نتایج جستجو برای: keywords chk2

تعداد نتایج: 1978979  

Journal: :The EMBO journal 2006
Antony W Oliver Angela Paul Katherine J Boxall S Elaine Barrie G Wynne Aherne Michelle D Garrett Sibylle Mittnacht Laurence H Pearl

The protein kinase Chk2 (checkpoint kinase 2) is a major effector of the replication checkpoint. Chk2 activation is initiated by phosphorylation of Thr68, in the serine-glutamine/threonine-glutamine cluster domain (SCD), by ATM. The phosphorylated SCD-segment binds to the FHA domain of a second Chk2 molecule, promoting dimerisation of the protein and triggering phosphorylation of the activation...

Journal: :Genetics 2003
Nisrine Masrouha Long Yang Sirine Hijal Stéphane Larochelle Beat Suter

Cell cycle checkpoints are signal transduction pathways that control the order and timing of cell cycle transitions, ensuring that critical events are completed before the occurrence of the next cell cycle transition. The Chk2 family of kinases is known to play a central role in mediating the cellular responses to DNA damage or DNA replication blocks in various organisms. Here we show through a...

Journal: :The Journal of biological chemistry 2000
B B Zhou P Chaturvedi K Spring S P Scott R A Johanson R Mishra M R Mattern J D Winkler K K Khanna

Recent evidence indicates that arrest of mammalian cells at the G(2)/M checkpoint involves inactivation and translocation of Cdc25C, which is mediated by phosphorylation of Cdc25C on serine 216. Data obtained with a phospho-specific antibody against serine 216 suggest that activation of the DNA damage checkpoint is accompanied by an increase in serine 216 phosphorylated Cdc25C in the nucleus af...

2011
Samah El Ghamrasni Ashwin Pamidi Marie Jo Halaby Miyuki Bohgaki Renato Cardoso Li Li Shriram Venkatesan Swaminathan Sethu Atsushi Hirao Tak W. Mak Manoor Prakash Hande Anne Hakem Razqallah Hakem

Chk2 is an effector kinase important for the activation of cell cycle checkpoints, p53, and apoptosis in response to DNA damage. Mus81 is required for the restart of stalled replication forks and for genomic integrity. Mus81(Δex3-4/Δex3-4) mice have increased cancer susceptibility that is exacerbated by p53 inactivation. In this study, we demonstrate that Chk2 inactivation impairs the developme...

Journal: :Community Literacy Journal 2012

Journal: :Osnabrücker Studien zur jüdischen und christlichen Bibel 2023

Free AccessImportant Keywordshttps://doi.org/10.14220/9783737013444.259SectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinkedInRedditEmail About Previous chapter Next FiguresReferencesRelatedDetails Download book coverOsnabrücker Studien zur Jüdischen und Christlichen Bibel.Volume 8 1st editionISBN: 978-3-8471-1344-7 eISBN: 978-3-7370-1344-4Hi...

Journal: :Human molecular genetics 2010
Kanae Iijima-Ando LiJuan Zhao Anthony Gatt Christopher Shenton Koichi Iijima

Hyperphosphorylation of the microtubule associated protein tau is detected in the brains of individuals with a range of neurodegenerative diseases including Alzheimer's disease (AD). An imbalance in phosphorylation and/or dephosphorylation of tau at disease-related sites has been suggested to initiate the abnormal metabolism and toxicity of tau in disease pathogenesis. However, the mechanisms u...

Journal: :The EMBO journal 2010
Hiroyuki Niida Kazuhiro Murata Midori Shimada Kumiko Ogawa Kumiko Ohta Kyoko Suzuki Hidetsugu Fujigaki Aik Kia Khaw Birendranath Banerjee M Prakash Hande Tomomi Miyamoto Ichiro Miyoshi Tomoyuki Shirai Noboru Motoyama Mireille Delhase Ettore Appella Makoto Nakanishi

Although the linkage of Chk1 and Chk2 to important cancer signalling suggests that these kinases have functions as tumour suppressors, neither Chk1+/- nor Chk2-/- mice show a predisposition to cancer under unperturbed conditions. We show here that Chk1+/-Chk2-/- and Chk1+/-Chk2+/- mice have a progressive cancer-prone phenotype. Deletion of a single Chk1 allele compromises G2/M checkpoint functi...

Journal: :Cancer research 2000
J Y Ahn J K Schwarz H Piwnica-Worms C E Canman

Eukaryotic cells activate an evolutionarily conserved set of proteins that rapidly induce cell cycle arrest to prevent replication or segregation of damaged DNA before repair is completed. In response to ionizing radiation (IR), the cell cycle checkpoint kinase, Chk2 (hCds1), is phosphorylated and activated in an ataxia telangiectasia mutated (ATM)-dependent manner. Here we show that the ATM pr...

2010
Xin Guo Michael D. Ward Jessica B. Tiedebohl Yvonne M. Oden Julius O. Nyalwidhe O. John Semmes

Chk2 is a critical regulator of the cellular DNA damage repair response. Activation of Chk2 in response to IR-induced damage is initiated by phosphorylation of the Chk2 SQ/TQ cluster domain at Ser(19), Ser(33), Ser(35), and Thr(68). This precedes autophosphorylation of Thr(383)/Thr(387) in the T-loop region of the kinase domain an event that is a prerequisite for efficient kinase activity. We c...

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