptor antagonist scopolamine rescues hippocampal neurons from death induced by glutamateA Rami
Center of Morphology, Department of Anatomy III, University Clinic, Theodor Stern Kai 7, 60590 Frankfurt, Germany
Brain Res 788:323-6. 1998..These data show that interactions between the NMDA, muscarinic receptors and their corresponding neurotransmitter inputs to hippocampal neurons may play a crucial role in neurodegeneration... - Synergetic effects of caspase 3 and mu-calpain in XIAP-breakdown upon focal cerebral ischemiaAbdelhaq Rami
Institute of Cellular and Molecular Anatomy, Dr Senckenbergische Anatomie, Johann Wolfgang Goethe University, Theodor Stern Kai 7, 60590, Frankfurt Main, Germany
Neurochem Res 32:2072-9. 2007..Therefore, degradation of XIAP by mu-calpain in our system may decrease the activation threshold of caspase-3 normally held in check by the IAPs and/or lead to auto-activation of other caspases... - Differential effects of scopolamine on neuronal survival in ischemia and glutamate neurotoxicity: relationships to the excessive vulnerability of the dorsoseptal hippocampusA Rami
Dr Senckenbergische Anatomie, , Frankfurt, Germany
J Chem Neuroanat 13:201-8. 1997..However, the mechanisms underlying the high vulnerability of dorsal hippocampus still remain enigmatic... 
TGF-{beta}1 activates two distinct type I receptors in neurons: implications for neuronal NF-{kappa}B signalingHans Georg König
Experimental Neurosurgery, Center for Neurology and Neurosurgery, Johann Wolfgang Goethe University Clinics, D 60590 Frankfurt, Germany
J Cell Biol 168:1077-86. 2005..Our data suggest that TGF-beta1 simultaneously activates two distinct receptor pathways in neurons and that the ALK1 pathway mediates TGF-beta1-induced NF-kappaB survival signaling...- Regulation of XIAP and Smac/DIABLO in the rat hippocampus following transient forebrain ischemiaM D Siegelin
Institute of Anatomy III, Dr Senckenbergische Anatomie, Clinic of the JWG University, Theodor Stern Kai 7, Frankfurt Main 60590, Germany
Neurochem Int 46:41-51. 2005..Smac/DIABLO expression was associated with alteration of the XIAP levels and the appearance of activated form of caspase-3 within the hippocampus during reperfusion in spatial and temporal manners... - Expression of the gene encoding the pro-apoptotic BNIP3 protein and stimulation of hypoxia-inducible factor-1alpha (HIF-1alpha) protein following focal cerebral ischemia in ratsJ Althaus
Institut für Molekulare und Zelluläre Anatomie, Universitatsklinikum, Theodor Stern Kai 7, 60590 Frankfurt Main, Germany
Neurochem Int 48:687-95. 2006..These findings open the possibility that the hypoxia-regulated pro-apoptotic protein BNIP3 enters the nucleus and could interact with other proteins involved in DNA structure, transcription or mRNA splicing after focal brain ischemia... - Induction and redistribution of XAF1, a new antagonist of XIAP in the rat brain after transient focal ischemiaM Siegelin
Institut für Anatomie III, Universitatsklinikum, Theodor Stern Kai 7, 60590 Frankfurt Main, Germany
Neurobiol Dis 20:509-18. 2005..These finding indicate that Smac/DIABLO, XAF1, and XIAP are implicated in the pathophysiological mechanisms of reperfusion injury... - Tissue plasminogen activator mediated blood-brain barrier damage in transient focal cerebral ischemia in rats: relevance of interactions between thrombotic material and thrombolytic agentTimo Kahles
Department of Neurology, University Hospital, JW Goethe University Frankfurt, Schleusenweg 2 16, ZNN, 60528 Frankfurt Main, Germany
Vascul Pharmacol 43:254-9. 2005..The results of the present study indicate a major role for thrombus-thrombolytic interaction in focal cerebral ischemia with subsequent increased BBB permeability... - Activation of sphingosine kinase 2 is an endogenous protective mechanism in cerebral ischemiaWaltraud Pfeilschifter
Department of Neurology, University Hospital, Goethe University Frankfurt
Biochem Biophys Res Commun 413:212-7. 2011..This suggests that SphK2 activity is an important endogenous protective mechanism in cerebral ischemia and corroborates that the protective effect of FTY720 is mediated via phospho-FTY720... - The serine protease Omi/HtrA2 is involved in XIAP cleavage and in neuronal cell death following focal cerebral ischemia/reperfusionJ Althaus
Institut für Zelluläre und Molekulare Anatomie Anatomie III, Johann Wolfgang von Goethe Universität, Theodor Stern Kai 7, 60590 Franfurt, Main, Germany
Neurochem Int 50:172-80. 2007..Blocking the proteolytic activity of Omi/HtrA2 with specific inhibitors, such as the ucf-101, could be a novel way to afford neuroprotection and minimize cellular damage in cerebral ischemia/reperfusion... - Gene expression during ER stress-induced apoptosis in neurons: induction of the BH3-only protein Bbc3/PUMA and activation of the mitochondrial apoptosis pathwayClaus Reimertz
Experimental Neurosurgery, Center for Biological Chemistry ZBC, HS 25 B, 4 OG, Johann Wolfgang Goethe University Clinics, Theodor Stern Kai 7, D 60590 Frankfurt, Germany
J Cell Biol 162:587-97. 2003..Our data suggest that the transcriptional induction of Bbc3/PUMA may be sufficient and necessary for ER stress-induced apoptosis... - Serum deprivation induced autophagy and predominantly an AIF-dependent apoptosis in hippocampal HT22 neuronsS Steiger-Barraissoul
Institute of Cellular and Molecular Anatomy, Clinics of the Wolfgang Goethe University, Frankfurt Main, Germany
Apoptosis 14:1274-88. 2009..The results of the current study suggest that SD induced predominantly caspase-independent apoptosis in hippocampal HT22 cells and that inhibition of autophagy is rather deleterious than protective... - The immunomodulatory sphingosine 1-phosphate analog FTY720 reduces lesion size and improves neurological outcome in a mouse model of cerebral ischemiaBozena Czech
Pharmazentrum Frankfurt, Klinikum der Johann Wolfgang Goethe Universitat, Theodor Stern Kai 7, 60590 Frankfurt am Main, Germany
Biochem Biophys Res Commun 389:251-6. 2009.... - Concomitant transitory up-regulation of X-linked inhibitor of apoptosis protein (XIAP) and the heterogeneous nuclear ribonucleoprotein C1-C2 in surviving cells during neuronal apoptosisA Spahn
Institute of Cellular and Molecular Anatomy Anatomie III, Clinic of Johann Wolfgang von Goethe University, Theodor Stern Kai 7, 60590, Franfurt Main, Germany
Neurochem Res 33:1859-68. 2008..The up-regulation of hnRNP-C1/C2 may foster the synthesis of XIAP as a protective pathway by which neurons try to counteract the initial deleterious effects of apoptosis... - Immunoreactivity for Bcl-2 and C-Jun/AP1 in hippocampal corpora amylacea after ischaemia in humansG Botez
Institute of Anatomy III, Clinic of the JWG-University, Frankfurt, Germany
Neuropathol Appl Neurobiol 27:474-80. 2001.... - Control of fetal growth and neonatal survival by the RasGAP-associated endoribonuclease G3BPLatifa Zekri
Institut de génétique moléculaire de Montpellier UMR 5535, IFR 122, Centre National de Recherche Scientifique, 1919 Route de Mende, 34293 Montpellier, France
Mol Cell Biol 25:8703-16. 2005..The results demonstrate that G3BP is essential for proper embryonic growth and development by mediating the coordinate expression of multiple imprinted growth-regulatory transcripts... - Guidelines for the use and interpretation of assays for monitoring autophagy in higher eukaryotesDaniel J Klionsky
Life Sciences Institute, University of Michigan, Ann Arbor, Michigan 48109 2216, USA
Autophagy 4:151-75. 2008..In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to verify an autophagic response...