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1.

001-es BibID:BIBFORM048561
Első szerző:Antonella Nadalutti, Cristina
Cím:Thioredoxin Is Involved in Endothelial Cell Extracellular Transglutaminase 2 Activation Mediated by Celiac Disease Patient IgA / Cristina Antonella Nadalutti, Ilma Rita Korponay-Szabo, Katri Kaukinen, Zhuo Wang, Martin Griffin, Markku Mäki, Katri Lindfors
Dátum:2013
ISSN:1932-6203
Megjegyzések:PURPOSE:To investigate the role of thioredoxin (TRX), a novel regulator of extracellular transglutaminase 2 (TG2), in celiac patients IgA (CD IgA) mediated TG2 enzymatic activation.METHODS:TG2 enzymatic activity was evaluated in endothelial cells (HUVECs) under different experimental conditions by ELISA and Western blotting. Extracellular TG2 expression was studied by ELISA and immunofluorescence. TRX was analysed by Western blotting and ELISA. Serum immunoglobulins class A from healthy subjects (H IgA) were used as controls. Extracellular TG2 enzymatic activity was inhibited by R281. PX12, a TRX inhibitor, was also employed in the present study.RESULTS:We have found that in HUVECs CD IgA is able to induce the activation of extracellular TG2 in a dose-dependent manner. Particularly, we noted that the extracellular modulation of TG2 activity mediated by CD IgA occurred only under reducing conditions, also needed to maintain antibody binding. Furthermore, CD IgA-treated HUVECs were characterized by a slightly augmented TG2 surface expression which was independent from extracellular TG2 activation. We also observed that HUVECs cultured in the presence of CD IgA evinced decreased TRX surface expression, coupled with increased secretion of the protein into the culture medium. Intriguingly, inhibition of TRX after CD IgA treatment was able to overcome most of the CD IgA-mediated effects including the TG2 extracellular transamidase activity.CONCLUSIONS:Altogether our findings suggest that in endothelial cells CD IgA mediate the constitutive activation of extracellular TG2 by a mechanism involving the redox sensor protein TRX.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Thioredoxin
IgA
TG2
Megjelenés:Plos One. - 8 : 10 (2013), p. e77277. -
További szerzők:Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Kaukinen, Katri Wang, Zhuo Griffin, Martin Mäki, Markku Lindfors, Katri
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2.

001-es BibID:BIBFORM011928
Első szerző:Caja, Sergio
Cím:Inhibition of transglutaminase 2 enzymatic activity ameliorates the anti-angiogenic effects of coeliac disease autoantibodies / Caja S., Myrsky E., Korponay-Szabo I., Nadalutti C., Sulic A. M., Lavric M., Sblattero D., Marzari R., Collighan R., Mongeot A., Griffin M., Maki M., Kaukinen K., Lindfors K.
Dátum:2010
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Scandinavian Journal of Gastroenterology. - 45 : 4 (2010), p. 421-427. -
További szerzők:Myrsky, Essi Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Nadalutti, Cristina Sulic, Ana-Marija Lavric, Miha Sblattero, Daniele Marzari, Roberto Collighan, Russell Mongeot, Alexandre Griffin, Martin Mäki, Markku Kaukinen, Katri Lindfors, Katri
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM069472
Első szerző:Kalliokoski, Suvi
Cím:Transglutaminase 2-specific coeliac disease autoantibodies induce morphological changes and signs of inflammation in the small-bowel mucosa of mice / Suvi Kalliokoski, Victoria Ortín Piqueras, Rafael Frías, Ana-Marija Sulic, Juha A. E. Määttä, Niklas Kähkönen, Keijo Viiri, Heini Huhtala, Arja Pasternack, Kaija Laurila, Daniele Sblattero, Ilma R. Korponay-Szabó, Markku Mäki, Sergio Caja, Katri Kaukinen, Katri Lindfors
Dátum:2017
ISSN:0939-4451 1438-2199
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Amino Acids 49 : 3 (2017), p. 529-540. -
További szerzők:Piqueras, Victoria Ortín Frías, Rafael Sulic, Ana-Marija Määttä, Juha A. E. Kähkönen, Niklas Viiri, Keijo Huhtala, Heini Pasternack, Arja Laurila, Kaija Sblattero, Daniele Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Mäki, Markku Caja, Sergio Kaukinen, Katri Lindfors, Katri
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4.

001-es BibID:BIBFORM056541
Első szerző:Kalliokoski, Suvi
Cím:Injection of celiac disease patient sera or immunoglobulins to mice reproduces a condition mimicking early developing celiac disease / Suvi Kalliokoski, Sergio Caja, Rafael Frias, Kaija Laurila, Outi Koskinen, Onni Niemelä, Markku Mäki, Katri Kaukinen, Ilma R. Korponay-Szabó, Katri Lindfors
Dátum:2015
ISSN:0946-2716
Megjegyzések:Typical features of celiac disease are small-bowel villus atrophy, crypt hyperplasia, and inflammation which develop gradually concomitant with ingestion of gluten. In addition, patients have anti-transglutaminase 2 (TG2) autoantibodies in their serum and tissues. The aim of this study was to establish whether celiac disease can be passively transferred to mice by serum or immunoglobulins. Serum aliquots or purified immunoglobulins (Ig) were intraperitoneally injected into Hsd:Athymic Nude-Foxn1nu mice for 8 or 27 days. As mice do not have proper IgA transport from peritoneum to blood, sera with a high content of IgG class anti-TG2 antibodies from untreated IgA-deficient celiac patients were used. Mouse sera were tested for celiac disease-specific autoantibodies, and several tissues were analyzed for autoantibody deposits targeted to TG2. Morphological assessment was made of the murine small intestinal mucosa. Injection of celiac disease patient sera or total IgG led to a significant delay in weight gain and mild diarrhea in a subset of mice. The mice injected with celiac patient sera or IgG had significantly decreased villus height crypt depth (Vh/CrD) ratios and celiac diseasespecific autoantibody deposits targeted to TG2 in several tissues, including the small intestine. None of these features were observed in control mice. We conclude that administration of IgA-deficient celiac disease patient serum or total IgG induces both deterioration of the intestinal mucosa and clinical features of celiac disease in mice. The experimentally induced condition in the mice injected with patient serum or IgG resembles early developing celiac disease in humans.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Autoantibodies
Celiac disease
Passivetransfer
Transglutaminase 2
Megjelenés:Journal of Molecular Medicine-Jmm 93 : 1 (2015), p. 51-62. -
További szerzők:Caja, Sergio Frías, Rafael Laurila, Kaija Koskinen, Outi Niemelä, Onni Mäki, Markku Kaukinen, Katri Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Lindfors, Katri
Pályázati támogatás:101788
OTKA
TÁMOP-4.2.2.A-11/1/KONV-2012-0023
TÁMOP
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Intézményi repozitóriumban (DEA) tárolt változat
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5.

001-es BibID:BIBFORM048568
035-os BibID:Article ID: e65887
Első szerző:Kalliokoski, Suvi
Cím:Celiac Disease-Specific TG2-Targeted Autoantibodies Inhibit Angiogenesis Ex Vivo and In Vivo in Mice by Interfering with Endothelial Cell Dynamics / Suvi Kalliokoski, Ana-Marija Sulic, Ilma R. Korponay-Szabo, Zsuzsa Szondy, Rafael Frias, Mileidys Alea Perez, Stefania Martucciello, Anne Roivainen, Lauri J. Pelliniemi, Carla Esposito, Martin Griffin, Daniele Sblattero, Markku Mäki, Katri Kaukinen, Katri Lindfors, Sergio Caja
Dátum:2013
ISSN:1932-6203
Megjegyzések:A characteristic feature of celiac disease is the presence of circulating autoantibodies targeted against transglutaminase 2 (TG2), reputed to have a function in angiogenesis. In this study we investigated whether TG2-specific autoantibodies derived from celiac patients inhibit angiogenesis in both ex vivo and in vivo models and sought to clarify the mechanism behind this phenomenon. We used the ex vivo murine aorta-ring and the in vivo mouse matrigel-plug assays to address aforementioned issues. We found angiogenesis to be impaired as a result of celiac disease antibody supplementation in both systems. Our results also showed the dynamics of endothelial cells was affected in the presence of celiac antibodies. In the in vivo angiogenesis assays, the vessels formed were able to transport blood despite impairment of functionality after treatment with celiac autoantibodies, as revealed by positron emission tomography. We conclude that celiac autoantibodies inhibit angiogenesis ex vivo and in vivo and impair vascular functionality. Our data suggest that the anti-angiogenic mechanism of the celiac disease-specific autoantibodies involves extracellular TG2 and inhibited endothelial cell mobility.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Plos One [electronic resource]. - 8 : 6 (2013), [8] p. -
További szerzők:Sulic, Ana-Marija Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Szondy Zsuzsanna (1959-) (molekuláris sejtbiológus, biokémikus) Frías, Rafael Perez, Mileidys Alea Martucciello, Stefania Roivainen, Anne Pelliniemi, Lauri J. Esposito, Carla Griffin, Martin Sblattero, Daniele Mäki, Markku Kaukinen, Katri Lindfors, Katri Caja, Sergio
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6.

001-es BibID:BIBFORM007714
Első szerző:Koskinen, Lotta L. E.
Cím:Myosin IXB gene region and gluten intolerance : linkage to coeliac disease and a putative dermatitis herpetiformis association / Koskinen, L. L. E., Korponay-Szabo, I. R., Viiri, K., Juuti-Uusitalo, K., Kaukinen, K., Lindfors, K., Mustalahti, K., Kurppa, K., Ádány, R., Pocsai, Z., Széles, G., Einarsdottir, E., Wijmenga, C., Mäki, M., Partanen, J., Kere, J., Saavalainen, P.
Dátum:2008
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal of Medical Genetics. - 45 : 4 (2008), p. 222-227. -
További szerzők:Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Viiri, Keijo Juuti-Uusitalo, K. Kaukinen, Katri Lindfors, Katri Mustalahti, Kirsi Kurppa, Kalle Ádány Róza (1952-) (megelőző orvostan és népegészségtan szakorvos) Pocsai Zsuzsanna (1970-) (népegészségügyi szakember) Széles György (1969-) (epidemiológus) Einarsdottir, Elisabet Wijmenga, Cisca Mäki, Markku Partanen, Jukka Kere, Juha Saavalainen, Päivi
Internet cím:elektronikus változat
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7.

001-es BibID:BIBFORM044279
Első szerző:Koskinen, Outi
Cím:Oats Do Not Induce Systemic or Mucosal Autoantibody Response in Children With Coeliac Disease / Koskinen Outi, Villanen Mikko, Korponay-Szabo Ilma, Lindfors Katri, Mäki Markku, Kaukinen Katri
Dátum:2009
ISSN:0277-2116
Megjegyzések:OBJECTIVES:A gluten-free diet omitting wheat, rye, and barley is the only effective treatment for coeliac disease. The necessity of excluding oats from the diet has remained controversial. We studied the toxicity of oats in children with coeliac disease during a 2-year follow-up by investigating jejunal transglutaminase 2 (TG2)-targeted IgA-class autoantibody deposits, a potentially more sensitive disease marker than serum antibodies or conventional histology.PATIENTS AND METHODS:Twenty-three coeliac children in remission were randomized to undergo oat or gluten challenge with wheat, rye, barley, and oats. When jejunal histological relapse was evident after gluten challenge, patients excluded wheat, rye, and barley but continued with oats. Mucosal morphology and TG2-targeted autoantibody deposits were studied in jejunal biopsies taken at baseline and after 6 and 24 months. Furthermore, serum IgA-class TG2 antibodies were measured.RESULTS:At baseline, serum TG2 antibodies were negative in all 23 patients, but 7 of them had minor mucosal deposits. In the oats group, there was no significant change in the intensity of the deposits within 2 years. In contrast, during the gluten challenge, the intensity of the deposits clearly increased and decreased again when wheat, rye, and barley were excluded but consumption of oats was continued; this was in line with serum autoantibodies. The intensity of the mucosal deposits correlated well with both villous morphology and serum autoantibody levels.CONCLUSIONS:Consumption of oats does not induce TG2 autoantibody production at mucosal level in children with coeliac disease. Measurement of small-intestinal mucosal autoantibody deposits is suitable for monitoring treatment in coeliac patients
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal Of Pediatric Gastroenterology And Nutrition. - 48 : 5 (2009), p. 559-565. -
További szerzők:Villanen, Mikko Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Lindfors, Katri Mäki, Markku Kaukinen, Katri
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8.

001-es BibID:BIBFORM044274
Első szerző:Martucciello, Stefania
Cím:RhoB is associated with the anti-angiogenic effects of celiac patient transglutaminase 2-targeted autoantibodies / Martucciello Stefania, Lavric Miha, Toth Boglarka, Korponay-Szabo Ilma, Nadalutti Cristina, Myrsky Essi, Rauhavirta Tiina, Esposito Carla, Sulic Ana-Marija, Sblattero Daniele, Marzari Roberto, Mäki Markku, Kaukinen Katri, Lindfors Katri, Caja Sergio
Dátum:2012
ISSN:0946-2716
Megjegyzések:Celiac patient-derived anti-transglutaminase 2 (TG2) antibodies disturb several steps in angiogenesis, but the detailed molecular basis is not known. Therefore, we here analyzed by microarray technology the expression of a set of genes related to angiogenesis and endothelial cell biology in order to identify factors that could explain our previous data related to vascular biology in the context of celiac disease. To this end, in vitro models using human umbilical vein endothelial cells (HUVECs) or in vivo models of angiogenesis were used. A total of 116 genes were analyzed after treatment with celiac patient autoantibodies against TG2. Compared to treatment with control IgA celiac patient, total IgA induced a consistent expression change of 10 genes, the up-regulation of four and down-regulation of six. Of these genes the up-regulated RhoB was selected for further studies. RhoB expression was found to be up-regulated at both messenger RNA and protein level in response to celiac patient total IgA as well as anti-TG2-specific antibody derived from a celiac patient. Interestingly, down-regulation of RhoB by specific small interfering RNA treatment in endothelial cells could rescue the deranged endothelial length and tubule formation caused by celiac disease autoantibodies. RhoB function is controlled by its post-translational modification by farnesylation. This modification of RhoB required for its correct function can be prevented by the cholesterol lowering drug simvastatin, which was also able to abolish the anti-angiogenic effects of celiac anti-TG2 autoantibodies. Taken together, our results would suggest that RhoB plays a key role in the response of endothelial cells to celiac disease-specific anti-TG2 autoantibodies
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal Of Molecular Medicine-Jmm. - 90 : 7 (2012), p. 817-826. -
További szerzők:Lavric, Miha Tóth Boglárka Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Nadalutti, Cristina Myrsky, Essi Rauhavirta, Tiina Esposito, Carla Sulic, Ana-Marija Sblattero, Daniele Marzari, Roberto Mäki, Markku Kaukinen, Katri Lindfors, Katri Caja, Sergio
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9.

001-es BibID:BIBFORM025026
Első szerző:Myrsky, Essi
Cím:Altered small-bowel mucosal vascular network in untreated coeliac disease / Myrsky E., Syrjänen M., Korponay-Szabo I. R., Mäki M., Kaukinen K., Lindfors K.
Dátum:2009
ISSN:0036-5521
Megjegyzések:It has recently been shown that serum autoantibodies targeted against transglutaminase 2 derived from untreated coeliac patients can disturb several steps of angiogenesis in vitro. The purpose of this study was to establish whether the small-bowel mucosal vasculature is altered in coeliac disease and whether the putative changes are gluten dependent. MATERIAL AND METHODS: The small-bowel mucosal microvessel architecture was examined in duodenal biopsy samples from coeliac patients before and after a gluten-free diet and from non-coeliac controls. In addition, the vasculature was subjected to a detailed morphometric analysis. Double immunofluorescent stainings of the vasculature with anti- alpha-smooth muscle actin antibody were performed in order to assess the maturity of mucosal vessels. Coeliac disease-specific transglutaminase 2-targeted autoantibody deposits in the vessel wall were studied using triple immunofluorescent stainings. RESULTS: On a gluten-containing diet the mucosal vasculature in the small intestine of untreated coeliac disease patients was altered in overall organization as well as in the number and maturity of the vessels when compared to healthy subjects. In patients on a gluten-free diet, the vasculature normalized parallel to mucosal recovery. CONCLUSIONS: In coeliac disease, ingestion of gluten leads to altered appearance of small-bowel mucosal microvasculature. It is thus conceivable that the small-bowel mucosal vascular biology might be involved in the pathogenesis of coeliac disease.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Scandinavian Journal Of Gastroenterology. - 44 : 2 (2009), p. 162-167. -
További szerzők:Syrjänen, Mari Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Mäki, Markku Kaukinen, Katri Lindfors, Katri
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10.

001-es BibID:BIBFORM025025
Első szerző:Myrsky, Essi
Cím:Coeliac disease-specific autoantibodies targeted against transglutaminase 2 disturb angiogenesis / Myrsky, E., Kaukinen, K., Syrjänen, M., Korponay-Szabó, I. R., Mäki, M., Lindfors, K.
Dátum:2008
ISSN:0009-9104
Megjegyzések:Coeliac disease is characterized by immunoglobulin-A (IgA)-class autoantibodies targeted against transglutaminase 2 (TG2), a multi-functional protein also with a role in angiogenesis. These antibodies are present in patient serum but are also found bound to TG2 below the epithelial basement membrane and around capillaries in the small intestinal mucosa. Based on these facts and the information that the mucosal vasculature of coeliac patients on a gluten-containing diet is disorganized, we studied whether the coeliac disease-specific autoantibodies targeted against TG2 would disturb angiogenesis. The effects of coeliac disease-specific autoantibodies on in vitro angiogenesis were studied in angiogenic cell cultures. The binding of the antibodies to cells, endothelial sprouting, migration of both endothelial and vascular mesenchymal cells, the integrity of the actin cytoskeleton in both cell types and the differentiation of vascular mesenchymal cells were recorded. In vitro, IgA derived from coeliac disease patients on a gluten-containing diet binds to surface TG2 on endothelial and vascular mesenchymal cells and this binding can be inhibited by the removal of TG2. In addition, coeliac disease-specific autoantibodies targeting TG2 disturb several steps of angiogenesis: endothelial sprouting and the migration of both endothelial and vascular mesenchymal cells. Furthermore, the autoantibodies cause disorganization of the actin cytoskeleton in both capillary cell types that account most probably for the defective cellular migration. We conclude that coeliac disease-specific autoantibodies recognizing TG2 inhibit angiogenesis in vitro. This disturbance of the angiogenic process could lead in vivo to the disruption of the mucosal vasculature seen in coeliac disease patients on a gluten-containing diet.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Clinical And Experimental Immunology. - 152 : 1 (2008), p. 111-119. -
További szerzők:Kaukinen, Katri Syrjänen, Mari Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Mäki, Markku Lindfors, Katri
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11.

001-es BibID:BIBFORM011940
Első szerző:Myrsky, Essi
Cím:Celiac disease IgA modulates vascular permeability in vitro through the activity of transglutaminase 2 and RhoA / Myrsky E., Caja S., Simon-Vecsei Z., Korponay-Szabo I., Nadalutti C., Collighan R., Mongeot A., Griffin M., Maki M., Kaukinen K., Lindfors K.
Dátum:2009
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Cellular and Molecular Life Sciences. - 66 : 20 (2009), p. 3375-3385. -
További szerzők:Caja, Sergio Simon-Vecsei Zsófia (1980-) (biológus) Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Nadalutti, Cristina Collighan, Russell Mongeot, Alexandre Griffin, Martin Mäki, Markku Kaukinen, Katri Lindfors, Katri
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12.

001-es BibID:BIBFORM048567
Első szerző:Nadalutti, Cristina Antonella
Cím:Celiac disease patient IgA antibodies induce endothelial adhesion and cell polarization defects via extracellular transglutaminase 2 / Cristina Antonella Nadalutti, Ilma Rita Korponay-Szabo, Katri Kaukinen, Martin Griffin, Markku Mäki, Katri Lindfors
Dátum:2014
ISSN:1420-682X
Megjegyzések:We have recently found that celiac disease patient serum-derived autoantibodies targeted against transglutaminase 2 interfere with several steps of angiogenesis, including endothelial sprouting and migration, though the mechanism involved remained to be fully characterized. This study now investigated the processes underlying the antiangiogenic effects exerted by celiac disease patient antibodies on endothelial cells, with particular regard to the adhesion, migration, and polarization signaling pathway. We observed that celiac IgA reduced endothelial cell numbers by affecting adhesion without increasing apoptosis. Endothelial cells in the presence of celiac IgA showed weak attachment, a high susceptibility to detach from fibronectin, and a disorganized extracellular matrix due to a reduction of protein cross-links. Furthermore, celiac patient IgA led to secretion of active transglutaminase 2 from endothelial cells into the culture supernatants. Additionally, cell surface transglutaminase 2 mediated integrin clustering in the presence of celiac IgA was coupled to augmented expression of ?1-integrin. We also observed that celiac patient IgA-treated endothelial cells had migratory defects and a less polarized phenotype when compared to control groups, and this was associated with the RhoA signaling pathway. These biological effects mediated by celiac IgA on endothelial cells were partially influenced but not completely abolished by R281, an irreversible extracellular transglutaminase 2 enzymatic activity inhibitor. Taken together, our results imply that celiac patient IgA antibodies disturb the extracellular protein cross-linking function of transglutaminase 2, thus altering cell-extracellular matrix interactions and thereby affecting endothelial cell adhesion, polarization, and motility.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Cellular and Molecular Life Sciences. - 71 : 7 (2014), p. 1315-1326. -
További szerzők:Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Kaukinen, Katri Griffin, Martin Mäki, Markku Lindfors, Katri
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