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204 results on '"Schmidt, Mirko H. H."'

3. Correction: EGFL7 loss correlates with increased VEGF-D expression, upregulating hippocampal adult neurogenesis and improving spatial learning and memory

Author

Barth, Kathrin, Vasić, Verica, McDonald, Brennan, Heinig, Nora, Wagner, Marc Christoph, Schumann, Ulrike, Röhlecke, Cora, Bicker, Frank, Schumann, Lana, Radyushkin, Konstantin, Baumgart, Jan, Tenzer, Stefan, Zipp, ·Frauke, Meinhardt, Matthias, Alitalo, Kari, Tegeder, Irmgard, and Schmidt, Mirko H. H.

Published
2023
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14. EGFL7 reduces CNS inflammation in mouse

Author

Larochelle, Catherine, Uphaus, Timo, Broux, Bieke, Gowing, Elizabeth, Paterka, Magdalena, Michel, Laure, Dudvarski Stankovic, Nevenka, Bicker, Frank, Lemaître, Florent, Prat, Alexandre, Schmidt, Mirko H. H., and Zipp, Frauke

Published
2018
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16. Gamma Irradiation Triggers Immune Escape in Glioma-Propagating Cells

Author

Hoppmann, Nicola, primary, Heinig, Nora, additional, Distler, Ute, additional, Kim, Ella, additional, Lennerz, Volker, additional, Krauß, Yvonne, additional, Schumann, Ulrike, additional, Giese, Alf, additional, Tenzer, Stefan, additional, Bitar, Lynn, additional, and Schmidt, Mirko H. H., additional

Published
2022
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20. SAMHD1 in cancer: curse or cure?

Author

Schott, Kerstin, primary, Majer, Catharina, additional, Bulashevska, Alla, additional, Childs, Liam, additional, Schmidt, Mirko H. H., additional, Rajalingam, Krishnaraj, additional, Munder, Markus, additional, and König, Renate, additional

Published
2021
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24. Acetylation-dependent regulation of endothelial Notch signalling by the SIRT1 deacetylase

Author

Guarani, Virginia, Deflorian, Gianluca, Franco, Claudio A., Krüger, Marcus, Phng, Li-Kun, Bentley, Katie, Toussaint, Louise, Dequiedt, Franck, Mostoslavsky, Raul, Schmidt, Mirko H. H., Zimmermann, Barbara, Brandes, Ralf P., Mione, Marina, Westphal, Christoph H., Braun, Thomas, Zeiher, Andreas M., Gerhardt, Holger, Dimmeler, Stefanie, and Potente, Michael

Published
2011
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25. Prevention of age-associated neuronal hyperexcitability with improved learning and attention upon knockout or antagonism of LPAR2

Author

Fischer, Caroline, primary, Endle, Heiko, additional, Schumann, Lana, additional, Wilken-Schmitz, Annett, additional, Kaiser, Julia, additional, Gerber, Susanne, additional, Vogelaar, Christina F., additional, Schmidt, Mirko H. H., additional, Nitsch, Robert, additional, Snodgrass, Isabel, additional, Thomas, Dominique, additional, Vogt, Johannes, additional, and Tegeder, Irmgard, additional

Published
2020
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28. Recommendations of the working group of the Anatomische Gesellschaft on reduction of formaldehyde exposure in anatomical curricula and institutes

Author

Waschke, Jens, Bergmann, Martin, Braeuer, Lars, Brenner, Erich, Buchhorn, Andreas, Deutsch, Arlette, Dokter, Martin, Egu, Desalegn Tadesse, Erguen, Suelleyman, Fassnacht, Ulrich, Fietz, Daniela, Gundlach, Stefanie, Heermann, Stephan, Hirt, Bernhard, Kugelmann, Daniela, Mueller-Gerbl, Magdalena, Neiss, Wolfram, Nimtschke, Ute, Plendl, Johanna, Pretterklieber, Michael, Redies, Christoph, Scaal, Martin, Schmidt, Mirko H. H., Schmiedl, Andreas, Schnittler, Hans-Joachim, Schomerus, Christof, Sebesteny, Tamas, Spittau, Bjoern, Steiniger, Birte, Tschernig, Thomas, Unverzagt, Axel, Viebahn, Christoph, Voigt, Ernst, Weigner, Janet, Weyers, Imke, Winkelmann, Andreas, Winkler, Merle, Paulsen, Friedrich, Waschke, Jens, Bergmann, Martin, Braeuer, Lars, Brenner, Erich, Buchhorn, Andreas, Deutsch, Arlette, Dokter, Martin, Egu, Desalegn Tadesse, Erguen, Suelleyman, Fassnacht, Ulrich, Fietz, Daniela, Gundlach, Stefanie, Heermann, Stephan, Hirt, Bernhard, Kugelmann, Daniela, Mueller-Gerbl, Magdalena, Neiss, Wolfram, Nimtschke, Ute, Plendl, Johanna, Pretterklieber, Michael, Redies, Christoph, Scaal, Martin, Schmidt, Mirko H. H., Schmiedl, Andreas, Schnittler, Hans-Joachim, Schomerus, Christof, Sebesteny, Tamas, Spittau, Bjoern, Steiniger, Birte, Tschernig, Thomas, Unverzagt, Axel, Viebahn, Christoph, Voigt, Ernst, Weigner, Janet, Weyers, Imke, Winkelmann, Andreas, Winkler, Merle, and Paulsen, Friedrich

Abstract

The practice of human and veterinary medicine is based on the science of anatomy and dissection courses are still irreplaceable in the teaching of anatomy. Embalming is required to preserve body donors, for which process formaldehyde (FA) is the most frequently used and well characterized biocidal substance. Since January 2016, a new occupational exposure limit (OEL) for FA of 0.37 mg/m(3) issued by the European Committee on Hazardous Substances is obligatory since FA has been classified as a human 1B carcinogen. The anatomical institutes in the German-speaking region are called upon to consolidate efforts to reduce use of FA in anatomical curricula and body donations. As a result, the Anatomische Gesellschaft (AG) has formed a Working Group for Reduction of Formaldehyde Exposure in Dissection Courses tasked with discussion and recommendation of measures to reduce FA. Based on the assessment of the Working Group, the AG has issued an official opinion to the effect that, at this point in time, embalming of body donors without FA completely is not feasible. Therefore, a combination of approaches are to be used to reduce FA exposure, including technical and structural (architectural) adaptations, modification of protocols for fixation and preservation as well as organizational measures. One structural measure considered unavoidable is the integration of air supply and exhaust of individual dissecting tables into the ventilation system of the anatomy building. To embalm human body donors, intra-arterial perfusion fixation with up to 4% FA and a total fluid volume of 150 mL/kg body weight will suffice. For animals where body weights and biology of bodies vary widely (i.e. special needs of fixation for ruminants, large animals as horses) perfusion fixation with up to 4% FA and a quantity of fixative solution of 10-15% of the body weight may be required. Preservation of body donors in storage (immersion) can be done with 40% ethanol or in a full bath preservation containin

Published
2019

30. The soluble form of pan-RTK inhibitor and tumor suppressor LRIG1 mediates downregulation of AXL through direct protein–protein interaction in glioblastoma

Author

Neirinckx, Virginie, primary, Hau, Ann-Christin, primary, Schuster, Anne, primary, Fritah, Sabrina, primary, Tiemann, Katja, primary, Klein, Eliane, primary, Nazarov, Petr V, primary, Matagne, André, primary, Szpakowska, Martyna, primary, Meyrath, Max, primary, Chevigné, Andy, primary, Schmidt, Mirko H H, primary, and Niclou, Simone P, primary

Published
2019
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33. Neurovascular EGFL7 regulates adult neurogenesis in the subventricular zone and thereby affects olfactory perception

Author

Bicker, Frank, Vasic, Verica, Horta, Guilherme, Ortega, Felipe, Nolte, Hendrik, Kavyanifar, Atria, Keller, Stefanie, Stankovic, Nevenka Dudvarski, Harter, Patrick N., Benedito, Rui, Lutz, Beat, Baeuerle, Tobias, Hartwig, Jens, Baumgart, Jan, Krueger, Marcus, Radyushkin, Konstantin, Alberi, Lavinia, Berninger, Benedikt, Schmidt, Mirko H. H., Bicker, Frank, Vasic, Verica, Horta, Guilherme, Ortega, Felipe, Nolte, Hendrik, Kavyanifar, Atria, Keller, Stefanie, Stankovic, Nevenka Dudvarski, Harter, Patrick N., Benedito, Rui, Lutz, Beat, Baeuerle, Tobias, Hartwig, Jens, Baumgart, Jan, Krueger, Marcus, Radyushkin, Konstantin, Alberi, Lavinia, Berninger, Benedikt, and Schmidt, Mirko H. H.

Abstract

Adult neural stem cells reside in a specialized niche in the subventricular zone (SVZ). Throughout life they give rise to adult-born neurons in the olfactory bulb (OB), thus contributing to neural plasticity and pattern discrimination. Here, we show that the neurovascular protein EGFL7 is secreted by endothelial cells and neural stem cells (NSCs) of the SVZ to shape the vascular stem-cell niche. Loss of EGFL7 causes an accumulation of activated NSCs, which display enhanced activity and re-entry into the cell cycle. EGFL7 pushes activated NSCs towards quiescence and neuronal progeny towards differentiation. This is achieved by promoting Dll4-induced Notch signalling at the blood vessel-stem cell interface. Fewer inhibitory neurons form in the OB of EGFL7-knockout mice, which increases the absolute signal conducted from the mitral cell layer of the OB but decreases neuronal network synchronicity. Consequently, EGFL7-knockout mice display severe physiological defects in olfactory behaviour and perception.

Published
2017

34. Neurovascular EGFL7 regulates adult neurogenesis in the subventricular zone and thereby affects olfactory perception

Author

Bicker, Frank, primary, Vasic, Verica, additional, Horta, Guilherme, additional, Ortega, Felipe, additional, Nolte, Hendrik, additional, Kavyanifar, Atria, additional, Keller, Stefanie, additional, Stankovic, Nevenka Dudvarski, additional, Harter, Patrick N., additional, Benedito, Rui, additional, Lutz, Beat, additional, Bäuerle, Tobias, additional, Hartwig, Jens, additional, Baumgart, Jan, additional, Krüger, Marcus, additional, Radyushkin, Konstantin, additional, Alberi, Lavinia, additional, Berninger, Benedikt, additional, and Schmidt, Mirko H. H., additional

Published
2017
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36. Pericytes in Vascular Development and Function

Author

Schmidt, Mirko H H, Liebner, Stefan, Schmidt, M H H ( Mirko H H ), Liebner, S ( Stefan ), Daneman, Richard, Keller, Annika, Schmidt, Mirko H H, Liebner, Stefan, Schmidt, M H H ( Mirko H H ), Liebner, S ( Stefan ), Daneman, Richard, and Keller, Annika

Abstract

Pericytes are perivascular cells that line the abluminal surface of the microvasculature. Recent years have witnessed tremendous progress in understanding the function of these cells. Pericytes have emerged as important regulators of vascular development and homeostasis. In addition, pericytes possess several organ-specific functions, including regulation of blood flow and modulation of the immune response. Pericytes are also emerging as therapeutic targets in pathological conditions such as tissue fibrosis, stroke, and tumors. In this chapter, we provide an overview of the ontogeny and morphology of pericytes, signaling pathways critical for pericyte recruitment to developing vessels, and various physiological roles of pericytes.

Published
2015

38. EGFL7 enhances surface expression of integrin α5β1 to promote angiogenesis in malignant brain tumors.

Author

Dudvarski Stanković, Nevenka, Bicker, Frank, Keller, Stefanie, Jones, David T. W., Harter, Patrick N., Kienzle, Arne, Gillmann, Clarissa, Arnold, Philipp, Golebiewska, Anna, Keunen, Olivier, Giese, Alf, von Deimling, Andreas, Bäuerle, Tobias, Niclou, Simone P., Mittelbronn, Michel, Ye, Weilan, Pfister, Stefan M., and Schmidt, Mirko H. H.

Abstract

Abstract: Glioblastoma (GBM) is a typically lethal type of brain tumor with a median survival of 15 months postdiagnosis. This negative prognosis prompted the exploration of alternative treatment options. In particular, the reliance of GBM on angiogenesis triggered the development of anti‐VEGF (vascular endothelial growth factor) blocking antibodies such as bevacizumab. Although its application in human GBM only increased progression‐free periods but did not improve overall survival, physicians and researchers still utilize this treatment option due to the lack of adequate alternatives. In an attempt to improve the efficacy of anti‐VEGF treatment, we explored the role of the egfl7 gene in malignant glioma. We found that the encoded extracellular matrix protein epidermal growth factor‐like protein 7 (EGFL7) was secreted by glioma blood vessels but not glioma cells themselves, while no major role could be assigned to the parasitic miRNAs miR‐126/126*. EGFL7 expression promoted glioma growth in experimental glioma models in vivo and stimulated tumor vascularization. Mechanistically, this was mediated by an upregulation of integrin α5β1 on the cellular surface of endothelial cells, which enhanced fibronectin‐induced angiogenic sprouting. Glioma blood vessels that formed in vivo were more mature as determined by pericyte and smooth muscle cell coverage. Furthermore, these vessels were less leaky as measured by magnetic resonance imaging of extravasating contrast agent. EGFL7‐inhibition using a specific blocking antibody reduced the vascularization of experimental gliomas and increased the life span of treated animals, in particular in combination with anti‐VEGF and the chemotherapeutic agent temozolomide. Data allow for the conclusion that this combinatorial regimen may serve as a novel treatment option for GBM. [ABSTRACT FROM AUTHOR]

Published
2018
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39. The Role of Microglia in Diabetic Retinopathy: Inflammation, Microvasculature Defects and Neurodegeneration.

Author

Altmann, Christine and Schmidt, Mirko H. H.

Subjects
*DIABETIC retinopathy, *MICROGLIA, *RETINAL diseases, *NEURONS, *APOPTOSIS, *BLINDNESS, *NEURODEGENERATION, *INFLAMMATION, *PREVENTION
Abstract

Diabetic retinopathy is a common complication of diabetes mellitus, which appears in one third of all diabetic patients and is a prominent cause of vision loss. First discovered as a microvascular disease, intensive research in the field identified inflammation and neurodegeneration to be part of diabetic retinopathy. Microglia, the resident monocytes of the retina, are activated due to a complex interplay between the different cell types of the retina and diverse pathological pathways. The trigger for developing diabetic retinopathy is diabetes-induced hyperglycemia, accompanied by leukostasis and vascular leakages. Transcriptional changes in activated microglia, mediated via the nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB) and extracellular signal-regulated kinase (ERK) signaling pathways, results in release of various pro-inflammatory mediators, including cytokines, chemokines, caspases and glutamate. Activated microglia additionally increased proliferation and migration. Among other consequences, these changes in microglia severely affected retinal neurons, causing increased apoptosis and subsequent thinning of the nerve fiber layer, resulting in visual loss. New potential therapeutics need to interfere with these diabetic complications even before changes in the retina are diagnosed, to prevent neuronal apoptosis and blindness in patients. [ABSTRACT FROM AUTHOR]

Published
2018
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41. Perivascular microglia promote blood vessel disintegration in the ischemic penumbra

Author

Jolivel, Valérie, primary, Bicker, Frank, additional, Binamé, Fabien, additional, Ploen, Robert, additional, Keller, Stefanie, additional, Gollan, René, additional, Jurek, Betty, additional, Birkenstock, Jérôme, additional, Poisa-Beiro, Laura, additional, Bruttger, Julia, additional, Opitz, Verena, additional, Thal, Serge C., additional, Waisman, Ari, additional, Bäuerle, Tobias, additional, Schäfer, Michael K., additional, Zipp, Frauke, additional, and Schmidt, Mirko H. H., additional

Published
2014
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42. EGFR and EGFRvIII Promote Angiogenesis and Cell Invasion in Glioblastoma: Combination Therapies for an Effective Treatment.

Author

Keller, Stefanie and Schmidt, Mirko H. H.

Subjects
*GLIOBLASTOMA multiforme, *GLIOBLASTOMA multiforme treatment, *EPIDERMAL growth factor receptors, *NEOVASCULARIZATION, *EXTRACELLULAR matrix, *PATIENTS
Abstract

Epidermal growth factor receptor (EGFR) and the mutant EGFRvIII are major focal points in current concepts of targeted cancer therapy for glioblastoma multiforme (GBM), the most malignant primary brain tumor. The receptors participate in the key processes of tumor cell invasion and tumor-related angiogenesis and their upregulation correlates with the poor prognosis of glioma patients. Glioma cell invasion and increased angiogenesis share mechanisms of the degradation of the extracellular matrix (ECM) through upregulation of ECM-degrading proteases as well as the activation of aberrant signaling pathways. This review describes the role of EGFR and EGFRvIII in those mechanisms which might offer new combined therapeutic approaches targeting EGFR or EGFRvIII together with drug treatments against proteases of the ECM or downstream signaling to increase the inhibitory effects of mono-therapies. [ABSTRACT FROM AUTHOR]

Published
2017
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43. Resilience and Vulnerability to Pain and Inflammation in the Hippocampus.

Author

Vasic, Verica and Schmidt, Mirko H. H.

Subjects
*HIPPOCAMPUS (Brain), *NEURODEGENERATION, *PATHOLOGICAL psychology, *NEUROPLASTICITY, *DEVELOPMENTAL neurobiology
Abstract

Increasing evidence demonstrates the importance of hippocampal neurogenesis, a fundamental mechanism of neuroplasticity associated with cognition and emotion, in correlation to neurodegenerative and psychiatric disorders. Neuropsychiatric disorders are often a result of chronic stress or pain followed by inflammation; all these conditions manifest cognitive deficits and impairments in neurogenesis. However, while some individuals are more susceptible to stress, others are able to adapt to new environments via mechanisms of resilience. In light of this emerging field and based on extensive research, the role of neurogenesis is summarized and presented as a potentially powerful therapeutic tool. [ABSTRACT FROM AUTHOR]

Published
2017
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44. CIN85 regulates dopamine receptor endocytosis and governs behaviour in mice

Author

Shimokawa, Noriaki, Haglund, Kaisa, Hölter, Sabine M, Grabbe, Caroline, Kirkin, Vladimir, Koibuchi, Noriyuki, Schultz, Christian, Rozman, Jan, Hoeller, Daniela, Qiu, Chun-Hong, Londoño, Marina B, Ikezawa, Jun, Jedlicka, Peter, Stein, Birgit, Schwarzacher, Stephan W, Wolfer, David P, Ehrhardt, Nicole, Heuchel, Rainer, Nezis, Ioannis, Brech, Andreas, Schmidt, Mirko H H, Fuchs, Helmut, Gailus-Durner, Valerie, Klingenspor, Martin, Bogler, Oliver, Wurst, Wolfgang, Deller, Thomas, de Angelis, Martin Hrabé, Dikic, Ivan, Shimokawa, Noriaki, Haglund, Kaisa, Hölter, Sabine M, Grabbe, Caroline, Kirkin, Vladimir, Koibuchi, Noriyuki, Schultz, Christian, Rozman, Jan, Hoeller, Daniela, Qiu, Chun-Hong, Londoño, Marina B, Ikezawa, Jun, Jedlicka, Peter, Stein, Birgit, Schwarzacher, Stephan W, Wolfer, David P, Ehrhardt, Nicole, Heuchel, Rainer, Nezis, Ioannis, Brech, Andreas, Schmidt, Mirko H H, Fuchs, Helmut, Gailus-Durner, Valerie, Klingenspor, Martin, Bogler, Oliver, Wurst, Wolfgang, Deller, Thomas, de Angelis, Martin Hrabé, and Dikic, Ivan

Abstract

Despite extensive investigations of Cbl-interacting protein of 85 kDa (CIN85) in receptor trafficking and cytoskeletal dynamics, little is known about its functions in vivo. Here, we report the study of a mouse deficient of the two CIN85 isoforms expressed in the central nervous system, exposing a function of CIN85 in dopamine receptor endocytosis. Mice lacking CIN85 exon 2 (CIN85(Deltaex2)) show hyperactivity phenotypes, characterized by increased physical activity and exploratory behaviour. Interestingly, CIN85(Deltaex2) animals display abnormally high levels of dopamine and D2 dopamine receptors (D2DRs) in the striatum, an important centre for the coordination of animal behaviour. Importantly, CIN85 localizes to the post-synaptic compartment of striatal neurons in which it co-clusters with D2DRs. Moreover, it interacts with endocytic regulators such as dynamin and endophilins in the striatum. Absence of striatal CIN85 causes insufficient complex formation of endophilins with D2DRs in the striatum and ultimately decreased D2DR endocytosis in striatal neurons in response to dopamine stimulation. These findings indicate an important function of CIN85 in the regulation of dopamine receptor functions and provide a molecular explanation for the hyperactive behaviour of CIN85(Deltaex2) mice.

Published
2010
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45. EGFL7 ligates αvβ3 integrin to enhance vessel formation

Author

Nikolić, Iva, primary, Stanković, Nevenka Dudvarski, additional, Bicker, Frank, additional, Meister, Jeannette, additional, Braun, Helene, additional, Awwad, Khader, additional, Baumgart, Jan, additional, Simon, Kirsten, additional, Thal, Serge C., additional, Patra, Chinmoy, additional, Harter, Patrick N., additional, Plate, Karl H., additional, Engel, Felix B., additional, Dimmeler, Stefanie, additional, Eble, Johannes A., additional, Mittelbronn, Michel, additional, Schäfer, Michael K., additional, Jungblut, Benno, additional, Chavakis, Emmanouil, additional, Fleming, Ingrid, additional, and Schmidt, Mirko H. H., additional

Published
2013
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46. Suppressors of T-cell receptor signaling Sts-1 and Sts-2 bind to Cbl and inhibit endocytosis of receptor tyrosine kinases

Author

Kowanetz, Katarzyna, Crosetto, Nicola, Haglund, Kaisa, Schmidt, Mirko H H, Heldin, Carl-Henrik, Dikic, Ivan, Kowanetz, Katarzyna, Crosetto, Nicola, Haglund, Kaisa, Schmidt, Mirko H H, Heldin, Carl-Henrik, and Dikic, Ivan

Abstract

The ubiquitin (Ub) ligase Cbl plays a critical role in attenuation of receptor tyrosine kinase (RTK) signaling by inducing ubiquitination of RTKs and promoting their sorting for endosomal degradation. Herein, we describe the identification of two novel Cbl-interacting proteins, p70 and Clip4 (recently assigned the names Sts-1 and Sts-2, respectively), that inhibit endocytosis of epidermal growth factor receptor (EGFR) and platelet-derived growth factor receptor. Sts-1 and Sts-2 contain SH3 domains that interacted with Cbl, Ub-associated domains, which bound directly to mono-Ub or to the EGFR/Ub chimera as well as phosphoglycerate mutase domains that mediated oligomerization of Sts-1/2. Ligand-induced recruitment of Sts-1/Sts-2 into activated EGFR complexes led to inhibition of receptor internalization, reduction in the number of EGFR-containing endocytic vesicles, and subsequent block of receptor degradation followed by prolonged activation of mitogenic signaling pathways. On the other hand, interference with Sts-1/Sts-2 functions diminished ligand-induced receptor degradation, cell proliferation, and oncogenic transformation in cultured fibroblasts. We suggest that Sts-1 and Sts-2 represent a novel class of Ub-binding proteins that regulate RTK endocytosis and control growth factor-induced cellular functions.

Published
2004
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47. CIN85 regulates dopamine receptor endocytosis and governs behaviour in mice

Author

Shimokawa, Noriaki, primary, Haglund, Kaisa, additional, Hölter, Sabine M, additional, Grabbe, Caroline, additional, Kirkin, Vladimir, additional, Koibuchi, Noriyuki, additional, Schultz, Christian, additional, Rozman, Jan, additional, Hoeller, Daniela, additional, Qiu, Chun-Hong, additional, Londoño, Marina B, additional, Ikezawa, Jun, additional, Jedlicka, Peter, additional, Stein, Birgit, additional, Schwarzacher, Stephan W, additional, Wolfer, David P, additional, Ehrhardt, Nicole, additional, Heuchel, Rainer, additional, Nezis, Ioannis, additional, Brech, Andreas, additional, Schmidt, Mirko H H, additional, Fuchs, Helmut, additional, Gailus-Durner, Valerie, additional, Klingenspor, Martin, additional, Bogler, Oliver, additional, Wurst, Wolfgang, additional, Deller, Thomas, additional, de Angelis, Martin Hrabé, additional, and Dikic, Ivan, additional

Published
2010
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49. Regulation of Epidermal Growth Factor Receptor Trafficking by Lysine Deacetylase HDAC6

Author

Lissanu Deribe, Yonathan, primary, Wild, Philipp, additional, Chandrashaker, Akhila, additional, Curak, Jasna, additional, Schmidt, Mirko H. H., additional, Kalaidzidis, Yannis, additional, Milutinovic, Natasa, additional, Kratchmarova, Irina, additional, Buerkle, Lukas, additional, Fetchko, Michael J., additional, Schmidt, Philipp, additional, Kittanakom, Saranya, additional, Brown, Kevin R., additional, Jurisica, Igor, additional, Blagoev, Blagoy, additional, Zerial, Marino, additional, Stagljar, Igor, additional, and Dikic, Ivan, additional

Published
2009
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50. Flt3-dependent transformation by inactivating c-Cbl mutations in AML

Author

Sargin, Bülent, primary, Choudhary, Chunaram, additional, Crosetto, Nicola, additional, Schmidt, Mirko H. H., additional, Grundler, Rebekka, additional, Rensinghoff, Marion, additional, Thiessen, Christine, additional, Tickenbrock, Lara, additional, Schwäble, Joachim, additional, Brandts, Christian, additional, August, Benjamin, additional, Koschmieder, Steffen, additional, Bandi, Srinivasa Rao, additional, Duyster, Justus, additional, Berdel, Wolfgang E., additional, Müller-Tidow, Carsten, additional, Dikic, Ivan, additional, and Serve, Hubert, additional

Published
2007
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