How dormant origins, the FA pathway and HELQ promote genome stability
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How dormant origins, the FA pathway and HELQ promote genome stability
~EN PB NW
ISBN: 9783659622236 bzw. 3659622230, vermutlich in Englisch, LAP Lambert Academic Publishing, Taschenbuch, neu.
Lieferung aus: Deutschland, Versandkostenfrei.
Von Händler/Antiquariat, BuchWeltWeit Inh. Ludwig Meier e.K. [57449362], Bergisch Gladbach, Germany.
Neuware - DNA replication is continually impeded by endogenous lesions that cause the stalling of replication forks. This threatens the integrity of the genome and may drive cancer development. Cells possess many mechanisms by which to deal with stalled forks including dormant (backup) origins, the Fanconi anemia pathway and the DNA helicase HELQ. However, their precise functions remained unclear. This book brings together multiple studies to shed light on how these mechanisms guard the genome. Using a unique mutant mouse model called Mcm4chaos3 exhibiting a decreased number of dormant origins, we provide evidence that origin-poor regions of the genome cannot finish replication until early M phase (or not all), leading to multiple forms of chromosome instability. A lack of dormant origins also leads to hyper-activation of the FA pathway, revealing its role in the recovery of stalled forks where origins are limited. Indeed, disruption of the FA pathway in Mcm4chaos3/chaos3 mice led to high perinatal lethality and accelerated tumor formation. Finally, we use the first Helq mutant mouse model to show that Helq works in parallel to the FA pathway to promote chromosome stability. 288 pp. Englisch.
Von Händler/Antiquariat, BuchWeltWeit Inh. Ludwig Meier e.K. [57449362], Bergisch Gladbach, Germany.
Neuware - DNA replication is continually impeded by endogenous lesions that cause the stalling of replication forks. This threatens the integrity of the genome and may drive cancer development. Cells possess many mechanisms by which to deal with stalled forks including dormant (backup) origins, the Fanconi anemia pathway and the DNA helicase HELQ. However, their precise functions remained unclear. This book brings together multiple studies to shed light on how these mechanisms guard the genome. Using a unique mutant mouse model called Mcm4chaos3 exhibiting a decreased number of dormant origins, we provide evidence that origin-poor regions of the genome cannot finish replication until early M phase (or not all), leading to multiple forms of chromosome instability. A lack of dormant origins also leads to hyper-activation of the FA pathway, revealing its role in the recovery of stalled forks where origins are limited. Indeed, disruption of the FA pathway in Mcm4chaos3/chaos3 mice led to high perinatal lethality and accelerated tumor formation. Finally, we use the first Helq mutant mouse model to show that Helq works in parallel to the FA pathway to promote chromosome stability. 288 pp. Englisch.
2
How dormant origins, the FA pathway and HELQ promote genome stability
~EN NW
ISBN: 9783659622236 bzw. 3659622230, vermutlich in Englisch, neu.
Lieferung aus: Vereinigtes Königreich Grossbritannien und Nordirland, Lieferzeit: 11 Tage, zzgl. Versandkosten.
DNA replication is continually impeded by endogenous lesions that cause the stalling of replication forks. This threatens the integrity of the genome and may drive cancer development. Cells possess many mechanisms by which to deal with stalled forks including dormant (backup) origins, the Fanconi anemia pathway and the DNA helicase HELQ. However, their precise functions remained unclear. This book brings together multiple studies to shed light on how these mechanisms guard the genome. Using a unique mutant mouse model called Mcm4chaos3 exhibiting a decreased number of dormant origins, we provide evidence that origin-poor regions of the genome cannot finish replication until early M phase (or not all), leading to multiple forms of chromosome instability. A lack of dormant origins also leads to hyper-activation of the FA pathway, revealing its role in the recovery of stalled forks where origins are limited. Indeed, disruption of the FA pathway in Mcm4chaos3/chaos3 mice led to high perinatal lethality and accelerated tumor formation. Finally, we use the first Helq mutant mouse model to show that Helq works in parallel to the FA pathway to promote chromosome stability.
DNA replication is continually impeded by endogenous lesions that cause the stalling of replication forks. This threatens the integrity of the genome and may drive cancer development. Cells possess many mechanisms by which to deal with stalled forks including dormant (backup) origins, the Fanconi anemia pathway and the DNA helicase HELQ. However, their precise functions remained unclear. This book brings together multiple studies to shed light on how these mechanisms guard the genome. Using a unique mutant mouse model called Mcm4chaos3 exhibiting a decreased number of dormant origins, we provide evidence that origin-poor regions of the genome cannot finish replication until early M phase (or not all), leading to multiple forms of chromosome instability. A lack of dormant origins also leads to hyper-activation of the FA pathway, revealing its role in the recovery of stalled forks where origins are limited. Indeed, disruption of the FA pathway in Mcm4chaos3/chaos3 mice led to high perinatal lethality and accelerated tumor formation. Finally, we use the first Helq mutant mouse model to show that Helq works in parallel to the FA pathway to promote chromosome stability.
3
How dormant origins, the FA pathway and HELQ promote genome stability
~EN PB NW
ISBN: 9783659622236 bzw. 3659622230, vermutlich in Englisch, LAP Lambert Academic Publishing, Taschenbuch, neu.
Lieferung aus: Deutschland, Versandkostenfrei.
How dormant origins, the FA pathway and HELQ promote genome stability: DNA replication is continually impeded by endogenous lesions that cause the stalling of replication forks. This threatens the integrity of the genome and may drive cancer development. Cells possess many mechanisms by which to deal with stalled forks including dormant (backup) origins, the Fanconi anemia pathway and the DNA helicase HELQ. However, their precise functions remained unclear. This book brings together multiple studies to shed light on how these mechanisms guard the genome. Using a unique mutant mouse model called Mcm4chaos3 exhibiting a decreased number of dormant origins, we provide evidence that origin-poor regions of the genome cannot finish replication until early M phase (or not all), leading to multiple forms of chromosome instability. A lack of dormant origins also leads to hyper-activation of the FA pathway, revealing its role in the recovery of stalled forks where origins are limited. Indeed, disruption of the FA pathway in Mcm4chaos3/chaos3 mice led to high perinatal lethality and accelerated tumor formation. Finally, we use the first Helq mutant mouse model to show that Helq works in parallel to the FA pathway to promote chromosome stability. Englisch, Taschenbuch.
How dormant origins, the FA pathway and HELQ promote genome stability: DNA replication is continually impeded by endogenous lesions that cause the stalling of replication forks. This threatens the integrity of the genome and may drive cancer development. Cells possess many mechanisms by which to deal with stalled forks including dormant (backup) origins, the Fanconi anemia pathway and the DNA helicase HELQ. However, their precise functions remained unclear. This book brings together multiple studies to shed light on how these mechanisms guard the genome. Using a unique mutant mouse model called Mcm4chaos3 exhibiting a decreased number of dormant origins, we provide evidence that origin-poor regions of the genome cannot finish replication until early M phase (or not all), leading to multiple forms of chromosome instability. A lack of dormant origins also leads to hyper-activation of the FA pathway, revealing its role in the recovery of stalled forks where origins are limited. Indeed, disruption of the FA pathway in Mcm4chaos3/chaos3 mice led to high perinatal lethality and accelerated tumor formation. Finally, we use the first Helq mutant mouse model to show that Helq works in parallel to the FA pathway to promote chromosome stability. Englisch, Taschenbuch.
4
How dormant origins, the FA pathway and HELQ promote genome stability (2014)
~EN PB NW
ISBN: 9783659622236 bzw. 3659622230, vermutlich in Englisch, 288 Seiten, LAP Lambert Academic Publishing, Taschenbuch, neu.
Lieferung aus: Deutschland, Versandkosten nach: Deutschland, Versandkostenfrei.
Von Händler/Antiquariat, Syndikat Buchdienst, [4235284].
DNA replication is continually impeded by endogenous lesions that cause the stalling of replication forks. This threatens the integrity of the genome and may drive cancer development. Cells possess many mechanisms by which to deal with stalled forks including dormant (backup) origins, the Fanconi anemia pathway and the DNA helicase HELQ. However, their precise functions remained unclear. This book brings together multiple studies to shed light on how these mechanisms guard the genome. Using a unique mutant mouse model called Mcm4chaos3 exhibiting a decreased number of dormant origins, we provide evidence that origin-poor regions of the genome cannot finish replication until early M phase (or not all), leading to multiple forms of chromosome instability. A lack of dormant origins also leads to hyper-activation of the FA pathway, revealing its role in the recovery of stalled forks where origins are limited. Indeed, disruption of the FA pathway in Mcm4chaos3/chaos3 mice led to high perinatal lethality and accelerated tumor formation. Finally, we use the first Helq mutant mouse model to show that Helq works in parallel to the FA pathway to promote chromosome stability. 2014, Taschenbuch / Paperback, Neuware, H: 220mm, B: 150mm, 288, Internationaler Versand, Selbstabholung und Barzahlung, PayPal, offene Rechnung, Banküberweisung.
Von Händler/Antiquariat, Syndikat Buchdienst, [4235284].
DNA replication is continually impeded by endogenous lesions that cause the stalling of replication forks. This threatens the integrity of the genome and may drive cancer development. Cells possess many mechanisms by which to deal with stalled forks including dormant (backup) origins, the Fanconi anemia pathway and the DNA helicase HELQ. However, their precise functions remained unclear. This book brings together multiple studies to shed light on how these mechanisms guard the genome. Using a unique mutant mouse model called Mcm4chaos3 exhibiting a decreased number of dormant origins, we provide evidence that origin-poor regions of the genome cannot finish replication until early M phase (or not all), leading to multiple forms of chromosome instability. A lack of dormant origins also leads to hyper-activation of the FA pathway, revealing its role in the recovery of stalled forks where origins are limited. Indeed, disruption of the FA pathway in Mcm4chaos3/chaos3 mice led to high perinatal lethality and accelerated tumor formation. Finally, we use the first Helq mutant mouse model to show that Helq works in parallel to the FA pathway to promote chromosome stability. 2014, Taschenbuch / Paperback, Neuware, H: 220mm, B: 150mm, 288, Internationaler Versand, Selbstabholung und Barzahlung, PayPal, offene Rechnung, Banküberweisung.
5
Symbolbild
How dormant origins, the FA pathway and HELQ promote genome stability
~EN PB NW
ISBN: 9783659622236 bzw. 3659622230, vermutlich in Englisch, 288 Seiten, LAP Lambert Academic Publishing, Taschenbuch, neu.
Lieferung aus: Deutschland, Versandkosten nach: Deutschland, Versandkostenfrei.
Von Händler/Antiquariat, AHA-BUCH GmbH, [4009276].
Neuware - DNA replication is continually impeded by endogenous lesions that cause the stalling of replication forks. This threatens the integrity of the genome and may drive cancer development. Cells possess many mechanisms by which to deal with stalled forks including dormant (backup) origins, the Fanconi anemia pathway and the DNA helicase HELQ. However, their precise functions remained unclear. This book brings together multiple studies to shed light on how these mechanisms guard the genome. Using a unique mutant mouse model called Mcm4chaos3 exhibiting a decreased number of dormant origins, we provide evidence that origin-poor regions of the genome cannot finish replication until early M phase (or not all), leading to multiple forms of chromosome instability. A lack of dormant origins also leads to hyper-activation of the FA pathway, revealing its role in the recovery of stalled forks where origins are limited. Indeed, disruption of the FA pathway in Mcm4chaos3/chaos3 mice led to high perinatal lethality and accelerated tumor formation. Finally, we use the first Helq mutant mouse model to show that Helq works in parallel to the FA pathway to promote chromosome stability. -, Taschenbuch, Neuware, 220x150x mm, 288, Internationaler Versand, PayPal, Kreditkarte, offene Rechnung, Banküberweisung, offene Rechnung (Vorkasse vorbehalten).
Von Händler/Antiquariat, AHA-BUCH GmbH, [4009276].
Neuware - DNA replication is continually impeded by endogenous lesions that cause the stalling of replication forks. This threatens the integrity of the genome and may drive cancer development. Cells possess many mechanisms by which to deal with stalled forks including dormant (backup) origins, the Fanconi anemia pathway and the DNA helicase HELQ. However, their precise functions remained unclear. This book brings together multiple studies to shed light on how these mechanisms guard the genome. Using a unique mutant mouse model called Mcm4chaos3 exhibiting a decreased number of dormant origins, we provide evidence that origin-poor regions of the genome cannot finish replication until early M phase (or not all), leading to multiple forms of chromosome instability. A lack of dormant origins also leads to hyper-activation of the FA pathway, revealing its role in the recovery of stalled forks where origins are limited. Indeed, disruption of the FA pathway in Mcm4chaos3/chaos3 mice led to high perinatal lethality and accelerated tumor formation. Finally, we use the first Helq mutant mouse model to show that Helq works in parallel to the FA pathway to promote chromosome stability. -, Taschenbuch, Neuware, 220x150x mm, 288, Internationaler Versand, PayPal, Kreditkarte, offene Rechnung, Banküberweisung, offene Rechnung (Vorkasse vorbehalten).
6
How dormant origins, the FA pathway and HELQ promote genome stability (2014)
EN PB NW
ISBN: 9783659622236 bzw. 3659622230, in Englisch, Lap Lambert Academic Publishing, Taschenbuch, neu.
Lieferung aus: Deutschland, Versandfertig in 1 - 2 Werktagen, Versandkostenfrei. Tatsächliche Versandkosten können abweichen.
Von Händler/Antiquariat, M & L aus Deutschland.
Die Beschreibung dieses Angebotes ist von geringer Qualität oder in einer Fremdsprache. Trotzdem anzeigen
Von Händler/Antiquariat, M & L aus Deutschland.
Die Beschreibung dieses Angebotes ist von geringer Qualität oder in einer Fremdsprache. Trotzdem anzeigen
7
How dormant origins the FA pathway and HELQ promote genome stability (2014)
DE NW
ISBN: 9783659622236 bzw. 3659622230, in Deutsch, LAP Lambert Academic Publishing, neu.
Lieferung aus: Deutschland, Versandkostenfrei.
Magazin Aziya, [3458207].
Die Beschreibung dieses Angebotes ist von geringer Qualität oder in einer Fremdsprache. Trotzdem anzeigen
Magazin Aziya, [3458207].
Die Beschreibung dieses Angebotes ist von geringer Qualität oder in einer Fremdsprache. Trotzdem anzeigen
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