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pro vyhledávání: ''
Autor:
Marius Hedtfeld, Andrea Musacchio, Tanja Bange, Stefano Maffini, Arsen Petrovic, Marion E. Pesenti, Priyanka Singh, Anupallavi Srinivasamani, Sara Carmignani
Publikováno v:
Molecular Cell
Summary Reflecting its pleiotropic functions, Polo-like kinase 1 (PLK1) localizes to various sub-cellular structures during mitosis. At kinetochores, PLK1 contributes to microtubule attachments and mitotic checkpoint signaling. Previous studies ident
Autor:
Stephanie Munk, Mark G. Frattini, Amnon Koren, Jesper V. Olsen, Camille Gelot, Ruth Santos, Kelly A. George, Yoshitaka Kawasoe, Tatsuro S. Takahashi, Prasad V. Jallepalli, Steven A. McCarroll, Mathew J. K. Jones
Publikováno v:
Mol Cell
Jones, M J K, Gelot, C, Munk, S, Koren, A, Kawasoe, Y, George, K A, Santos, R E, Olsen, J V, McCarroll, S A, Frattini, M G, Takahashi, T S & Jallepalli, P V 2021, ' Human DDK rescues stalled forks and counteracts checkpoint inhibition at unfired origins to complete DNA replication ', Molecular Cell, vol. 81, no. 3, pp. 426-441.e8 . https://doi.org/10.1016/j.molcel.2021.01.004
Jones, M J K, Gelot, C, Munk, S, Koren, A, Kawasoe, Y, George, K A, Santos, R E, Olsen, J V, McCarroll, S A, Frattini, M G, Takahashi, T S & Jallepalli, P V 2021, ' Human DDK rescues stalled forks and counteracts checkpoint inhibition at unfired origins to complete DNA replication ', Molecular Cell, vol. 81, no. 3, pp. 426-441.e8 . https://doi.org/10.1016/j.molcel.2021.01.004
Eukaryotic genomes replicate via spatially and temporally regulated origin firing. Cyclin-dependent kinase (CDK) and Dbf4-dependent kinase (DDK) promote origin firing, whereas the S phase checkpoint limits firing to prevent nucleotide and RPA exhaust
Autor:
Kyosuke Nakamura, Constance Alabert, Moritz Völker-Albert, Chunaram Choudhary, Shankha Satpathy, Axel Imhof, Georg Kustatscher, Niels Mailand, Ignasi Forné, Martina Hödl, Tracey E. Beyer, Anja Groth, Juri Rappsilber
Publikováno v:
Molecular Cell
Nakamura, K, Kustatscher, G, Alabert, C, Hödl, M, Forne, I, Völker-Albert, M, Satpathy, S, Beyer, T E, Mailand, N, Choudhary, C, Imhof, A, Rappsilber, J & Groth, A 2021, ' Proteome dynamics at broken replication forks reveal a distinct ATM-directed repair response suppressing DNA double-strand break ubiquitination ', Molecular Cell, vol. 81, no. 3 . https://doi.org/10.1016/j.molcel.2020.12.025
Nakamura, K, Kustatscher, G, Alabert, C, Hödl, M, Forne, I, Völker-Albert, M, Satpathy, S, Beyer, T E, Mailand, N, Choudhary, C, Imhof, A, Rappsilber, J & Groth, A 2021, ' Proteome dynamics at broken replication forks reveal a distinct ATM-directed repair response suppressing DNA double-strand break ubiquitination ', Molecular Cell, vol. 81, no. 5, pp. P1084-1099.E6 . https://doi.org/10.1016/j.molcel.2020.12.025
Nakamura, K, Kustatscher, G, Alabert, C, Hödl, M, Forne, I, Völker-Albert, M, Satpathy, S, Beyer, T E, Mailand, N, Choudhary, C, Imhof, A, Rappsilber, J & Groth, A 2021, ' Proteome dynamics at broken replication forks reveal a distinct ATM-directed repair response suppressing DNA double-strand break ubiquitination ', Molecular Cell, vol. 81, no. 3 . https://doi.org/10.1016/j.molcel.2020.12.025
Nakamura, K, Kustatscher, G, Alabert, C, Hödl, M, Forne, I, Völker-Albert, M, Satpathy, S, Beyer, T E, Mailand, N, Choudhary, C, Imhof, A, Rappsilber, J & Groth, A 2021, ' Proteome dynamics at broken replication forks reveal a distinct ATM-directed repair response suppressing DNA double-strand break ubiquitination ', Molecular Cell, vol. 81, no. 5, pp. P1084-1099.E6 . https://doi.org/10.1016/j.molcel.2020.12.025
Summary Cells have evolved an elaborate DNA repair network to ensure complete and accurate DNA replication. Defects in these repair machineries can fuel genome instability and drive carcinogenesis while creating vulnerabilities that may be exploited
Autor:
Mark R. Bray, Tak W. Mak, Jacqueline M. Mason, Heiko Blaser, Kelsie L. Thu, Carmen Dominguez-Brauer
Publikováno v:
Molecular Cell. 60(4):524-536
The cell cycle is an evolutionarily conserved process necessary for mammalian cell growth and development. Because cell-cycle aberrations are a hallmark of cancer, this process has been the target of anti-cancer therapeutics for decades. However, des
Publikováno v:
Molecular Cell. 60:7-20
Damaged mitochondria are detrimental to cellular homeostasis. One mechanism for removal of damaged mitochondria involves the PINK1-PARKIN pathway, which poly-ubiquitylates damaged mitochondria to promote mitophagy. We report that assembly of ubiquiti
Publikováno v:
Molecular Cell. 56(4):595-607
Oncogenic mutations in PIK3CA, the gene encoding the catalytic subunit of phosphoinositide 3-kinase (PI 3-K), occur with high frequency in breast cancer. The protein kinase Akt is considered to be the primary effector of PIK3CA, although mechanisms b
Autor:
Junbin Qian, Pascual Sanz, Gerd Van der Hoeven, Miguel López de Heredia, Mathieu Bollen, Monique Beullens, Maria Giulia Manzione, Maria Adelaida Garcia-Gimeno, Juan Carlos Igual, Lendert Gelens
Publikováno v:
Molecular cell. 68(4)
The spindle assembly checkpoint (SAC) generates a diffusible protein complex that prevents anaphase until all chromosomes are properly attached to spindle microtubules. A key step in SAC initiation is the recruitment of MAD1 to kinetochores, which is
Publikováno v:
ResearcherID
As cells enter mitosis, the two centrosomes separate and grow dramatically, each forming a nascent spindle pole that nucleates a radial array of microtubules. Centrosome growth (and associated microtubule nucleation surge), termed maturation, involve
Autor:
Christopher R. Vakoc, Junwei Shi
Publikováno v:
Molecular Cell. 54:728-736
The bromodomain and extra-terminal (BET) protein Brd4 recruits transcriptional regulatory complexes to acetylated chromatin. While Brd4 is considered to be a general transcriptional regulator, pharmacological inhibition of BET proteins shows therapeu
Publikováno v:
Molecular Cell. 52(5):734-745
Summary The mitosis-specific phosphorylation of histone H3 at Thr3 (H3T3ph) plays an important role in chromosome segregation by recruiting Aurora B. H3T3 phosphorylation is catalyzed by Haspin, an atypical protein kinase whose kinase domain is intri