Pardo, Luis A.

[["dc.bibliographiccitation.artnumber","1600253"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","BioEssays"],["dc.bibliographiccitation.volume","39"],["dc.contributor.author","Pedersen, Stine F."],["dc.contributor.author","Novak, Ivana"],["dc.contributor.author","Alves, Frauke"],["dc.contributor.author","Schwab, Albrecht"],["dc.contributor.author","Pardo, Luis A."],["dc.date.accessioned","2018-10-10T13:25:55Z"],["dc.date.available","2018-10-10T13:25:55Z"],["dc.date.issued","2017"],["dc.description.abstract","We present here the hypothesis that the unique microenvironmental pH landscape of acid-base transporting epithelia is an important factor in development of epithelial cancers, by rendering the epithelial and stromal cells pre-adapted to the heterogeneous extracellular pH (pHe ) in the tumor microenvironment. Cells residing in organs with net acid-base transporting epithelia such as the pancreatic ductal and gastric epithelia are exposed to very different, temporally highly variable pHe values apically and basolaterally. This translates into spatially and temporally non-uniform intracellular pH (pHi ) patterns. Disturbed pHe - and pHi -homeostasis contributes to essentially all hallmarks of cancer. Our hypothesis, that the physiological pHe microenvironment in acid-base secreting epithelia shapes cancers arising in these tissues, can be tested using novel imaging tools. The acidic tumor pHe in turn might be exploited therapeutically. Pancreatic cancers are used as our prime example, but we propose that this concept is also relevant for other cancers of acid-base transporting epithelia."],["dc.fs.pkfprnr","66887"],["dc.identifier.doi","10.1002/bies.201600253"],["dc.identifier.fs","631974"],["dc.identifier.pmid","28440551"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/15964"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","1521-1878"],["dc.title","Alternating pH landscapes shape epithelial cancer initiation and progression: Focus on pancreatic cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Pharmacology"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Hartung, Franziska"],["dc.contributor.author","Krüwel, Thomas"],["dc.contributor.author","Shi, Xiaoyi"],["dc.contributor.author","Pfizenmaier, Klaus"],["dc.contributor.author","Kontermann, Roland"],["dc.contributor.author","Chames, Patrick"],["dc.contributor.author","Alves, Frauke"],["dc.contributor.author","Pardo, Luis A."],["dc.date.accessioned","2021-04-14T08:26:27Z"],["dc.date.available","2021-04-14T08:26:27Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.3389/fphar.2020.00686"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81946"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1663-9812"],["dc.title","A Novel Anti-Kv10.1 Nanobody Fused to Single-Chain TRAIL Enhances Apoptosis Induction in Cancer Cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","589"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","American Journal Of Pathology"],["dc.bibliographiccitation.lastpage","598"],["dc.bibliographiccitation.volume","171"],["dc.contributor.author","Herrero-Herranz, Eva"],["dc.contributor.author","Pardo, Luis A."],["dc.contributor.author","Bunt, Gertrude"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Stühmer, Walter"],["dc.contributor.author","Linker, Ralf A."],["dc.date.accessioned","2018-11-07T10:59:44Z"],["dc.date.available","2018-11-07T10:59:44Z"],["dc.date.issued","2007"],["dc.description.abstract","Mechanisms of lesion repair in multiple sclerosis are incompletely understood. To some degree, remyelination can occur, associated with an increase of proliferating oligodendroglial cells. Recently, the expression of potassium channels has been implicated in the control of oligodendrocyte precursor cell proliferation in vitro. We investigated the expression of Kv1.4 potassium channels in myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis, a model of multiple sclerosis. Confocal microscopy revealed expression of Kv1.4 in AN2-positive oligodendrocyte precursor cells and pre-myelinating oligodendrocytes in vitro but neither in mature oligodendrocytes nor in the spinal cords of healthy adult mice. After induction of myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis, Kv1.4 immunoreactivity was detected in or around lesions already during disease onset with a peak early and a subsequent decrease in the late phase of the disease. Kv1.4 expression was confined to 2',3'-cyclic nucleotide 3'-phosphodiesterase-positive oligodendroglial cells, which were actively proliferating and ensheathed naked axons. After a demyelinating episode, the number of Kv1.4 and 2',3'-cyclic nucleotide 3'-phosphodiesterase double-positive cells was greatly reduced in ciliary neurotrophic factor knockout mice, a model with impaired lesion repair. in summary, the re-expression of an oligodendroglial potassium channel may have a functional implication on oligodendroglial cell cycle progression, thus influencing tissue repair in experimental autoimmune encephalomyelitis and multiple sclerosis."],["dc.identifier.doi","10.2353/ajpath.2007.061241"],["dc.identifier.isi","000248496300022"],["dc.identifier.pmid","17600124"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50766"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0002-9440"],["dc.title","Re-expression of a developmentally restricted potassium channel in autoimmune demyelination - Kv1.4 is implicated in oligodendroglial proliferation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1143"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Molecular Psychiatry"],["dc.bibliographiccitation.lastpage","1149"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Hammer, Christian"],["dc.contributor.author","Stepniak, Beata"],["dc.contributor.author","Schneider, Anja"],["dc.contributor.author","Papiol, Sergi"],["dc.contributor.author","Tantra, Martesa"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Sirén, Anna-Leena"],["dc.contributor.author","Pardo, Luis A."],["dc.contributor.author","Sperling, Swetlana"],["dc.contributor.author","Mohd Jofrry, Sue"],["dc.contributor.author","Gurvich, Artem"],["dc.contributor.author","Jensen, Niels"],["dc.contributor.author","Ostmeier, Katrin"],["dc.contributor.author","Lühder, F."],["dc.contributor.author","Probst, Christian"],["dc.contributor.author","Martens, Henrik"],["dc.contributor.author","Gillis, M."],["dc.contributor.author","Saher, Gesine"],["dc.contributor.author","Assogna, F."],["dc.contributor.author","Spalletta, Gianfranco"],["dc.contributor.author","Stöcker, W."],["dc.contributor.author","Schulz, Thomas F."],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:37Z"],["dc.date.available","2017-09-07T11:46:37Z"],["dc.date.issued","2014"],["dc.description.abstract","In 2007, a multifaceted syndrome, associated with anti-NMDA receptor autoantibodies (NMDAR-AB) of immunoglobulin-G isotype, has been described, which variably consists of psychosis, epilepsy, cognitive decline and extrapyramidal symptoms. Prevalence and significance of NMDAR-AB in complex neuropsychiatric disease versus health, however, have remained unclear. We tested sera of 2817 subjects (1325 healthy, 1081 schizophrenic, 263 Parkinson and 148 affective-disorder subjects) for presence of NMDAR-AB, conducted a genome-wide genetic association study, comparing AB carriers versus non-carriers, and assessed their influenza AB status. For mechanistic insight and documentation of AB functionality, in vivo experiments involving mice with deficient blood-brain barrier (ApoE(-/-)) and in vitro endocytosis assays in primary cortical neurons were performed. In 10.5% of subjects, NMDAR-AB (NR1 subunit) of any immunoglobulin isotype were detected, with no difference in seroprevalence, titer or in vitro functionality between patients and healthy controls. Administration of extracted human serum to mice influenced basal and MK-801-induced activity in the open field only in ApoE(-/-) mice injected with NMDAR-AB-positive serum but not in respective controls. Seropositive schizophrenic patients with a history of neurotrauma or birth complications, indicating an at least temporarily compromised blood-brain barrier, had more neurological abnormalities than seronegative patients with comparable history. A common genetic variant (rs524991, P=6.15E-08) as well as past influenza A (P=0.024) or B (P=0.006) infection were identified as predisposing factors for NMDAR-AB seropositivity. The >10% overall seroprevalence of NMDAR-AB of both healthy individuals and patients is unexpectedly high. Clinical significance, however, apparently depends on association with past or present perturbations of blood-brain barrier function."],["dc.identifier.doi","10.1038/mp.2013.110"],["dc.identifier.gro","3150565"],["dc.identifier.pmid","23999527"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7339"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.title","Neuropsychiatric disease relevance of circulating anti-NMDA receptor autoantibodies depends on blood-brain barrier integrity"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","5540"],["dc.bibliographiccitation.issue","20"],["dc.bibliographiccitation.journal","The EMBO Journal"],["dc.bibliographiccitation.lastpage","5547"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Pardo, L. A."],["dc.date.accessioned","2022-03-01T11:46:43Z"],["dc.date.available","2022-03-01T11:46:43Z"],["dc.date.issued","1999"],["dc.identifier.doi","10.1093/emboj/18.20.5540"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/103777"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.eissn","1460-2075"],["dc.title","Oncogenic potential of EAG K+ channels"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2850"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","FEBS Letters"],["dc.bibliographiccitation.lastpage","2852"],["dc.bibliographiccitation.volume","580"],["dc.contributor.author","Stuhmer, Walter"],["dc.contributor.author","Alves, Frauke"],["dc.contributor.author","Hartung, Franziska"],["dc.contributor.author","Zientkowska, M."],["dc.contributor.author","Pardo, L. A."],["dc.date.accessioned","2018-11-07T09:48:45Z"],["dc.date.available","2018-11-07T09:48:45Z"],["dc.date.issued","2006"],["dc.description.abstract","An increasing number of ion channels are being found to be causally involved in diseases, giving rise to the new field of \"channelopathies\". Cancer is no exception, and several ion channels have been linked to tumour progression. Among them is the potassium channel EAG (Ether-a-go-go). Over 75% of tumours have been tested positive using a monoclonal antibody specific for EAG, while inhibition of this channel decreased the proliferation of EAG expressing cells. The inhibition of EAG is accomplished using RNA interference, functional anti-EAG1 antibodies, or (unspecific) EAG channel blockers. Fluorescently labelled recombinant Fab fragments recognizing EAG allow the distribution of EAG to be visualized in an in vivo mouse tumour model. (c) 2006 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.febslet.2006.03.062"],["dc.identifier.isi","000238167200009"],["dc.identifier.pmid","16783874"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35368"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0014-5793"],["dc.title","Potassium channels as tumour markers"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2247"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Human Molecular Genetics"],["dc.bibliographiccitation.lastpage","2262"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Ufartes, Roser"],["dc.contributor.author","Schneider, Tomasz"],["dc.contributor.author","Mortensen, Lena Suenke"],["dc.contributor.author","de Juan Romero, Camino"],["dc.contributor.author","Hentrich, Klaus"],["dc.contributor.author","Knoetgen, Hendrik"],["dc.contributor.author","Beilinson, Vadim"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Tarabykin, Victor"],["dc.contributor.author","Alves, Frauke"],["dc.contributor.author","Pardo, Luis A."],["dc.contributor.author","Rawlins, J. Nicholas P."],["dc.contributor.author","Stühmer, Walter"],["dc.date.accessioned","2018-11-07T09:24:20Z"],["dc.date.available","2018-11-07T09:24:20Z"],["dc.date.issued","2013"],["dc.description.abstract","K(v)10.1 (Eag1), member of the K(v)10 family of voltage-gated potassium channels, is preferentially expressed in adult brain. The aim of the present study was to unravel the functional role of K(v)10.1 in the brain by generating knockout mice, where the voltage sensor and pore region of K(v)10.1 were removed to render non-functional proteins through deletion of exon 7 of the KCNH1 gene using the '3 Lox P strategy'. K(v)10.1-deficient mice show no obvious alterations during embryogenesis and develop normally to adulthood; cortex, hippocampus and cerebellum appear anatomically normal. Other tests, including general health screen, sensorimotor functioning and gating, anxiety, social behaviour, learning and memory did not show any functional aberrations in K(v)10.1 null mice. K(v)10.1 null mice display mild hyperactivity and longer-lasting haloperidol-induced catalepsy, but there was no difference between genotypes in amphetamine sensitization and withdrawal, reactivity to apomorphine and haloperidol in the prepulse inhibition tests or to antidepressants in the haloperidol-induced catalepsy. Furthermore, electrical properties of K(v)10.1 in cerebellar Purkinje cells did not show any difference between genotypes. Bearing in mind that K(v)10.1 is overexpressed in over 70 of all human tumours and that its inhibition leads to a reduced tumour cell proliferation, the fact that deletion of K(v)10.1 does not show a marked phenotype is a prerequisite for utilizing K(v)10.1 blocking and/or reduction techniques, such as siRNA, to treat cancer."],["dc.description.sponsorship","Max Planck Society"],["dc.identifier.doi","10.1093/hmg/ddt076"],["dc.identifier.isi","000319432000011"],["dc.identifier.pmid","23424202"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29798"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0964-6906"],["dc.title","Behavioural and functional characterization of K(v)10.1 (Eag1) knockout mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","675"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Current Medicinal Chemistry"],["dc.bibliographiccitation.lastpage","682"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Pardo, L. A."],["dc.contributor.author","Gomez-Varela, David"],["dc.contributor.author","Major, Felix"],["dc.contributor.author","Sansuk, K."],["dc.contributor.author","Leurs, R."],["dc.contributor.author","Downie, B. R."],["dc.contributor.author","Tietze, Lutz Friedjan"],["dc.contributor.author","Stühmer, Walter"],["dc.date.accessioned","2018-11-07T09:13:48Z"],["dc.date.available","2018-11-07T09:13:48Z"],["dc.date.issued","2012"],["dc.description.abstract","K(V)10.1 has recently become generally accepted as a promising cancer target, as it is ectopically expressed in the majority of solid tumors. Due to its cell-surface accessibility, K(V)10.1 has a strong potential for tumor treatment and diagnosis. Given that its mode of action is likely independent of conventional cancer pathways such as tyrosine kinases, K(V)10.1 opens a novel window for treating cancer. In this review we will give an overview of the current status of data linking K(V)10.1 to cancer, and propose techniques that could exploit K(V)10.1's properties for the management of cancer."],["dc.identifier.isi","000300443700005"],["dc.identifier.pmid","22204340"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27252"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0929-8673"],["dc.title","Approaches Targeting K(V)10.1 Open a Novel Window for Cancer Diagnosis and Therapy"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","307"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Neuropathology and Experimental Neurology"],["dc.bibliographiccitation.lastpage","324"],["dc.bibliographiccitation.volume","72"],["dc.contributor.author","Barrantes-Freer, Alonso"],["dc.contributor.author","Kim, Ella L."],["dc.contributor.author","Bielanska, Joanna"],["dc.contributor.author","Giese, Alf"],["dc.contributor.author","Mortensen, Lena Suenke"],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Pardo, Luis A."],["dc.date.accessioned","2018-11-07T09:26:43Z"],["dc.date.available","2018-11-07T09:26:43Z"],["dc.date.issued","2013"],["dc.description.abstract","Glioma-initiating cells (GICs) represent a potential important therapeutic target because they are likely to account for the frequent recurrence of malignant gliomas; however, their identity remains unsolved. Here, we characterized the cellular lineage fingerprint of GICs through a combination of electrophysiology, lineage marker expression, and differentiation assays of 5 human patient-derived primary GIC lines. Most GICs coexpressed nestin, NG2 proteoglycan, platelet-derived growth factor receptor-alpha, and glial fibrillary acidic protein. Glioma-initiating cells could be partially differentiated into astrocytic but not oligodendroglial or neural lineages. We also demonstrate that GICs have a characteristic electrophysiologic profile distinct from that of well-characterized tumor bulk cells. Together, our results suggest that GICs represent a unique type of cells reminiscent of an immature phenotype that closely resembles but is not identical to NG2 glia with respect to marker expression and functional membrane properties."],["dc.identifier.doi","10.1097/NEN.0b013e31828afdbd"],["dc.identifier.isi","000316944200004"],["dc.identifier.pmid","23481707"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30362"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0022-3069"],["dc.title","Human Glioma-Initiating Cells Show a Distinct Immature Phenotype Resembling but Not Identical to NG2 Glia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","95"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.volume","275"],["dc.contributor.author","Barrantes-freer, Alonso"],["dc.contributor.author","Mortensen, Lena Sünke"],["dc.contributor.author","Lohrberg, Melanie"],["dc.contributor.author","Götz, Alexander"],["dc.contributor.author","Hanisch, Uwe-karsten"],["dc.contributor.author","Pardo, Luis A."],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Stadelmann-Nessler, Christine"],["dc.date.accessioned","2022-03-01T11:45:14Z"],["dc.date.available","2022-03-01T11:45:14Z"],["dc.date.issued","2014"],["dc.identifier.doi","10.1016/j.jneuroim.2014.08.255"],["dc.identifier.pii","S0165572814004883"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/103259"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.issn","0165-5728"],["dc.title","MyD88 signaling mediates the effects of the innate immune response in cerebellar short-term synaptic plasticity"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]