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The metalloproteinase ADAM10 requires its activity to sustain surface expression

The metalloproteinase ADAM10 requires its activity to sustain surface expression

glutamate for the catalytic mechanism and the zinc ion and water coordination may be affected, whereas in the H394E mutant, the zinc ion is displaced but its coordination with water should be unaffected [ 42 , 43 ] (Fig.  7 a). Importantly, these changes should not affect the substrate binding pock- ets or other parts of the metalloproteinase structure. These murine variants as well as murine wild-type ADAM10 were then expressed in a HEK293 cell line with knockout of endogenous ADAM10. Activity of wild-type ADAM10 and activity loss of the variants was confirmed by means of a betacellulin cleavage assay (suppl. Fig. 6A). Western blot analysis revealed that all variants were expressed at a comparable level with respect to their proforms. By contrast, the mature forms of the inactive variants were expressed at a much lower level compared to that of wild-type ADAM10 further demonstrating that inactivation of ADAM10 causes downregulation of its mature form (Fig.  7 b). Moreover, GI treatment only reduced the expression of murine wild-type ADAM10, but did not further suppress the residual surface expression of the inactive variants (Fig.  7 c). Nevertheless, at this stage, it could not be excluded that the mutants differ in their ability to bind the small molecule inhibitor which then might have led to differences in downregulation of the protease variants. We, therefore, used a Cy5.5-labelled deri- vate of the small molecule inhibitor MN8 against ADAM10. The inhibitor caused similar ADAM10 downregulation as GI254023X (compare suppl. Fig. 1E) and via its fluores- cence, it also allows to investigate binding of the inhibitor to ADAM10. In fact, flow cytometric experiments indicated that the relative binding of the small molecule inhibitor was not compromised by introducing the mutations (Fig.  7 d, suppl. Fig. 6BC). Thus, the observed differences in GI- induced downregulation of mature ADAM10 between the mutants and wild-type ADAM10 (Fig.  7 c) were not due to differences in their inhibitor binding but rather differences in their proteolytic activity.
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Hypercapnia impairs ENaC cell surface expression and function by promoting phosphorylation and polyubiquitination of ENaC beta-subunit in alveolar epithelial cells

Hypercapnia impairs ENaC cell surface expression and function by promoting phosphorylation and polyubiquitination of ENaC beta-subunit in alveolar epithelial cells

In the lungs, ENaC is expressed in airway epithelial cells including Clara cells located in the distal airways and in both types of alveolar epithelial cells, in which it is responsible for maintaining alveolar fluid balance and consequently for optimal gas exchange (Matalon et al. 2002; Matalon et al. 2015). In this regards, abnormalities in ENaC function are associated with several diseases such as an inherited, autosomal-dominant salt-sensitive form of hypertension (Liddle’s syndrome), a disorder that is directly linked to changes in ENaC cell surface expression due to the presence of characteristic mutations within the PY motif of the β- and γ-subunits that affect channel endocytosis (Abriel et al. 1999). Interestingly, a commonly used mouse model to study CF is characterized by β-ENaC overexpression. Mall and colleagues presented that overexpression of β-ENaC in mice leads to hyperabsorption of Na + and lung dehydration most probably due to abnormally high ENaC trafficking to the cellular surface (Mall et al. 2004). In contrary, reduction in ENaC function leads to an excess of lung fluid resulting from impaired Na + and water reabsorption. This type of ENaC dysfunction is observed in patients with type I pseudohypoaldosteronism (PHA1) (Kerem and Bistritzer 1999) and pulmonary edema (Matalon et al. 2002; Matalon et al. 2015).
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Surface expression and genotypes of Toll-like receptors 2 and 4 in patients with juvenile idiopathic arthritis and systemic lupus erythematosus

Surface expression and genotypes of Toll-like receptors 2 and 4 in patients with juvenile idiopathic arthritis and systemic lupus erythematosus

Although the results of this study for surface expression of TLR2 and TLR4 within JIA and SLE patients differ, in some aspects, from the results of other studies, they do not necessarily contradict them. In our own experiments (unpublished data) we have shown that the technical im- plementation affects the density of TLRs on monocytes significantly: Unstimulated monocytes expressed TLR2, TLR4, and CD14 in whole blood with an identical pattern to that seen in purified peripheral blood mononuclear cells (PBMC), although with lower mean fluorescences than were seen in purified cells. After stimulation with Lipopolysaccharid (TLR4) or Zymosan (TLR2) in whole blood we observed the expected increase of TLR2 respect- ively TLR4 on monocytes. In contrast, in purified PBMC populations we found as a result of Zymosan stimulation a significant decrease of TLR2 density (dMFI unstimu- lated: median 100, dMFI stimulated: median −400) and an increase of TLR4 density (dMFI unstimulated: median 30, dMFI stimulated: median 600) on monocytes.
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Surface expression and genotypes of Toll-like receptors 2 and 4 in patients with juvenile idiopathic arthritis and systemic lupus erythematosus

Surface expression and genotypes of Toll-like receptors 2 and 4 in patients with juvenile idiopathic arthritis and systemic lupus erythematosus

Although the results of this study for surface expression of TLR2 and TLR4 within JIA and SLE patients differ, in some aspects, from the results of other studies, they do not necessarily contradict them. In our own experiments (unpublished data) we have shown that the technical im- plementation affects the density of TLRs on monocytes significantly: Unstimulated monocytes expressed TLR2, TLR4, and CD14 in whole blood with an identical pattern to that seen in purified peripheral blood mononuclear cells (PBMC), although with lower mean fluorescences than were seen in purified cells. After stimulation with Lipopolysaccharid (TLR4) or Zymosan (TLR2) in whole blood we observed the expected increase of TLR2 respect- ively TLR4 on monocytes. In contrast, in purified PBMC populations we found as a result of Zymosan stimulation a significant decrease of TLR2 density (dMFI unstimu- lated: median 100, dMFI stimulated: median −400) and an increase of TLR4 density (dMFI unstimulated: median 30, dMFI stimulated: median 600) on monocytes.
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Relax, Cool Down and Scaffold: How to Restore Surface Expression of Folding-Deficient Mutant GPCRs and SLC6 Transporters

Relax, Cool Down and Scaffold: How to Restore Surface Expression of Folding-Deficient Mutant GPCRs and SLC6 Transporters

Neither inhibitors of HSP90 nor HSP70 are universally effective in rescuing folding deficient mutants. This can be rationalized by taking into account the fact that their action depends on the point, at which the folding intermediates are stalled in the folding trajectory. Accordingly, when combined with the pharmacochaperone noribogaine, all possible types of interactions were observed: depending on the nature of the mutation in SERT, HSP inhibitors (i) potentiated the action of noribogaine by shifting the concentration of noribogaine to the left; (ii) they were additive by increasing the maximum effect on cell surface expression without any appreciable change in EC50 of noribogaine or (iii) they shifted the concentration-response curve to the right [ 57 ]. It is also worth noting that HSP70 inhibitors are not equivalent, because they target different domains in the protein [ 106 ]. Pifithrin-µ binds to the C-terminal substrate/peptide-biding domain and suppresses the association between HSP70 and some of its co-factors/co-chaperones (e.g., HSP40) [ 107 ]. In contrast, VER155008, for instance, is an adenosine derivative that mimics the action of ADP in the HSP70 cycle and thus traps the substrate–HSP70 complex [ 108 ]. Contrary to pifithin-µ, VER155008 does not rescue folding-deficient SERT mutants but increases their accumulation in the ER [ 57 ].
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The regulation of gp130 surface expression on monocytes : implications in chronic inflammation

The regulation of gp130 surface expression on monocytes : implications in chronic inflammation

RESULTS 34 We therefore focused on this population and performed live-cell imaging to investigate the influence of IL-1β on gp130 surface expression. After isolation PBMCs were allowed to settle down. A reduction of lymphocytes and an enrichment of adherent monocytes was achieved by washing the cells stringently. The cells were labeled with antibodies against gp130 and CD14 and analyzed by confocal fluorescence microscopy. Figure 3-2 A shows representative images of cells left untreated (upper panel) compared to samples stimulated with recombinant IL-1β (lower panel). Pictures were taken immediately after subjecting the samples to microscopy and every 10 min. While a localization of the gp130-staining could be detected mainly at the cell membrane in untreated cells, monocytes exhibited less clear membrane staining in the presence of IL-1β. Instead, gp130 was distributed throughout the cell and some rafts were visible (see arrowheads). In figure 3-2 B a statistical analysis of two individual microscopy experiments can be seen. According to the degree of internalization, cells were assessed based on a scoring system (table 2-12). There was a certain rate of constitutive internalization during the experiment, which explains how the internalization score had reached almost 0.5 at time point 2 min and rose further even in the absence of IL-1β. However, in the presence of IL-1β internalization was significantly higher compared to untreated cells.
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Expression von Inhibin und Aktivin in Ovarialkarzinomen

Expression von Inhibin und Aktivin in Ovarialkarzinomen

Die unter die benignen, nur fakultativ bösartigen, Keimstrangstromatumoren subsummierten Granulosa- und Sertoli-Leydig-Zelltumoren wurden von Yamashita et al. ebenfalls auf Expression sowie Sekretion der Inhibindimere A und B untersucht. Sie fanden heraus, dass sowohl die α- wie auch die β-Fraktionen in den nur zu 30% maligne entartenden Granulosazelltumoren exprimiert werden. Eine spezifische Färbereaktion für Leydigtumorzellen beobachteten sie für die α-Untereinheit, in den Sertolitumorzellen die spezifische Färbereaktion für die βA-Kette. Die βB-Subunit wiesen sie für beide Zellklassen nach. Korrespondierend dazu waren die Serumspiegel der Inhibin A- und B-Dimere präoperativ stark erhöht, fielen aber nach der operativen Entfernung der Neubildungen wieder auf normale Werte ab [91]. Die Vermutung liegt daher auch hier nahe, dass die α-Untereinheit in benignen Geweben als Tumorsuppressor fungiert und eine maligne Entartung zu verhindern scheint.
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Expression des Urokinase-Systems bei Magenkarzinomen

Expression des Urokinase-Systems bei Magenkarzinomen

Die Proteolyse entsteht aus der Interaktion einer großen Anzahl von Enzymsystemen; einer Reihe von Serin und Serpinproteasen, dem Urokinasesystem, verschiedenen Subtypen der Kollagenase IV, weiteren Metalloproteinasen und anderen extrazellulären Enzymen. In verschiedensten Studien konnten Hinweise auf eine Aktivierung dieser Enzymsysteme bei der Tumorprogression, speziell durch die tumorbedingte Expression des Urokinasesystems erbracht werden (Allgayer H. et al 1995, Blasi F. et al 1988, Blasi F.et al 1993, Blasi F.et al 1997, Pappot H. et al 1995, Danǿ K.et al 1985, Danǿ K.et al 1994). In diesen Studien wird eine entscheidende Rolle des Urokinasesystems bei der Zellinvasion und Metastasierung beschrieben, dies insbesondere durch Promotion der extrazellulären Proteolyse, der Zelladhäsion und der Chemotaxis.
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Cometary Comae-Surface Links

Cometary Comae-Surface Links

A yet different approach to inverting the nadir MIRO measurements taken around the equinox conditions in May 2015 is described in the multi-instrument study of coma data in Marschall et al. (2019). In the present section we treat only the noteworthy details of the inverse problem related to the MIRO spectra, while the general 3D DSMC modelling and comparisons to multi-instrument data are further discussed in Sect. 4.2 in this chapter. In the cited paper, the simultaneous inversion of the two water transitions (H 16 2 O and H 18 2 O) was performed in a framework very similar to the one of optimal estimation formalism as used in Lee et al. (2015). However, the vertical profiles of density, temperature, and velocity along the LOS were discretised along the radial direction (along the LOS). The physical and stabilising factor of this non-linear inversion was to start the retrieval from self-consistent a-priori profiles and co-variance matrices constructed from the output of a 3D DSMC model. The retrieval iteration was allowed to rigorously fit the measured signal, which revealed several never before reported features that remain a challenge to explain with the current understanding of gas flow physics near the nucleus. An alternative explanation is that discrepancies in the results are due to some missing physical processes driving the rotational populations of water molecules not taken into account in the current radiative transfer models. The first such surprise was an ubiquitous presence of a “red” emission wing in the nadir absorption spectra at the 557 GHz transition (see e.g. Fig. 10). The MIRO observations record enhanced radiance above the continuum temperatures for red-shifted frequencies of the line, implying a stagnant (not expanding) or tangential flow to the MIRO’s LOS of the near-nucleus gas field which is also significantly warmer (by 10–20 K or more) than the surface (the near sub-surface in the case of sub-mm wavelengths). The second unexpected finding was a temperature enhancement for several studied cases in the altitude region of 30–80 km. There were several speculations offered how to explain this feature, but rigorous physical modelling is yet to be constructed. Currently there is no indication that this feature is an artefact of the data calibration. In addition, the retrieved velocity profiles show evidence just above the 2-σ uncertainty levels that acceleration continues up to an altitude of 20–40 km, and the radial profiles where the transition into free-molecular flow is expected are not necessarily smooth. Finally, the retrieved water column densities are found at least a factor 2 smaller than the modelled ones, which also seems to be a robust result. Figure 10 illustrates these features.
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Surface erosion of Titan

Surface erosion of Titan

Erosional processes: Surface conditions on Titan are different from that on Earth. However discharge of fluids are also driven by the gravity and to a first order estimate we can model flows and discharges on Titan based on Earth-analogues for surface runoff. Liquid methane (CH 4 ) is suggested to be the main fluid on Titan. Its viscosity at surface temperature (95° K) is 1.8 10 -4 Pa s which is approximately five times smaller than water at 298° K (1.8 10 -4 Pa s) [4,5]. Thus, liquid methane will produce turbulent flows on Titan’s sur- face that have significant erosional power. On Earth an empirical function relates channel width W to dis- charge Q in a first order approach, for alluvial uncon- fined sand-bedded channels with sand or silt banks carrying bankfull floods with relative short recurrence intervals [6]:
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Microscopy and surface analytics

Microscopy and surface analytics

Probing different depths by ADXPS shows en- hanced abundance of hydroxide at the outermost sur- face of the pellet. A homogeneous layer model con- sisting of an adventitious hydrocarbon layer at the outermost surface, a hydroxylated layer, and U4O9 beneath is employed to estimate the extent of hydrox- ide formation. Since the adventitious hydrocarbon layer does not contain significant amounts of oxygen (only in traces of carboxylic and COH groups), Strohmeier´s equation [9] and C2 equation for electron effective attenuation lengths [10] are employed for calculation of the thickness of hydroxylated layer by use of curve-fits to O 1s spectra. The thickness of the hydroxylated layer is about 0.5 nm, calculated at 45° between surface normal and analyzer axis. Since the results for the thickness vary at various angles by about 10%, a gradient of the hydroxide concentration is likely, similar to results by Marchetti [11], who immersed UO2 in 18 O labelled water and applied SIMS depth profiling. The thickness of the adventitious hydrocarbon layer is calculated to 0.8 nm by compari- son of the C 1s intensity with that of low density- polyethylene as a model substance for adventitious hydrocarbon.
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Surface Polariton Mode Densities 

Surface Polariton Mode Densities 

F o r the description of these excitations we defined a local density of states including all bulk and surface contributions on both sides of the boundary: the bulk polaritons, the s[r]

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Classification of Dawn/VIR data reveals homogeneous surface units on Ceres surface

Classification of Dawn/VIR data reveals homogeneous surface units on Ceres surface

The NASA Dawn spacecraft [1] orbits around Ceres since March 2015, and is now completing the second extended phase of the mission. The large amount of data acquired by Dawn are fundamental in understanding the chemical and physical properties undergoing on Ceres surface [2]. Dawn’s payload is made up of three instruments: the Framing Camera (FC) [3], the Visible and InfraRed mapping spectrometer (VIR) [4], and the Gamma Ray and Neutron Detector (GRaND) [5]. VIR is a key instrument for deciphering Ceres surface mineralogy at unprecedented spatial resolution [4]. The spatial resolution depends on the altitude of the spacecraft over the mean surface, which changes from one phase to another. The main Dawn mission phases at Ceres, in the two-year period 2015-2016, were: Survey (1.1 km/pixel), High Altitude Mapping Orbit (HAMO) (0.38 km/px), and Low Altitude Mapping Orbit (LAMO) (0.095 km/pixel) [1]. After LAMO, the mission was extended to perform a first extended mission phase in 2016-2017, which was divided in a number of sub-phases where the altitude of the spacecraft raised back to ~19,500 km. In 2018, the Dawn spacecraft was finally injected into an elliptical orbit to perform the second and last extended mission phase (XM2). The combination of broad coverage and varying pixel resolution allow both a global analysis and a local study of features of interest. In particular, several VIR-derived mineralogical maps have been produced [6, 7]. The global mineralogy of Ceres is consistent with a large abundance of a low- albedo, carbonaceous chondrite-like spectral endmember, mixed with Mg- and NH 4 -bearing phyllosilicates [6, 7] and Mg-carbonates, whereas
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Expression antimikrobieller Peptide in Bronchialkarzinomen

Expression antimikrobieller Peptide in Bronchialkarzinomen

Angiogenese und Formation neugebildeter Gefäße im Tumor sind entscheidend für seine Entwicklung und Progression. Die Gefäße zeigen inkomplette und unreife Strukturen mit veränderter Funktion. Die Morphologie variiert in verschiedenen Tumoren von vorläufigen Endothelzellproliferationen bis hin zu großen Gefäßen mit dicker Wand ohne Muskelschicht. Es zeigt sich ein unkontrolliertes, nichtlimitiertes Wachstum und Hypertrophie der Endothelzellen. Hypoxie ist ein wichtiger Stimulus in der Tumorangiogenese. Im Tumorgewebe bewirkt Hypoxie Zelltod und induziert die Expression verschiedener Angiogenesefaktoren (Bian et al 2004). Auch Chemokine und ihre Rezeptoren tragen durch direkte Aktivierung von Tumorzellen und Förderung der Angiogenese via Endothelzellen zum Tumorwachstum bei (Balkwill 2004; Wang et al 1998).
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Expression von Oberflächenrezeptoren beim Bronchialkarziom

Expression von Oberflächenrezeptoren beim Bronchialkarziom

Deutliche tumorspezifische Unterschiede konnten in der Expression von CD44v6 zwischen den unterschiedlichen histologischen Subtypen beobachtet werden. Plattenepithelkarzinome und Bronchioalveolarkarzinome exprimierten diese Isoform in über 80% der untersuchten Fälle, andere Subtypen hingegen kaum. Die anderen untersuchten Isoformen, wie v5 und v7/8, zeigten kein klares histiotypisches Auftreten in primären Lungentumoren (siehe Tab. 20). Diese Befunde wurden später durch Studien anderer Arbeitsgruppen, in denen Biopsiematerial von Plattenepithelkarzinomen ebenfalls eine hohe Expression von CD44H, -v5 und -v6, aber nur eine geringe Expression von CD44v7 und v10 aufwies, belegt (Givehchian et al., 1996). Die Expression von CD44v6 in SCC könnte die Expression von Basalzellen des normalen Epithels, wie sie auch in der Haut, dem Ösophagus und den Bronchien (Mackay et al., 1994; Heider et al., 1993) gefunden wird, widerspiegeln. Da Epithelien häufig hyperplastische Basalzellen beherbergen, die zu SCC transformieren können (Gazdar und Linnoila, 1988), könnte die v6 Expression in SCC ein konservierter histiotypischer Marker sein.
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Expression der humanen und murinen Guanidinoacetatmethyltransferase

Expression der humanen und murinen Guanidinoacetatmethyltransferase

gaprime DNA Labelling markiertem dCTP (Amersh m Biosciences, Freiburg, AA0005-250µCi) hergestellt. Nach Inkubation mit Prähybridisierungslösung für 30 min wurde die Membran für 1h mit der radioaktiven Probe in Hybridisierungslösung inkubiert. Im Anschluß wurde die Membran mit 2xSSC/0,1%SDS, mit 0,2xSSC/0,1%SDS und mit 0,1xSSC/0,1%SDS bei 50°C für 2x15 min gewaschen. Die Membran wurde in Plastikfolie gehüllt und durch Autoradiographie markierte Bereiche dargestellt. Abbildung 10 zeigt das Expressionsmuster der mGAMT mRNA in adultem Mausgewebe. Ähnlich dem gewebsspezifischen Expressionsmuster der hGAMT-mRNA (Abschnitt 4.3) lässt sich die mGAMT mRNA am stärksten in Leber und im Skelettmuskel detektieren. Hohe mGAMT Expression findet sich auch in den Gonaden (Hoden und Eierstöcke), in der Niere und in verschiedenen Hirnarealen.
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Expression und Funktion von Arzneistofftransportproteinen in der Plazenta

Expression und Funktion von Arzneistofftransportproteinen in der Plazenta

Funktion der Transportproteine beeinflussen kann. Zu den häufigsten Störungen in der Schwangerschaft gehören Präeklampsie und Gestationshypertonie. Diese Erkrankungen betreffen bis zu 7 % aller Schwangeren und sind ein Hauptgrund für die maternale und neonatale Morbidität und Mortalität (67;68). Als Gestationshypertonie bezeichnet man neu nach der 20. Schwangerschaftswoche aufgetretene Hypertonie (über 140/90 mmHg) ohne Proteinurie. Präeklampsie ist neben einem hohen Blutdruck (über 140/90 mmHg) auch eine durch Proteinurie (> 300 mg Protein im 24-Stunden-Sammelurin) gekennzeichnete Erkrankung, die sich erst in der zweiten Schwangerschaftshälfte manifestiert. Meist leiden die Frauen auch unter vermehrter Flüssigkeitseinlagerung und dadurch bedingte Ödeme. Bis heute sind die Ursachen, die zu Präeklampsie oder Gestatioshypertonie führen, nicht geklärt. Die Vasokonstriktion, die bei diesen Erkrankungen beobachtet wird, wurde mit Veränderungen des Transport und Stoffwechsels von vasoaktiven Monoaminen wie z.B. Norepinephrin, Serotonin und Histamin in Verbindung gebracht (69-71). Diese Vermutung wird auch von einer Studie, die geringere mRNA-Expression von
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Expression von Somatostatinrezeptoren in Hepatozellulären Karzinomen

Expression von Somatostatinrezeptoren in Hepatozellulären Karzinomen

differenziert, bzw. es muss bei der Probengewinnung sehr genau darauf geachtet werden, dass ausschließlich Tumorgewebe untersucht wird. Diese Entscheidung ist makroskopisch am Resektat oftmals schwierig. Bei den Untersuchungen zu dieser Arbeit stellte sich das umgebende, in vielen Fällen zirrhotisch veränderte Lebergewebe häufig in der Immunfärbung SSTR-positiv dar. Ein Befund, der sich mit den Ergebnissen von Reynaert et al. deckt, die in einer kleinen Anzahl unter- suchter Proben SSTR in zirrhotischem Gewebe (und ebenfalls in HCCs, aber nicht in normalen Hepatozyten) mittels Immunhistochemie nachweisen konnten [81]. Dies könnte bei RT-PCR-Untersuchungen zu falsch-positiven Resultaten führen. Ebenso kann durch den Nachweis des mRNA-Transkripts keine Aussage darüber getroffen werden, ob tatsächlich auf Proteinebene ein funktionsfähiger Rezeptor hergestellt und in die Zellmembran überführt wird. Weiterhin ist durch RT-PCR eine quantifizierende Beurteilung und ein Nachweis fokaler Expression im Tumor nicht möglich.
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Membrane Hsp70 expression in gliomas

Membrane Hsp70 expression in gliomas

In non-glial tumors, membrane Hsp70 was found to be a specific structure on tumor cells but not on other cell types (Multhoff, 2007). In GBM, the current study further distinguished the cellular subtypes within the heterogenous GBM cell conglomerate which expressed the membrane Hsp70, so distinct subpopulations including primary tumor cell cultures, CD133-positive cells, endothelial cells and mesenchymal stem-like cells were isolated from primary GBM tissues for checking membrane Hsp70 expression. In FACS-analysis results, selectively CD133-positive cells and primary tumor cell cultures expressed membrane Hsp70, which also could be expressed on GBM cell lines U87 and U373. CD133-positive cells were identified as a subpopulation of so-called cancer stem cells within glioblastoma tissue with an unlimited capacity for self-renewal and tumor-initiation (Chen et al., 2010). Mesenchymal stem cells, which have the ability of homing to tumor tissue, differentiation in
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THY1-Expression im Neuroblastom als Prognosemarker

THY1-Expression im Neuroblastom als Prognosemarker

41 könnte ein frühzeitiger Nachweis hier zu einer geringeren Mortalität führen. Besonders für Patienten im Kindesalter, deren Körper in vielerlei Hinsicht empfindlicher als Erwachsene reagiert, ist dieser Aspekt möglicherweise bedeutsam. Aus diesem Grund ist es von außerordentlicher Bedeutung, für dieses Patientenklientel, eine möglichst eindeutige Definition für ein niedriges Risiko zu erzielen (Evans und D´Angio 2005). Wie unsere Fälle zeigen, kann der Nachweis von THY1-Expression als Prognosemarker ergänzend zu den bislang üblichen Patienten in günstigere Risikogruppen eingestuft werden. Ein Teil unserer Ergebnisse zeigt, dass einige Patienten durch den Nachweis von THY1 auf ihrem Tumorgewebe in günstigere Risikogruppen eingestuft werden könnten, als es mit den bisherigen Prognosemarkern der Fall ist. Dessen Konsequenz wäre bezüglich des Therapiestufenschemas eine weniger
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