Function of LMP2B in EBV-positive Burkitt's Lymphoma: Virus and cancer (German Edition)

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9783838106601: Function of LMP2B in EBV-positive Burkitt's Lymphoma: Virus and cancer (German Edition)

Epstein-Barr virus (EBV) is a human γ-herpesvirus that persists latently in the memory B-cell pool. EBV is linked to malignancies including Burkitt’s lymphoma (BL) where it expresses specific latency genes. Among these genes, latent membrane protein (LMP)2A and LMP2B seem to be involved in the regulation of EBV latency. LMP2A blocks B-cell receptor (BCR) signalling after its engagement, which activates as well lytic EBV infection. Therefore, LMP2A contributes to the persistence of EBV. By contrast, the function of LMP2B, a splice variant of LMP2A, is still not resolved. The experimental setup presented in this book revealed for the first time that silencing of LMP2B resulted in reduced expression of lytic EBV mRNA and proteins upon BCR cross-linking. By contrast, overexpression of LMP2B resulted in the opposite. We could further demonstrate that LMP2A and LMP2B physically interact and that LMP2B resides predominantly in intracellular compartments. In conclusion, these observations support the hypothesis that LMP2B exhibits a negative regulatory effect on the ability of LMP2A to maintain latent EBV by preventing the switch to lytic infection.

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About the Author:

Markus Rechsteiner was born 20.12.1976 in Zurich, Switzerland.After completing his master studies in Biotechnology at the ETHZurich, he worked at the University UNESP, Brasil and Agroscope FAL Reckenholz, Switzerland. From 2005-06 he did his PhD thesis in the group of Prof. D. Nadal at the University Children’s Hospital Zurich.

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Rechsteiner, Markus
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Descripción Estado de conservación: New. Publisher/Verlag: Südwestdeutscher Verlag für Hochschulschriften | Virus and cancer | Epstein-Barr virus (EBV) is a human -herpesvirus that persists latently in the memory B-cell pool. EBV is linked to malignancies including Burkitt's lymphoma (BL) where it expresses specific latency genes. Among these genes, latent membrane protein (LMP)2A and LMP2B seem to be involved in the regulation of EBV latency. LMP2A blocks B-cell receptor (BCR) signalling after its engagement, which activates as well lytic EBV infection. Therefore, LMP2A contributes to the persistence of EBV. By contrast, the function of LMP2B, a splice variant of LMP2A, is still not resolved. The experimental setup presented in this book revealed for the first time that silencing of LMP2B resulted in reduced expression of lytic EBV mRNA and proteins upon BCR cross-linking. By contrast, overexpression of LMP2B resulted in the opposite. We could further demonstrate that LMP2A and LMP2B physically interact and that LMP2B resides predominantly in intracellular compartments. In conclusion, these observations support the hypothesis that LMP2B exhibits a negative regulatory effect on the ability of LMP2A to maintain latent EBV by preventing the switch to lytic infection. | Format: Paperback | 128 gr | 220x150x4 mm | 84 pp. Nº de ref. de la librería K9783838106601

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Descripción Sudwestdeutscher Verlag Fur Hochschulschriften AG 2009-05-04, 2009. paperback. Estado de conservación: New. Nº de ref. de la librería 9783838106601

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Markus Rechsteiner
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Descripción Südwestdeutscher Verlag Für Hochschulschriften AG Co. KG Aug 2015, 2015. Taschenbuch. Estado de conservación: Neu. Neuware - Epstein-Barr virus (EBV) is a human -herpesvirus that persists latently in the memory B-cell pool. EBV is linked to malignancies including Burkitt's lymphoma (BL) where it expresses specific latency genes. Among these genes, latent membrane protein (LMP)2A and LMP2B seem to be involved in the regulation of EBV latency. LMP2A blocks B-cell receptor (BCR) signalling after its engagement, which activates as well lytic EBV infection. Therefore, LMP2A contributes to the persistence of EBV. By contrast, the function of LMP2B, a splice variant of LMP2A, is still not resolved. The experimental setup presented in this book revealed for the first time that silencing of LMP2B resulted in reduced expression of lytic EBV mRNA and proteins upon BCR cross-linking. By contrast, overexpression of LMP2B resulted in the opposite. We could further demonstrate that LMP2A and LMP2B physically interact and that LMP2B resides predominantly in intracellular compartments. In conclusion, these observations support the hypothesis that LMP2B exhibits a negative regulatory effect on the ability of LMP2A to maintain latent EBV by preventing the switch to lytic infection. 84 pp. Deutsch. Nº de ref. de la librería 9783838106601

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Markus Rechsteiner
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Descripción Südwestdeutscher Verlag Für Hochschulschriften AG Co. KG Aug 2015, 2015. Taschenbuch. Estado de conservación: Neu. Neuware - Epstein-Barr virus (EBV) is a human -herpesvirus that persists latently in the memory B-cell pool. EBV is linked to malignancies including Burkitt's lymphoma (BL) where it expresses specific latency genes. Among these genes, latent membrane protein (LMP)2A and LMP2B seem to be involved in the regulation of EBV latency. LMP2A blocks B-cell receptor (BCR) signalling after its engagement, which activates as well lytic EBV infection. Therefore, LMP2A contributes to the persistence of EBV. By contrast, the function of LMP2B, a splice variant of LMP2A, is still not resolved. The experimental setup presented in this book revealed for the first time that silencing of LMP2B resulted in reduced expression of lytic EBV mRNA and proteins upon BCR cross-linking. By contrast, overexpression of LMP2B resulted in the opposite. We could further demonstrate that LMP2A and LMP2B physically interact and that LMP2B resides predominantly in intracellular compartments. In conclusion, these observations support the hypothesis that LMP2B exhibits a negative regulatory effect on the ability of LMP2A to maintain latent EBV by preventing the switch to lytic infection. 84 pp. Deutsch. Nº de ref. de la librería 9783838106601

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Markus Rechsteiner
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Descripción Südwestdeutscher Verlag Für Hochschulschriften AG Co. KG Aug 2015, 2015. Taschenbuch. Estado de conservación: Neu. This item is printed on demand - Print on Demand Neuware - Epstein-Barr virus (EBV) is a human -herpesvirus that persists latently in the memory B-cell pool. EBV is linked to malignancies including Burkitt's lymphoma (BL) where it expresses specific latency genes. Among these genes, latent membrane protein (LMP)2A and LMP2B seem to be involved in the regulation of EBV latency. LMP2A blocks B-cell receptor (BCR) signalling after its engagement, which activates as well lytic EBV infection. Therefore, LMP2A contributes to the persistence of EBV. By contrast, the function of LMP2B, a splice variant of LMP2A, is still not resolved. The experimental setup presented in this book revealed for the first time that silencing of LMP2B resulted in reduced expression of lytic EBV mRNA and proteins upon BCR cross-linking. By contrast, overexpression of LMP2B resulted in the opposite. We could further demonstrate that LMP2A and LMP2B physically interact and that LMP2B resides predominantly in intracellular compartments. In conclusion, these observations support the hypothesis that LMP2B exhibits a negative regulatory effect on the ability of LMP2A to maintain latent EBV by preventing the switch to lytic infection. 84 pp. Deutsch. Nº de ref. de la librería 9783838106601

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Markus Rechsteiner
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Descripción Sudwestdeutscher Verlag Fur Hochschulschriften AG, United States, 2015. Paperback. Estado de conservación: New. Language: English . Brand New Book. Epstein-Barr virus (EBV) is a human -herpesvirus that persists latently in the memory B-cell pool. EBV is linked to malignancies including Burkitt s lymphoma (BL) where it expresses specific latency genes. Among these genes, latent membrane protein (LMP)2A and LMP2B seem to be involved in the regulation of EBV latency. LMP2A blocks B-cell receptor (BCR) signalling after its engagement, which activates as well lytic EBV infection. Therefore, LMP2A contributes to the persistence of EBV. By contrast, the function of LMP2B, a splice variant of LMP2A, is still not resolved. The experimental setup presented in this book revealed for the first time that silencing of LMP2B resulted in reduced expression of lytic EBV mRNA and proteins upon BCR cross-linking. By contrast, overexpression of LMP2B resulted in the opposite. We could further demonstrate that LMP2A and LMP2B physically interact and that LMP2B resides predominantly in intracellular compartments. In conclusion, these observations support the hypothesis that LMP2B exhibits a negative regulatory effect on the ability of LMP2A to maintain latent EBV by preventing the switch to lytic infection. Nº de ref. de la librería KNV9783838106601

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Markus Rechsteiner
Editorial: Sudwestdeutscher Verlag Fur Hochschulschriften AG
ISBN 10: 3838106601 ISBN 13: 9783838106601
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Descripción Sudwestdeutscher Verlag Fur Hochschulschriften AG. Paperback. Estado de conservación: New. 84 pages. Dimensions: 8.7in. x 5.9in. x 0.2in.Epstein-Barr virus (EBV) is a human -herpesvirusthat persists latently in the memory B-cell pool. EBVis linked to malignancies including Burkittslymphoma (BL) where it expresses specific latencygenes. Among these genes, latent membrane protein(LMP)2A and LMP2B seem to be involved in theregulation of EBV latency. LMP2A blocks B-cellreceptor (BCR) signalling after its engagement, whichactivates as well lytic EBV infection. Therefore, LMP2A contributes to the persistence of EBV. Bycontrast, the function of LMP2B, a splice variant ofLMP2A, is still not resolved. The experimental setuppresented in this book revealed for the first timethat silencing of LMP2B resulted in reducedexpression of lytic EBV mRNA and proteins upon BCRcross-linking. By contrast, overexpression of LMP2Bresulted in the opposite. We could furtherdemonstrate that LMP2A and LMP2B physically interactand that LMP2B resides predominantly in intracellularcompartments. In conclusion, these observationssupport the hypothesis that LMP2B exhibits a negativeregulatory effect on the ability of LMP2A to maintainlatent EBV by preventing the switch to lytic infection. This item ships from multiple locations. Your book may arrive from Roseburg,OR, La Vergne,TN. Paperback. Nº de ref. de la librería 9783838106601

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